bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects of cocaine on plasma catecholamine and muscle glycogen concentrations during exercise in the rat
Authors: Conlee R. K. , Barnett D. W. , Kelly K. P. , Han D. H.
Published: December 2017

This study was designed to test the hypothesis that cocaine (C) alters the normal physiological responses to exercise. Male rats were injected with saline (S) or C (12.5 mg/kg) either intravenously (iv) or intraperitoneally (ip). After injection the animals were allowed to rest for 30 min or were run on the treadmill (26 m/min, 10% grade). At rest plasma epinephrine values were 245 +/- 24 pg/ml in the S group and 411 +/- 43 (ip) and 612 +/- 41 (iv) pg/ml in the C groups (P less than 0.05 between S and C). During exercise plasma epinephrine levels were 615 +/- 32 pg/ml in S and 1,316 +/- 58 (ip) and 1,208 +/- 37 (iv) pg/ml in the C groups (P less than 0.05 between S and C). Similar results were obtained for norepinephrine. Glycogen content in the white vastus lateralis muscle was reduced to 31 +/- 2 mumol/g in S after exercise, but after C and exercise the values were 12 +/- 4 (ip) and 16 +/- 3 (iv) mumol/g (P less than 0.05 between S and C). There was no effect of the drug on this parameter at rest. Blood lactate rose to 4.8 +/- 1.0 (ip) and 5.8 +/- 1.3 (iv) mM in the C groups but to only 3.0 +/- 0.2 in the S group after exercise (P less than 0.05 between S and C). These results show that C and exercise combined exert a more dramatic effect on plasma catecholamine, muscle glycogen, and blood lactate concentrations than do C and exercise alone. They provide further insight into explaining the adverse effects of C on exercise endurance observed previously (Bracken et al., J. Appl. Physiol. 66: 377-383, 1989).
Effects of prior exercise on the thermic effect of glucose and fructose
Authors: Balon T. W. , Welk G. J.
Published: December 2017

It has been previously observed that the thermic effect of a glucose load is potentiated by prior exercise. To determine whether this phenomenon is observed when different carbohydrates are used and to ascertain the role of insulin, the thermic effects of fructose and glucose were compared during control (rest) and postexercise trials. Six male subjects ingested 100 g fructose or glucose at rest or after recovery from 45 min of treadmill exercise at 70% of maximal O2 consumption. Measurements of O2 consumption, respiratory exchange ratio, and plasma concentrations of glucose, insulin, glycerol, and lactate were measured for 3 h postingestion. Although glucose and fructose increased net energy expenditure by 44 and 51 kcal, respectively, over baseline during control trials, exercise increased the thermic effect of both carbohydrate challenges an additional 20-25 kcal (P less than 0.05). Glucose ingestion was associated with large (P less than 0.05) increases in plasma insulin concentration during control and exercise trials, in contrast to fructose ingestion. Because fructose, which is primarily metabolized by liver, and glucose elicited a similar postexercise potentiation of thermogenesis, the results indicate that the thermogenic phenomenon is not limited to skeletal muscle. These results also demonstrate that carbohydrate-induced postexercise thermogenesis is not related to an incremental increase in plasma insulin concentration.
Extracellular potassium homeostasis in the cat medulla during progressive brain hypoxia
Authors: Melton J. E. , Chae L. O. , Neubauer J. A. , Edelman N. H.
Published: December 2017

Brain extracellular potassium [( K+]ec) in the ventral respiratory group of the medulla and the phrenic neurogram were recorded in anesthetized vagotomized peripherally chemodenervated ventilated cats during progressive isocapnic carbon monoxide (CO) hypoxia. During hypoxia, the phrenic neurogram was progressively depressed and became silent when arterial O2 content (CaO2) was reduced by 62 +/- 3% (SE). Gasping was seen in the phrenic neurogram when CaO2 was reduced by 78 +/- 1%. Medullary [K+]ec, an indicator of energy production failure due to O2 insufficiency, was 3.2 +/- 0.4 mM before hypoxia and was statistically unchanged at the onset of phrenic apnea during CO hypoxia (4 +/- 0.7 mM). By the onset of gasping, [K+]ec had increased to 6.1 +/- 1 mM, a value that tended to be different from control (P less than 0.1). After initiation of gasping, the rate of rise of [K+]ec increased, and [K+]ec reached a maximum value of 14.3 +/- 2.7 mM before hypoxia was terminated. With reoxygenation, [K+]ec returned to control levels within 20 min. On the basis of these results, we have drawn two major conclusions. 1) Hypoxic depression to the point of phrenic apnea does not appear to be caused by medullary energy insufficiency as measured by loss of [K+]ec homeostasis. 2) The rapid rise in [K+]ec in the medulla that characterizes severe hypoxia is closely associated with the onset of gasping in the phrenic neurogram, suggesting that gasping may serve as a marker for loss of medullary ionic homeostasis and thus onset of medullary energy insufficiency during hypoxia.
Endurance training increased HDL cholesteryl ester metabolism in rats
Authors: Pels A. E. , Terpstra A. H. , White T. P.
Published: December 2017

We studied the effects of endurance training on the metabolism of high-density lipoprotein (HDL, 1.063 less than density less than 1.15 kg/l) cholesteryl ester and proteins in rats fed a cholesterol-rich (1%) semipurified diet. The HDL were labeled with 131I in the apoproteins and with cholesteryl-[1-14C]oleate in the esters. The HDL were intravenously administered to endurance-trained (n = 10) and cage-sedentary (n = 10) rats. Blood samples were taken over the next 36 h while the rats were conscious and feeding. The trained rats had higher plasma HDL cholesterol (0.72 vs. 0.28 mM) and HDL apoprotein (461 vs. 267 mg/l) concentrations than the sedentary rats. The production or disposal rate of HDL cholesteryl ester was higher in the trained rats (1.36 mumol/h) than in the sedentary rats (0.72 mumol/h), whereas the production or disposal rate of HDL apoproteins was similar in the trained (0.64 mg/h) and sedentary (0.60 mg/h) rats. The residence time of the HDL cholesteryl esters (4.72 +/- 0.22 vs. 3.37 +/- 0.21 h) and HDL apoprotein (7.65 +/- 0.36 vs. 4.55 +/- 0.28 h) was longer for the trained than for the sedentary rats. These data indicate that endurance training resulted in a significant change in the metabolism of HDL cholesteryl esters and apoproteins as well as an increase in their concentrations.
Umbilical cord occlusion stimulates breathing independent of blood gases and pH
Authors: Adamson S. L. , Kuipers I. M. , Olson D. M.
Published: December 2017

The role of umbilical cord occlusion in the initiation of breathing at birth was investigated by use of 16 unanesthetized fetal sheep near full term. Artificial ventilation with high-frequency oscillation was used to control fetal arterial blood gas tensions. At baseline, PCO2 was maintained at control fetal values and PO2 was elevated to between 25 and 50 Torr. In the first study on six intact and four vagotomized fetuses, arterial PCO2 and PO2 were maintained constant during two 30-min periods of umbilical cord occlusion. Nevertheless, the mean fetal breathing rate increased significantly when the umbilical cord was occluded. In the second study on six intact fetuses, hypercapnia (68 Torr) was imposed by adding CO2 to the ventilation gas. When the umbilical cord was occluded, there was a significantly greater stimulation of breathing (rate, incidence, and amplitude) in response to hypercapnia than in response to hypercapnia alone. During cord occlusion, plasma prostaglandin E2 concentration decreased significantly. Results indicate that cord occlusion stimulates breathing possibly by causing the removal of a placentally produced respiratory inhibitor such as prostaglandin E2 from the circulation.
PET evaluation of pulmonary vascular permeability: a structure-function correlation
Authors: Velazquez M. , Weibel E. R. , Kuhn C. , Schuster D. P.
Published: December 2017

We compared regional measurements of the pulmonary transcapillary escape rate (rPTCER) for 68Ga-transferrin, obtained by positron emission tomography (PET), with morphometric data obtained from corresponding tissue samples in six anesthetized mechanically ventilated dogs, 1 h after oleic acid administration to either the left caudal lobe (0.015 ml/kg; Lobar group, n = 3) or the right atrium (0.08 ml/kg; Diffuse group, n = 3). Data were obtained from 48 regions in both injured and control lobes (right caudal lobes from the Lobar group). The volume density of edematous or hemorrhagic alveoli at the light-microscopic level was directly related to rPTCER (r = 0.82 for regions with rPTCER values less than 700 x 10(-4) min-1). Likewise, the relative surface of abnormal capillary endothelium and alveolar epithelium at the electron-microscopic level correlated well with rPTCER (r = 0.87 for regions with rPTCER less than 1,200 X 10(-4) min-1). We conclude that the rPTCER measurements obtained with PET reflect the morphological heterogeneity present in oleic acid-damaged lung tissue. Thus rPTCER measurements should be useful as a noninvasive quantitative index of lung injury. Furthermore, the tomographic image display of rPTCER may allow PET to be used as a "physiological probe" to guide tissue excision for later histological evaluation when lung injury is heterogeneous.
Respiratory-related recruitment of the masseter: response to hypercapnia and loading
Authors: Hollowell D. E. , Bhandary P. R. , Funsten A. W. , Suratt P. M.
Published: December 2017

To test the hypothesis that a muscle that closes the jaw, the masseter, can be recruited by ventilatory stimuli, we studied the electromyographic activation of the masseter and genioglossus in seven normal awake males who were exposed in random order to progressive hyperoxic hypercapnia, inspiratory threshold loading (-40 cmH2O), and combined hypercapnia and loading. With hypercapnia, the masseter was generally recruited after the genioglossus had been activated. Once recruited, activation of both muscles increased linearly with increasing CO2. Combined hypercapnia and loading produced more activation than either stimulus alone. These data indicate that the masseter is activated by ventilatory stimuli that activate the genioglossus. Earlier recruitment of the genioglossus suggests that activation of the masseter serves to stabilize the mandible and allow the genioglossus to function as a more efficient dilator of the upper airway.
Respiratory neuronal activity during apnea and other breathing patterns induced by laryngeal stimulation
Authors: Lawson E. E. , Richter D. W. , Czyzyk-Krzeska M. F. , Bischoff A. , Rudesill R. C.
Published: December 2017

Respiration cycles through three distinct phases (inspiration, postinspiration, and expiration) each having corresponding medullary cells that are excited during one phase and inhibited during the other two. Laryngeal stimulation is known to induce apnea in newborn animals, but the cellular mechanisms underlying this effect are not known. Intracellular recording of ventral respiratory group neurons was accomplished in intact anesthetized, paralyzed, and mechanically ventilated piglets. Apnea was induced by insufflation of the larynx with ammonia-saturated air, smoke, or water. Laryngeal insufflation induced phrenic nerve apnea, stimulation of postinspiratory neurons, and stable membrane potentials in inspiratory and expiratory cells consistent with postinspiratory inhibition. Usually the membrane potential of each neuronal type cycled through an expiratory level before onset of the first recovery breath. Variants of the apnea response, probably reflecting the aspiration reflex or sniffing, sneezing, coughing, and swallowing, were also observed. These latter patterns showed oscillation between inspiration and postinspiration without an apparent intervening stage II expiratory phase. However, stage II expiratory activity always preceded onset of the first ramp inspiration after such a pattern. These findings suggest that activation of postinspiratory mechanisms causes profound alterations in the respiratory pattern and that stage II expiration importantly modulates recovery of ramp inspiratory activity. The mechanism of this latter effect may be inhibition of early inspiratory neurons with consequent postinhibitory rebound.
Fractal perspectives in pulmonary physiology
Authors: McNamee J. E.
Published: December 2017

Like other organs that exchange substantial quantities of material with blood, the lung accommodates a large two-dimensional surface in a component three-dimensional volume. The lung's structure shows a resemblance to certain one- and two-dimensional mathematical functions that possess plane- and space-filling properties. When viewed from a conventional geometric perspective, many of the familiar forms and functions of pulmonary tissue appear to possess unusual qualities that defy explanation. Mathematically, they behave as though they had a fractional geometric dimension. This property is shared by a class of functions known as fractals. Fractals are described, and practical techniques are presented to measure the properties of the edges and surfaces of the lung. The consequences of fractal structure are also considered for the bronchial tree, pulmonary vasculature, and microcirculation. Insights arising from viewing the lung in this new perspective are summarized.
Enhanced exercise-induced rise of aldosterone and vasopressin preceding mountain sickness
Authors: Bartsch P. , Maggiorini M. , Schobersberger W. , Shaw S. , Rascher W. , Girard J. , Weidmann P. , Oelz O.
Published: December 2017

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4–7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Pentoxifylline does not attenuate acute lung injury in the absence of granulocytes
Authors: Yonemaru M. , Hatherill J. R. , Hoffmann H. , Zheng H. , Ishii K. , Raffin T. A.
Published: December 2017

Pentoxifylline (PTX), a methylxanthine, can suppress polymorphonuclear leukocyte (PMN) activation and attenuate sepsis-induced acute lung injury. We investigated whether PTX prevents non-PMN-dependent lung injury. First we studied four groups of granulocyte-depleted guinea pigs (control, PTX, Escherichia coli, and E. coli + PTX). Lung injury was assessed by wet-to-dry lung weight (W/D) ratio and lung tissue-to-plasma 125I-albumin ratio (albumin index, AI). The E. coli group showed a significant increase in the lung W/D ratio and AI compared with the control and PTX groups. However, PTX did not prevent the E. coli-induced increase in the lung W/D ratio and AI. Next we investigated the effects of PTX on endothelial cell monolayer permeability and adenosine 3′,5′-cyclic monophosphate (cAMP) levels. Whereas E. coli lipopolysaccharide (LPS) alone increased the endothelial permeability, PMNs added to the endothelial monolayers and exposed to LPS enhanced the increase. PTX attenuated the permeability increase mediated by LPS-exposed PMNs. PTX did not prevent the LPS-induced increase in permeability when PMNs were not present, although PTX increased endothelial cell cAMP levels. These data demonstrate that 1) PTX does not prevent lung injury in granulocyte-depleted guinea pigs; 2) PTX does not prevent LPS-induced increases in endothelial cell permeability, despite increased cAMP levels; and 3) PTX attenuates PMN-dependent increases in endothelial cell permeability.
Effect of triiodothyronine-induced thyrotoxicosis on airway hyperresponsiveness
Authors: Hollingsworth H. M. , Pratter M. R. , Dubois J. M. , Braverman L. E. , Irwin R. S.
Published: December 2017

To determine whether thyrotoxicosis has an effect on the asthmatic state in subjects with mild asthma, airway responsiveness, lung function, and exercise capacity were measured in a randomized double-blind placebo-controlled trial before and after liothyronine (triiodothyronine, T3)-induced thyrotoxicosis. Baseline evaluation of 15 subjects with mild asthma included clinical evaluation, thyroid and routine pulmonary function tests, airway responsiveness assessment by methacholine inhalation challenge, and a symptom-limited maximal exercise test. For all subjects, the initial testing revealed that the dose of methacholine which provoked a 20% fall in forced expiratory volume in 1s (PD20) was in a range consistent with symptomatic asthma. There was no significant change in pulmonary function tests, airway reactivity (PD20), or exercise capacity in either the placebo or the T3-treated groups. Thyroid function tests confirmed mild sustained thyrotoxicosis in the T3-treated groups. We conclude that mild T3-induced thyrotoxicosis of 4-wk duration had no effect on lung function, airway responsiveness, or exercise capacity in subjects with mild asthma.
Relationships between abdominal and diaphragmatic volume displacements
Authors: Knight H. , Petroll W. M. , Rochester D. F.
Published: December 2017

We investigated the relationship between the volumes displaced by the diaphragm and the abdominal wall during spontaneous breathing in supine anesthetized dogs. Diaphragmatic volume displacement (Vdi) was calculated from measurements taken from anteroposterior fluoroscopic images employing a previously described geometric model. The volume displacement of the abdominal wall (Vabd) was measured with a calibrated Respitrace. Shortening of single diaphragm muscle bundles in costal and crural regions was measured as the distance between radiopaque beads sutured to the peritoneal surface of the muscle. We found that Vdi always exceeded Vabd, but Vabd/Vdi was larger in animals in which the abdominal wall was more compliant. In this preparation, Vdi is better correlated with costal than with crural shortening. Vabd did not correlate with either costal or crural shortening. We infer that the difference between Vdi and Vabd reflects the volume displacement of the lower rib cage caused by diaphragm contraction. This volume difference was tightly correlated with costal shortening. We conclude from these data that coupling between Vdi and Vabd is influenced by the relative compliances of the chest wall and abdomen. Shortening of regions of the diaphragm may have variable relationships to the measured volume displacement, but costal shortening is intimately related to expansion of the lower rib cage.
Passive heat exposure leads to delayed increase in plasma levels of atrial natriuretic peptide in humans
Authors: Leppaluoto J. , Arjamaa O. , Vuolteenaho O. , Ruskoaho H.
Published: December 2017

The effects of passive heat exposure on atrial natriuretic peptide (ANP) were studied in six healthy men staying in a Finnish sauna at +92 degrees C for 20 min. Their rectal temperature increased by 0.4 degrees C, and evaporative water loss was 0.92 +/- 0.14 (SD) kg. Heart rate and systolic blood pressure increased significantly during the 20-min exposure. Serum osmolality and plasma arginine vasopressin levels increased during the exposure, then declined, and increased significantly again at 90–120 min. Plasma renin activity and aldosterone increased by two- to fourfold in 20 min. Plasma ANP levels rose from 13 +/- 7 to 39 +/- 15 ng/l at 60 min and to 41 +/- 13 ng/l at 120 min (P less than 0.01 for both). We conclude that transient increases in heart rate and systolic blood pressure or changes in blood volume as inferred from the weight loss do not contribute to the increased plasma ANP levels observed after the heat exposure. Instead, increased secretions of pressor hormones could explain the elevated plasma ANP levels observed after the thermal stress.
Lung edema formation following inhalation injury: role of the bronchial blood flow
Authors: Abdi S. , Herndon D. N. , Traber L. D. , Ashley K. D. , Stothert J. C. , Maguire J. , Butler R. , Traber D. L.
Published: December 2017

We investigated the contribution of the bronchial blood flow to the lung lymph flow (QL) and lung edema formation after inhalation injury in sheep (n = 18). The animals were equally divided into three groups and chronically prepared by implantation of cardiopulmonary catheters and a flow probe on the common bronchial artery. Groups 1 and 2 sheep were insufflated with 48 breaths of cotton smoke while group 3 received only room air. Just before injury, the bronchial artery of group 2 animals was occluded. The occlusion was maintained for the duration of the 24-h study period. At the end of the investigation, samples of lung were taken for determination of blood-free wet weight-to-dry weight ratio (W/D). Inhalation injury induced a sevenfold increase in QL in group 1 (7 +/- 1 to 50 +/- 9 ml/h; P less than 0.05) but only a threefold increase in group 2 (10 +/- 2 to 28 +/- 7 ml/h; P less than 0.05). The mean W/D value of group 1 animals was 23% higher than that of group 2 (5.1 +/- 0.4 vs. 3.9 +/- 0.2; P less than 0.05). Our data suggest that the bronchial circulation contributes to edema formation in the lung that is often seen after the acute lung injury with smoke inhalation.
Short-term potentiation of breathing in humans
Authors: Fregosi R. F.
Published: December 2017

The purpose of this study was to determine if the increase in ventilation induced by hypoxic stimulation of the carotid bodies (CB) persists after cessation of the stimulus in humans. I reasoned that a short-term potentiation (STP) of breathing, sometimes called an “afterdischarge,” could be unmasked by combining hypoxia with exercise, because ventilation increases synergistically under these conditions. Seven young healthy men performed mild bicycle exercise (30% peak power) while breathing O2 for 1.5 min (“control” state), and their CB were then stimulated by 1.5 min of hypoxic exercise (10% O2--balance N2). CB stimulation was then terminated by changing the inspirate back to O2 as exercise continued. Inspiratory and expiratory duration (TI and TE) and inspiratory flow and its time integral [tidal volume (VT)] were measured with a pneumotachometer. Inspired minute ventilation (VI) and mean inspiratory flow (VT/TI) declined exponentially after the cessation of CB stimulation, with first-order time constants of 28.6 +/- 6.7 and 24.6 +/- 1.6 (SD) s, respectively. The slow decay of VI was due primarily to potentiation of both TI and TE, although the effect on the latter predominated. Additional experiments in six subjects showed that brief intense CB stimulation with four to five breaths of N2 during mild exercise induced STP of similar magnitude to that observed in the hypoxic exercise experiments. Finally, the imposition of hyperoxia during air breathing exercise at a level of respiratory drive similar to that induced by the hypoxic exercise did not change VI significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of perfusate buffer capacity on capillary CO2-HCO3(-)-H+ reactions: theory
Authors: Bidani A. , Heming T. A.
Published: December 2017

The importance of perfusate nonbicarbonate buffer capacity (beta nonHCO3) to intracapillary CO2-HCO3(-)-H+ reactions was assessed by theoretical analysis of CO2 exchange in saline-perfused pulmonary capillaries. Time courses for perfusate PCO2, [HCO3-], and [H+] were computed for capillaries containing different activities of luminal vascular carbonic anhydrase and different amounts of perfusate nonbicarbonate buffers. Mobilization of perfusate HCO3- toward CO2 during capillary transit is determined by the availability of HCO3- and H+. A supply of protons from the nonbicarbonate buffer pool is necessary to maintain a high rate of HCO3- dehydration. The analyses indicate that beta nonHCO3 has marked nonlinear effects on transcapillary CO2 exchange and intravascular pH equilibration. These nonlinear effects differ from those previously computed for CO2 reactions in an open system because the present model system consists of a sequential combination of open (within capillary proper) and closed (within postcapillary vasculature) systems. The role of luminal vascular carbonic anhydrase in capillary CO2 reactions is strongly dependent on beta nonHCO3. Perfusate nonbicarbonate buffer capacity must be considered when the results of experimental studies of transcapillary CO2 exchange and/or intravascular pH equilibration are interpreted.
Internal carotid flow velocity with exercise before and after acclimatization to 4,300 m
Authors: Huang S. Y. , Tawney K. W. , Bender P. R. , Groves B. M. , McCullough R. E. , McCullough R. G. , Micco A. J. , Manco-Johnson M. , Cymerman A. , Greene E. R. , et al.
Published: December 2017

Cerebral blood flow and O2 delivery during exercise are important for well-being at altitude but have not been studied. We expected flow to increase on arrival at altitude and then to fall as O2 saturation and hemoglobin increased, thereby maintaining cerebral O2 delivery. We used Doppler ultrasound to measure internal carotid artery flow velocity at sea level and on Pikes Peak, CO (4,300 m). In an initial study (1987, n = 7 men) done to determine the effect of brief (5-min) exercises of increasing intensity, we found at sea level that velocity [24.8 +/- 1.4 (SE) cm/s rest] increased by 15 +/- 7, 30 +/- 6, and 22 +/- 8% for cycle exercises at 33, 71, and 96% of maximal O2 uptake, respectively. During acute hypobaric hypoxia in a decompression chamber (inspired PO2 = 83 Torr), velocity (23.2 +/- 1.4 cm/s rest) increased by 33 +/- 6, 20 +/- 5, and 17 +/- 9% for exercises at 45, 72, and 98% of maximal O2 uptake, respectively. After 18 days on Pikes Peak (inspired PO2 = 87 Torr), velocity (26.6 +/- 1.5 cm/s rest) did not increase with exercise. A subsequent study (1988, n = 7 men) of the effect of prolonged exercise (45 min at approximately 100 W) found at sea level that velocity (24.8 +/- 1.7 cm/s rest) increased by 22 +/- 6, 13 +/- 5, 17 +/- 4, and 12 +/- 3% at 5, 15, 30, and 45 min.(ABSTRACT TRUNCATED AT 250 WORDS)
Forearm vascular resistance increases during static exercise in heart transplant recipients
Authors: Morgan B. J. , DeBoer L. W. , Pease M. O. , Scherrer U. , Vissing S. F. , Hanson P.
Published: December 2017

In heart transplant recipients but not in normal humans, total peripheral vascular resistance increases during static exercise. To determine whether this augmented vasoconstriction limits the vasodilation normally seen in the nonexercising forearm, we measured arterial pressure, heart rate, and forearm blood flow during 30% maximal static handgrip in 9 heart transplant recipients and 10 control subjects. Handgrip evoked comparable increases in mean arterial pressure in the transplant recipients and control subjects (+19 +/- 2 vs. +20 +/- 2 mmHg). Heart rates increased by 14 +/- 3 beats/min in the control subjects but did not change in the transplant recipients. Directionally opposite patterns of forearm vascular resistance were observed in the two groups. In the control subjects, forearm resistance fell during handgrip (-8.8 +/- 1.9 units, P less than 0.05). In contrast, in the transplant recipients, forearm resistance rose during this intervention (+9.0 +/- 2.9 units, P less than 0.05). Thus the vasodilation that normally occurs in the nonexercising forearm during static handgrip is reversed in heart transplant recipients. Vasoconstriction in the forearm contributes to the increase in total peripheral resistance that occurs during static exercise in these individuals.
Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge
Authors: Fryer A. D. , Wills-Karp M.
Published: December 2017

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Heat stress and thermal dehydration: lactacidemia and plasma volume regulation
Authors: Zurovski Y. , Eckstein L. , Horowitz M.
Published: December 2017

This investigation was undertaken to study heat stress and dehydration effects on 1) plasma lactic acid (LA) concentration and 2) plasma LA effect on plasma volume conservation during thermal dehydration. Experiments were performed on conscious nonacclimated and heat-acclimated laboratory rats subjected to various levels of heat stress and/or dehydration (37–42 degrees C with and without drinking water). During the exposures, rectal temperature (Tre), plasma LA pyruvic acids, and hematocrit were measured. From these data, excess LA, indicative of anaerobic metabolism, was calculated. In separate experiments, transvascular protein efflux (half time of Evans blue-labeled albumin) was measured before and after plasma LA elevation, either by LA infusion or thermal dehydration. The results show that elevation of plasma LA was associated with a rise in Tre, with accelerated elevation within a Tre range of 41–42 degrees C. LA concentrations were similar for the same Tre in all experimental groups. In nonacclimated rats, this rise was accompanied by a significant rise in excess LA. In acclimated rats, only a minor rise in excess LA was observed. A positive correlation was found between plasma LA elevation and the increase in plasma protein efflux. It is concluded that there is a temperature threshold for the rise in plasma LA. In nonacclimated rats, local hypoxia may contribute to this rise. The data also suggest that, in nonacclimated rats, lactacidemia accelerates plasma protein and fluid loss, leading to circulatory failure during acute thermal dehydration.
Muscle carnitine after strenuous endurance exercise
Authors: Decombaz J. , Gmuender B. , Sierro G. , Cerretelli P.
Published: December 2017

The effect of very long endurance exercise on muscle carnitine was studied. Eighteen cross-country skiers took part in a race in the Alps (average inspired partial pressure of O2 100–110 Torr) that lasted on average 13 h 26 min. Carnitine intake, evaluated for 2 wk before the event, was 50 +/- 4 (SE) mg/day. Muscle (vastus lateralis) total carnitine concentration, measured twice with a 2-yr interval on eight rested subjects, did not change with time (17 vs. 16 mumol/g dry wt, NS) but showed consistent interindividual differences (range 12–22, P = 0.001) with no correlation with intake. After exercise, total muscle carnitine was unaltered (from 17.9 +/- 1.0 at rest to 18.3 +/- 0.8 mumol/g dry wt postexercise in the 15 subjects who completed the race, NS), but muscle free carnitine decreased 20% (from 14.9 +/- 0.8 mumol/g, P = 0.01) and short-chain acylcarnitine increased 108% (from 3.5 +/- 0.4 mumol/g, P = 0.01). These results suggest that carnitine deficiency will probably not result from strenuous aerobic exercise in trained subjects who consume a moderate amount of carnitine in their food.
Assessment of papain-induced lung injury in isolated lungs by measurements of aerosol deposition and mixing
Authors: Rosenthal F. S. , Wright S.
Published: December 2017

Aerosol bolus inspirations were used to assess lung injury in 15 isolated dog lungs exposed to low (0–375 units) or high doses (600–1,200 units) of papain. Effective air space size (EAD) was determined from aerosol deposition during a 5-s breath hold. Convective mixing was assessed by the spreading of the expired bolus with respect to expired volume, quantified by a coefficient of dispersion (CD) equal to the square root of the difference in the variances of the expired and inspired boluses divided by the volumetric penetration of the bolus. After exposure, CD measured with deeply penetrating boluses increased by an average of 2.5% in the low-exposure group (P greater than 0.05) and 28.0% in the high-exposure group (P less than 0.0001). CD measured with shallowly penetrating boluses decreased by 4.3% (P less than 0.0001) in the low-exposure group and increased by an average of 18.3% in the high-exposure group (P less than 0.05). Papain exposure caused EAD to increase in some lungs and decrease in others. For deep bolus penetrations, EAD changed by an average of -0.8% in the low-exposure group (P greater than 0.05) and +21.1% in the high-exposure group (P greater than 0.05). Both EAD and CD appeared to be sensitive to lung injury. However, changes in EAD were less consistent than those in CD, possibly due to changes caused by lung injury in the regional distribution of inspired aerosol.
Coronary and systemic vascular response to inspiratory resistive breathing
Authors: Peters J. , Ihle P.
Published: December 2017

To evaluate the coronary and systemic cardiovascular response to graded inspiratory resistive breathing, seven dogs were studied 2–4 wk after chronic instrumentation to measure circumflex coronary artery and ascending aortic blood flows as well as aortic and left ventricular (LV) blood pressures. The experiments were performed under chloralose anesthesia (to exclude any confounding emotional effects by dyspnea on cardiovascular variables) and hyperoxic conditions (to prevent chemoreflex activation by hypoxemia). In a randomized fashion, the dogs were subjected to graded inspiratory resistive breathing (spontaneous breathing alone and moderate and severe resistive loading, corresponding to resistances of approximately 0, 40, and 110 cmH2O.s.l-1, respectively). Each run lasted 10 min. Compared with mechanical ventilation with the respiratory muscles at rest, spontaneous breathing alone and moderate and severe inspiratory resistive loading induced pronounced and significant increases in circumflex coronary blood flow (19, 32, and 62%, respectively), which were almost exclusively accounted for by significant decrements in coronary vascular resistance and were paralleled (r = 0.88, P less than 0.0001) by significant increments (18, 31, and 57%) in heart rate transmural-aortic pressure product, an indicator of LV myocardial O2 demand. An increase in myocardial O2 consumption during resistive breathing was confirmed by analysis of coronary sinus blood samples in additional experiments (n = 3). Cardiac output significantly increased (10, 14, and 35%) because of increases in heart rate (15, 24, and 49%), with LV stroke volume and diastolic dimensions remaining unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Interpretation of EMG spectral alterations and alteration indexes at sustained contraction
Authors: Hagg G. M.
Published: December 2017

Alterations of the electromyographic power spectrum have been studied extensively to assess fatigue development in the neuromuscular system. Usually, a data reduction has been applied to create an index based on the mean power frequency or the median frequency. The physiological origin of the spectrum alterations has been (and to some extent still is) incompletely known. However, during the 1980s, substantial progress has been made in this field. The factors affecting the electromyographic power spectrum discussed in this review are action potential velocity decrease, firing statistics alterations, action potential modification, muscle temperature, additional recruitment at fatigue, and force level. Their impact on three commonly used fatigue indexes, mean power frequency, median frequency, and zero crossing rate, is also reviewed.
Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat
Authors: Tankersley C. G. , Nicholas W. C. , Deaver D. R. , Mikita D. , Kenney W. L.
Published: December 2017

Thermoregulatory, cardiovascular, and body fluid responses during exercise in the heat were tested in five middle-aged (48 +/- 2 yr) women before and after 14–23 days of estrogen replacement therapy (ERT). The heat and exercise challenge consisted of a 40-min rest period followed by semirecumbent cycle exercise (approximately 40% maximal O2 uptake) for 60 min. At rest, the ambient temperature was elevated from a thermoneutral (dry bulb temperature 25 degrees C; wet bulb temperature 17.5 degrees C) to a warm humid (dry bulb temperature 36 degrees C; wet bulb temperature 27.5 degrees C) environment. Esophageal (Tes) and rectal (Tre) temperatures were measured to estimate body core temperature while arm blood flow and sweating rate were measured to assess the heat loss response. Mean arterial pressure and heart rate were measured to evaluate the cardiovascular response. Blood samples were analyzed for hematocrit (Hct), hemoglobin ([Hb]), plasma 17 beta-estradiol (E2), progesterone (P4), protein, and electrolyte concentrations. Plasma [E2] was significantly (P < 0.05) elevated by ERT without affecting the plasma [P4] levels. After ERT, Tes and Tre were significantly (P < 0.05) depressed by approximately 0.5 degrees C, and the Tes threshold for the onset of arm blood flow and sweating rate was significantly (P < 0.05) lower during exercise. After ERT, heart rate during exercise was significantly lower (P < 0.05) without notable variation in mean arterial pressure. Isotonic hemodilution occurred with ERT evident by significant (P < 0.05) reductions in Hct and [Hb], whereas plasma tonicity remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Retrofacial lesions: effects on CO2-sensitive phrenic and sympathetic nerve activity
Authors: Nattie E. E. , Blanchford C. , Li A.
Published: December 2017

We made unilateral chemical (10- or 50-nl microinjections; 4.7 mM kainic acid) or electrolytic (5–15 mA; 15 s) lesions in a region of the rostral ventrolateral medulla (VLM) caudal to the retrotrapezoid nucleus in 10 decerebrate, paralyzed, vagotomized, and servo-ventilated cats. The lesions were 3.0–4.2 mm lateral to the midline, within 2 mm caudal to the facial nucleus, and within 2.5 mm of the VLM surface. Four control injections (mock cerebrospinal fluid and fluorescent beads alone) produced small and inconsistent effects over 3–5 h. The predominant effect of the lesions was a significant decrease in baseline integrated phrenic nerve amplitude (PNA) (apnea in 2 cases), total respiratory cycle duration, and the response to increased CO2 (slope < 15% of control in 3 cases). The respiratory-related peak amplitude of the integrated sympathetic signal, blood pressure, and the sympathetic nerve activity response to CO2 were also decreased after the majority of lesions. Not all lesions produced all effects, and some lesions resulted in increased PNA and respiratory cycle duration. The lesioned region appears functionally to represent a caudal extension of the retrotrapezoid nucleus containing neurons necessary for normal baseline PNA and CO2 sensitivity. In addition, it contains neurons involved in the determination of resting respiratory frequency and normal sympathetic activity and blood pressure. The pattern of mixed responses among animals suggests that a heterogeneity of function is present within a relatively small VLM region.
Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs
Authors: Kawada T. , Kambara K. , Arakawa M. , Segawa T. , Ando F. , Hirakawa S. , Emura S. , Shoumura S. , Isono H.
Published: December 2017

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.
A model of ventilatory instability induced in the unrestrained rat
Authors: Thomas A. J. , Austin W. , Friedman L. , Strohl K. P.
Published: December 2017

A classic conditioning paradigm was used to examine the hypothesis that perturbations during sleep in the neonate rat can have a lasting impact on breathing. During the first 4 wk of life, stimuli were presented to rats during behaviorally defined sleep. In a conditioned hypoxic (CH) group, brief periods of hypoxic gas were used as the unconditioned stimulus. Tactile and auditory stimuli were used as the conditioned stimuli. In a conditioned control (CC) group, air was used as the unconditioned stimulus. A third group of unconditioned control (UC) rats was not exposed to the conditioning paradigm. Animals were provided routine care for 3.5 mo; ventilation was then assessed using plethysmography. Conditioning during neonatal life produced increased ventilatory irregularities and apnea during behaviorally defined sleep in adult rats. Both CH and CC rats showed a significantly greater number of apneic events compared with UC rats. Over a 2-h sleep period, CH rats exhibited a total of 105.1 +/- 9.4 (SE) apneic events, CC rats 69.4 +/- 4.2 events, and UC rats 42.1 +/- 3.1 events [F(2,18) = 25.568; P < 0.0001]. These findings suggest that experiences in the first few weeks of life will alter ventilatory patterning in the adult animal.
Diaphragmatic microcirculation during halothane and isoflurane exposure in pentobarbital-anesthetized rats
Authors: Leon A. , Boczkowski J. , Dureuil B. , Vicaut E. , Aubier M. , Desmonts J. M.
Published: December 2017

We investigated the effects of halothane and isoflurane on diaphragmatic microcirculation in pentobarbital-anesthetized rats by in vivo video microscopy. After a baseline period, rats were randomly allocated into three groups according to administration of 0.5, 0.75, and 1 minimal alveolar concentration (MAC) of either halothane (group Hal, n = 16), isoflurane (group Iso, n = 14), or no halogenated agent (group C, n = 20) in three succeeding steps of 15 min. Mean arterial blood pressure (MAP), arteriolar diameters, and functional capillary density were analyzed in the last 3 min of each step. MAP remained unchanged in group C but decreased in a dose-dependent manner in both halogenated receiving groups. MAP was significantly lower in rats breathing Hal compared with those breathing Iso. Arterioles were classified in second (A2, n = 39), third (A3, n = 24), and fourth (A4, n = 30) order according to their relative location in the network. No changes in A2 and A3 diameters were noted in either group. A4 diameters remained unchanged in groups C and Iso, whereas a significant reduction was found in group Hal at 0.75 and 1 MAC exposure (P < 0.05 compared with baseline and with groups C and Iso, respectively). During Iso exposure, functional capillary density was not significantly different when compared with baseline and group C, whereas in group Hal it decreased significantly at 0.5, 0.75, and 1 MAC, amounting to 61.1 +/- 9, 30.7 +/- 10.3, and 22.8 +/- 6.3%, respectively, of baseline (P < 0.01 vs. baseline and P < 0.05 vs. groups Iso and C for 0.75 and 1 MAC).(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of acetazolamide on cerebral blood flow and capillary patency
Authors: Frankel H. M. , Garcia E. , Malik F. , Weiss J. K. , Weiss H. R.
Published: December 2017

This study investigated the effects 2 h after administration of acetazolamide on cerebral blood flow and the pattern of cerebral capillary perfusion. Arterial blood pressure, heart rate, arterial blood gases, and pH were recorded in two groups of rats along with either regional cerebral blood flow or the percentage of capillary volume per cubic millimeter and number per square millimeter perfused as determined in cortical, thalamic, pontine, and medullary regions of the brain. Blood pressure, heart rate, and arterial PCO2 were not significantly different between the rats receiving acetazolamide (100 mg/kg) and the controls. Arterial blood pH was significantly lower in the acetazolamide rats. Blood flow increased significantly in the cortical (+ 102%), thalamic (+ 89%), and pontine (+ 88%) regions receiving acetazolamide. In control rats, approximately 60% of the capillaries were perfused in all of the examined regions. The percentage of capillaries per square millimeter perfused was significantly greater in the cortical (+ 52%), thalamic (+ 49%), and pontine (+ 47%) regions of acetazolamide rats compared with controls. In the medulla the increases in blood flow and percentage of capillaries perfused were not significant. Thus in the regions that acetazolamide increased cerebral blood flow, it also increased the percentage of capillaries perfused.
Differential effects of long-term hypoxia on norepinephrine turnover in brain stem cell groups
Authors: Soulier V. , Cottet-Emard J. M. , Pequignot J. , Hanchin F. , Peyrin L. , Pequignot J. M.
Published: December 2017

The influence of long-term hypoxia on noradrenergic cell groups in the brain stem was assessed by estimating the changes in norepinephrine (NE) turnover in A1, A2 (subdivided into anterior and posterior parts), A5, and A6 groups in rats exposed to hypoxia (10% O2–90% N2) for 14 days. The NE turnover was decreased in A5 and A6 groups but failed to change significantly in A1. The NE turnover was increased in the posterior part of A2 and remained unaltered in the anterior part. In normoxic rats, the hypotensive drug dihydralazine induced a reverse effect, namely increased NE turnover in anterior A2 and no change in posterior A2. The neurochemical responses to hypoxia were abolished by transection of carotid sinus nerves. The results show that long-term hypoxia exerts differential effects on the noradrenergic cell groups located in the brain stem. Peripheral chemosensory inputs control the hypoxia-induced noradrenergic alterations. The A2 cell group displays a functional subdivision: the posterior part is influenced by peripheral chemosensory inputs, whereas the anterior part may be concerned with barosensitivity.