bluuebunny/crossref_metadata_2025 huggingface dataset:
Postural cardiovascular reflexes: comparison of responses of forearm and calf resistance vessels
Authors: Essandoh L. K. , Duprez D. A. , Shepherd J. T.
Published: December 2017

Simultaneous measurements were made of changes in vascular resistance in the forearm and calf in response to moving from supine to sitting or to head-down tilt. The subjects were healthy male volunteers, 21–63 yr. Blood flows were measured by venous occlusion plethysmography using mercury-in-Silastic strain-gauges. The gauges were maintained at the same level relative to the heart during the postural changes. Arterial blood pressure was measured by auscultation; heart rate was counted from the plethysmograms. Changing from supine to sitting caused a decrease in forearm blood flow from 4.13 +/- 0.14 to 2.16 +/- 0.19 ml.100 ml-1.min-1. Corresponding calf flows were 4.21 +/- 0.32 and 4.40 +/- 0.59 ml.100 ml-1.min-1. There was no change in mean arterial blood pressure, and heart rate increased by 8.0 +/- 1.5 beats/min. Arrest of the circulation of both legs with occlusion cuffs on the thighs before sitting, to prevent pooling of blood in them, reduced the degree of forearm vasoconstriction. Neck suction (40 Torr) during sitting, to oppose the decrease in transmural pressure at the carotid sinuses, inhibited the vasoconstriction. During a 30 degrees head-down tilt, there was a dilatation of forearm but not of calf resistance vessels. A Valsalva maneuver caused a similar constriction of both vascular beds. Thus, when changes in vascular resistance in forearm and calf are compared, the major reflex adjustments to changes in posture take place in the forearm.
Exercise-induced satellite cell activation in growing and mature skeletal muscle
Authors: Darr K. C. , Schultz E.
Published: December 2017

The time course and extent of satellite cell activation were studied in the soleus (m-SOL) and extensor digitorum longus (m-EDL) muscles of untrained growing and mature rats after a single bout of prolonged eccentric treadmill running. At 24, 48, 72, and 120 h postexercise, satellite cell mitotic activity was quantitated in autoradiographs of whole-fiber segments after injection of [3H]thymidine. Fiber damage and localization of labeled cells were also examined in muscle cross sections. Labeling in growing muscles progressively increased to peak levels (approximately 250% of control) at 72 h postexercise, whereas mature muscles exhibited an earlier peak (approximately 250% of control) at 24 (m-SOL) and 48 (m-EDL) h, followed by a more rapid decline to control levels by 120 h postexercise. In all exercised muscles the calculated satellite cell activation was far greater than required to repair the small number (less than 3.0%) of necrotic fibers identified at the light-microscopic level. These results suggest that satellite cells were activated not only on fibers exhibiting overt necrosis but also on those with lesions not discernible with light microscopy.
Effects of voluntary constraining of thoracic displacement during hypercapnia
Authors: Chonan T. , Mulholland M. B. , Cherniack N. S. , Altose M. D.
Published: December 2017

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.
Comparison of calibration methods for respiratory inductive plethysmography in infants
Authors: Revow M. D. , England S. J. , Stogryn H. A. , Wilkes D. L.
Published: December 2017

In infants under the age of 6 mo respiratory inductive plethysmograph (RIP)-calculated tidal volumes (VT) were compared with simultaneously measured volumes using a pneumotachograph (PNT) to 1) assess whether using multiple points (MP) along the inspiratory profile of a breath is superior to using only VT when calculating volume-motion (VM) coefficients, 2) verify the assumption of independent contributions of the abdomen and rib cage to VT, which was accomplished by extending the normal RIP model to include a term representing interaction between these two compartments, and 3) investigate whether VM coefficients are sleep-state dependent. Neither use of multiple points nor inclusion of the interacting term improved the performance of the RIP over that observed using a simple two-compartment model with VT measurements. However, VM coefficients obtained during quiet sleep (QS) were not reliable when used during rapid-eye-movement (REM) sleep, suggesting that coefficients obtained during one sleep state may not be applicable to another state where there is a substantial change in the relative abdominal/rib cage contributions to VT.
Antiarrhythmic agents diminish thiourea-induced pulmonary vascular protein leak in rats
Authors: Stelzner T. J. , Welsh C. H. , Berger E. , McCullough R. G. , Morris K. , Repine J. E. , Weil J. V.
Published: December 2017

Drugs possessing membrane stabilizing activity might act to diminish the augmented microvascular permeability resulting from acute lung injury. To test this rats were pretreated with quinidine, procainamide, or lidocaine and then given the lung injury-inducing agent thiourea. Vascular permeability, assessed as the extravascular accumulation of radiolabeled protein, was increased more than threefold by thiourea. This increase was diminished by 29, 34, and 43% after pretreatment with procainamide, quinidine, and lidocaine, respectively. Lidocaine also returned the thiourea-induced increase in lung wet weight-to-dry weight ratios to control levels. This protection was not likely due to hemodynamic effects of these agents, since no differences were noted in cardiac output between pretreated rats and those receiving thiourea alone and a small increase in mean pulmonary arterial pressure in the lidocaine-pretreatment group was the only difference noted. O2 metabolites have been implicated in the pathogenesis of thiourea-induced lung injury. None of these agents scavenged O2- or H2O2 directly, but quinidine and procainamide diminished in vitro neutrophil O2- and H2O2 production, and lidocaine inhibited neutrophil H2O2 production. However, neutropenia (PMN less than 100/ml) induced with either vinblastine or cyclophosphamide (Cytoxan) failed to prevent thiourea-induced increases in pulmonary vascular protein leak. In conclusion, procainamide, quinidine, and lidocaine diminished lung injury in rats after thiourea. Although these agents diminish PMN O2 metabolite production in vitro their salutary role in thiourea-induced lung injury appears to be through an unknown mechanism that is independent of their effects on neutrophil O2 metabolite-dependent toxicity.
Effects of temperature on cholinergic contractility of rabbit airway muscle
Authors: Bratton D. L. , Tanaka D. T. , Grunstein M. M.
Published: December 2017

To elucidate the mechanism underlying temperature-induced changes in airway cholinergic contractility, the effects of organ bath cooling were evaluated in isolated rabbit airway smooth muscle (ASM) segments isometrically contracted with methacholine (METH) (10(-8)-10(-3) M) and electrical field stimulation (ES), wherein the ES stimulus frequency was varied between 1 and 100 Hz. Cooling from 37 to 25 degrees C produced systematic increases (P less than 0.01) in isometric tension at various administered doses of METH and at different levels of ES. Since the potentiated contractions to ES significantly exceeded (P less than 0.001) the corresponding increases in METH-induced contractility, we evaluated whether the latter was attributed to temperature-mediated changes in intrinsic airway neuronal acetylcholine (ACh) release. Accordingly, the effects of ASM cooling were independently determined before and after inhibition of the Na+-K+ electrogenic pump with ouabain (10(-5) M), and depletion of intrinsic neuronal ACh stores with hemicholinium-3 (HC-3) (10(-3) M). In the presence of either ouabain or HC-3 the above responses to temperature reduction were reversed, and airway cooling was associated with abrupt relaxation of ASM segments precontracted with METH. In contrast, neither inhibition of cyclooxygenase products with indomethacin (10(-6) M) nor cholinesterase inhibition with neostigmine (10(-3) M) notably influenced the ASM responses to organ bath cooling. Thus these findings demonstrate that 1) both METH-induced and neurally mediated cholinergic contractility are augmented during airway cooling; 2) the potentiated cholinergic responses are attributed to enhanced presynaptic release of ACh at the airway neuromuscular junction.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute anemic hypoxemia produces a transient depression in fetal respiratory activity
Authors: Bissonnette J. M. , Hohimer A. R.
Published: December 2017

Isovolemic anemia was produced in 11 unanesthetized fetal sheep by withdrawal of blood and replacement with saline-dextran. Fetal hematocrit fell from 36 +/- 1 to 19 +/- 1% (SE). Fetal breathing movements, which were present during 34.4 +/- 5.5% of 3 h before the anemia, occurred 10.1 +/- 5.3, 14.8 +/- 4.4, and 27.1 +/- 6.7% in the 3 h following. The anemia caused a fall in arterial O2 concentration from 8.4 +/- 0.3 to 3.6 +/- 0.1 vol% and sagittal vein PO2 fell from 15.4 +/- 0.5 to 12.4 +/- 0.3 Torr. Cerebral metabolic rate during the period of anemia was 2.9 +/- 0.1 ml.100 g-1.min-1, which was unchanged from the control value of 3.0 +/- 0.2 ml.100 g-1.min-1. Sagittal vein PCO2 (54.2 +/- 1.4 Torr) remained constant after the fetus was made anemic. We conclude that respiratory activity in the sheep fetus is depressed by anemic hypoxemia but that the effect is transient.
Monokine-induced acute lung injury in rabbits
Authors: Goldblum S. E. , Jay M. , Yoneda K. , Cohen D. A. , McClain C. J. , Gillespie M. N.
Published: December 2017

Interleukin-1 (IL-1) mediates components of the acute phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied in unanesthetized rabbits the effects of intravenous divided dose infusions of a murine monokine preparation containing IL-1 activity, on circulating granulocytes, their sequestration within the pulmonary microvasculature, pulmonary edema formation, and changes in pulmonary vascular permeability. Monokine administration induced significant (P less than 0.01) granulocytopenia as well as a significant (P less than 0.001) increase in mean alveolar septal wall granulocytes per high power field (HPF) compared with saline-injected controls. Infusions of the monokine preparation significantly (P less than 0.005) increased lung wet-to-dry weight ratios as well as significantly (P less than 0.025) increased pulmonary extravasation of radiolabeled albumin. Electron microscopic analysis of lung sections obtained from monokine-infused animals demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural tracer. We conclude that a monokine preparation containing IL-1 activity can induce profound granulocytopenia, pulmonary leukostasis, and acute pulmonary vascular endothelial injury.
Subunit composition of rodent isomyosins and their distribution in hindlimb skeletal muscles
Authors: Tsika R. W. , Herrick R. E. , Baldwin K. M.
Published: December 2017

Three adult skeletal muscle sarcomeric myosin heavy chain (MHC) genes have been identified in the rat, suggesting that the expressed native myosin isoforms can be differentiated, in part, on the basis of their MHC composition. This study was undertaken to ascertain whether the five major native isomyosins [3 fast (Fm1, Fm2, Fm3), 1 slow (Sm), and 1 intermediate (Im)], typically expressed in the spectrum of adult rat skeletal muscles comprising the hindlimb, could be further differentiated on the basis of their MHC profiles in addition to their light chain composition. Results show that in muscles comprised exclusively of fast-twitch glycolytic (FG) fibers and consisting of Fm1, Fm2, and Fm3, such as the tensor fasciae latae, only one MHC, designated as fast type IIb, could be resolved. In soleus muscle, comprised of both slow-twitch oxidative and fast-twitch oxidative-glycolytic fibers and expressing Sm and Im, two MHC bands were resolved and designated as slow/cardiac beta-MHC and fast type IIa MHC. In muscles expressing a mixture of all three fiber types and a full complement of isomyosins, as seen in the plantaris, the MHC could be resolved into three bands. Light chain profiles were characterized for each muscle type, as well as for the purified isomyosins. These data suggest that Im (IIa) consists of a mixture of fast and slow light chains, whereas Fm (IIb) and Sm (beta) isoforms consist solely of fast- and slow-type light chains, respectively. Polypeptide mapping of denatured myosin extracted from muscles expressing contrasting isoform phenotypes suggests differences in the MHC primary structure between slow, intermediate, and fast myosin isotypes. These findings demonstrate that 1) Fm, Im, and Sm isoforms are differentiated on the bases of both their heavy and light chain components and 2) each isomyosin is distributed in a characteristic fashion among rat hindlimb skeletal muscles. Furthermore, these data suggest that the ratio of isomyosins in a given muscle or muscle region is of physiological importance to the function of that muscle during muscular activity.
Regional distribution of blood flow of dogs during graded dynamic exercise
Authors: Musch T. I. , Friedman D. B. , Pitetti K. H. , Haidet G. C. , Stray-Gundersen J. , Mitchell J. H. , Ordway G. A.
Published: December 2017

The regional blood flow response to progressive treadmill exercise was measured with radioactive microspheres in 25 untrained mongrel dogs. Incremental increases in work intensity resulted in corresponding increases in blood flows to the gracilis, gastrocnemius, semimembranosus, and semitendinosus muscles of the hindlimb and to the heart. During maximal exercise, blood flow was greatest in the semimembranosus muscle and lowest in the semitendinosus muscle (342 and 134 ml–1.100 g tissue-1.min-1, respectively). Exercise produced a decrease in blood flow to the temporalis muscle, which was classified as nonlocomotive in function. Blood flows to the stomach, pancreas, and large intestine decreased at the lowest exercise work load and remained diminished throughout the continuum to maximal exercise. Blood flows to the small intestine and spleen were maintained during submaximal exercise but were reduced by 50% at maximal O2 consumption (VO2max). No changes in blood flows to the kidneys, adrenal glands, liver, and brain were found. These results demonstrate that 1) renal blood flow is maintained at resting levels during exercise in untrained dogs; 2) blood flow changes in the various organs of the splanchnic region of dogs during exercise are heterogeneous; and 3) blood flows to the working skeletal muscles of dogs progressively increase with increasing work loads up to VO2max.
Increased carotid body hypoxic sensitivity during acclimatization to hypobaric hypoxia
Authors: Vizek M. , Pickett C. K. , Weil J. V.
Published: December 2017

Mechanisms of ventilatory acclimatization to chronic hypoxia remain unclear. To determine whether the sensitivity of peripheral chemoreceptors to hypoxia increases during acclimatization, we measured ventilatory and carotid sinus nerve responses to isocapnic hypoxia in seven cats exposed to simulated altitude of 15,000 ft (barometric pressure = 440 Torr) for 48 h. A control group (n = 7) was selected for hypoxic ventilatory responses matched to the preacclimatized measurements of the experimental group. Exposure to 48 h of hypobaric hypoxia produced acclimatization manifested as decrease in end-tidal PCO2 (PETCO2) in normoxia (34.5 +/- 0.9 Torr before, 28.9 +/- 1.2 after the exposure) as well as in hypoxia (28.1 +/- 1.9 Torr before, 21.8 +/- 1.9 after). Acclimatization produced an increase in hypoxic ventilatory response, measured as the shape parameter A (24.9 +/- 2.6 before, 35.2 +/- 5.6 after; P less than 0.05), whereas values in controls remained unchanged (25.7 +/- 3.2 and 23.1 +/- 2.7; NS). Hypoxic exposure was associated with an increase in the carotid body response to hypoxia, similarly measured as the shape parameter A (24.2 +/- 4.7 in control, 44.5 +/- 8.2 in acclimatized cats). We also found an increased dependency of ventilation on carotid body function (PETCO2 increased after unilateral section of carotid sinus nerve in acclimatized but not in control animals). These results suggest that acclimatization is associated with increased hypoxic ventilatory response accompanied by enhanced peripheral chemoreceptor responsiveness, which may contribute to the attendant rise in ventilation.
Role of substance P in hypercapnic excitation of carotid chemoreceptors
Authors: Prabhakar N. R. , Mitra J. , Cherniack N. S.
Published: December 2017

Experiments were performed on 17 anesthetized, paralyzed, and artificially ventilated cats to evaluate the importance of substance P-like peptide (SP) on the carotid body responses to CO2. Single or paucifiber carotid chemoreceptor activity was recorded from the peripheral end of the cut carotid sinus nerve. In eight of the cats the influence of SP on hyperoxic hypercapnic responses was studied. While the animals breathed 100% O2, intracarotid infusion of SP (1 microgram.kg-1.min-1, 3 min) increased chemoreceptor activity by +4.8 +/- 0.3 impulses/s. After SP infusion, inhalation of CO2 in O2 caused a rapid increase in activity that reached a peak and then adapted to a lower level, whereas similar levels of CO2 before SP caused only a gradual increase in carotid body discharge rate without any overshoot in response. Furthermore SP significantly increased the magnitude and slope of the CO2 response. In the other nine cats the effect of intracarotid infusion of an SP antagonist, [D-Pro2,D-Trp7,9] SP (10–15 micrograms.kg-1.min-1), on carotid body responses to 1) hyperoxic hypercapnia (7% CO2–93% O2), 2) isocapnic hypoxia (11% O2–89% N2), and 3) hypoxic hypercapnia (11% O2–7% CO2–82% N2) was examined. SP antagonist had no effect on carotid body response to hyperoxic hypercapnia but significantly attenuated the chemoreceptor excitation caused by isocapnic hypoxia and hypoxic hypercapnia. These results suggest that 1) SP may play an important role in carotid body responses to hypoxia but not to CO2, and 2) the mechanisms of stimulation of the carotid body by hypercapnia and by hypoxia differ.
Effect of aerobic training on the plasma ACTH response to exercise
Authors: Buono M. J. , Yeager J. E. , Sucec A. A.
Published: December 2017

The purpose of this study was to reexamine the effect of training on plasma adrenocorticotropin (ACTH) levels during exercise. Ten adult volunteers were split into a control and an experimental group. The experimental group participated in a 12-wk training program that resulted in a significant 11% increase in their mean maximal O2 uptake. The plasma ACTH response to a 150-W work rate was measured in both groups before and after the training program. The experimental group demonstrated a significant reduction in the ACTH response (11 vs. 4 pg/ml) to the work rate, whereas the control group demonstrated an unchanged response (16 vs. 13 pg/ml) over the course of the study. These data suggest that the ACTH response to an absolute submaximal work rate is blunted after training.
Effects of metabolic blockade on distribution of blood flow to respiratory muscles
Authors: Johnson R. L. , Reid M. B.
Published: December 2017

Sublethal inhibition of citrate metabolism in the tricarboxylic acid (TCA) cycle with monofluoroacetate (MFA) has been shown to cause a fivefold increase in myocardial blood flow without any change in cardiac output, blood pressure, or O2 consumption (C. Liang, J. Clin. Invest. 60: 61-69, 1977); however, blood flow did not increase to any organs examined other than the heart, including resting limb skeletal muscle. Preferential inhibition of glycolysis with iodoacetate (IA) failed to cause similar changes in distribution of blood flow. This unique response of myocardium to TCA cycle inhibition suggested a unique metabolic control of cardiac vasodilation. An alternate explanation is that MFA is preferentially concentrated in active muscle. After MFA, tissue citrate accumulates behind the block and the highest levels are reported in the heart and diaphragm, suggesting enhanced blockade or enhanced compensation in these two continuously active muscles. To test the hypothesis that vasodilation in the heart after MFA is not unique and that similar vasodilation will be evoked in active respiratory muscles, we measured blood flow to the myocardium, kidney, diaphragm, intercostals, transverse abdominals, and triceps brachii in anesthetized dogs using radionuclide-labeled microspheres, before and after MFA, and in another set of dogs before and after IA. Before MFA or IA, inspiratory loading significantly increased blood flow to active muscles of breathing in proportion to the added load. After MFA, blood flow to active muscles of breathing as well as to the heart became abnormally elevated with respect to mechanical work, and loading evoked no further increase in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Ventilatory and PaCO2 responses to voluntary and electrically induced leg exercise
Authors: Brice A. G. , Forster H. V. , Pan L. G. , Funahashi A. , Lowry T. F. , Murphy C. L. , Hoffman M. D.
Published: December 2017

We studied the role of central command mediation of exercise hyperpnea by comparing the ventilatory and arterial CO2 partial pressure (PaCO2) responses to voluntary (ExV) and electrically induced (ExE) muscle contractions in normal, awake human subjects. We hypothesized that if central command signals are critical to a normal ventilatory response, then ExE should cause a slower ventilatory response resulting in hypercapnia at the onset of exercise. ExE was induced through surface electrodes placed over the quadriceps and hamstring muscles. ExE and ExV produced leg extension (40/min) against a spring load that increased CO2 production (VCO2) 100-1,000 ml/min above resting level. PaCO2 and arterial pH during work transitions and in the steady state did not differ significantly from rest (P greater than 0.05) or between ExE and ExV. The temporal pattern of ventilation, tidal volume, breathing frequency, and inspired and expired times, and the ventilation-VCO2 relationship were similar between ExE and ExV. We conclude that since central command was reduced and/or eliminated by ExE, central command is not requisite for the precise matching of alveolar ventilation to increases in VCO2 during low-intensity muscle contractions.
Is the hyperpnea of muscular contractions critically dependent on spinal afferents?
Authors: Brice A. G. , Forster H. V. , Pan L. G. , Funahashi A. , Hoffman M. D. , Murphy C. L. , Lowry T. F.
Published: December 2017

We studied the role of spinal afferent pathways in the hyperpnea of electrically induced muscle contractions (ExE). The ventilatory (VE) and arterial CO2 partial pressure (PaCO2) responses were measured at rest and during two levels of ExE in awake human paraplegic subjects with clinically complete lesions of the spinal cord (range T4-T11). We hypothesized that if peripheral neural drive is critical to a normal ventilatory response, then ExE in the absence of intact pathways should cause a lower ventilatory response resulting in hypercapnia at the onset of ExE. ExE was induced by stimulation of the quadriceps and hamstring muscles that approximately doubled the resting level of CO2 production (VCO2). PaCO2 during work transitions and in the latter stages of ExE did not differ significantly from that at rest. Arterial pH progressively declined over time during ExE (P less than 0.01) as a result of increased lactate concentration (P less than 0.01). The linear relationship between VE and VCO2 was similar to that found for normal human subjects during ExE (P = 0.73). These data suggest that VE and presumably alveolar ventilation (VA) can be appropriately matched to VCO2 during low-intensity muscle contractions of the lower extremities in the absence of intact spinal afferent pathways. Moreover, since it is unlikely that postulated "central command" mechanisms were initiated during ExE in these paraplegic subjects, the data provide support for our previous conclusion that central command is not obligatory for matching VA to VCO2 (J. Appl. Physiol. 64: 218-225, 1988).
Autoregulation of diaphragmatic blood flow in dogs
Authors: Hussain S. N. , Roussos C. , Magder S.
Published: December 2017

In eight anesthetized spontaneously breathing dogs, we determined whether diaphragmatic blood flow is dependent on arterial blood pressure (Pa) or whether it is autoregulated. We also determined whether diaphragmatic muscular activity affects the degree of autoregulation. We measured blood flow through the left phrenic artery (Qphr) with an electromagnetic flow probe and decreased Pa in steps by controlled hemorrhage. Phrenic venous blood was sampled to allow the calculation of diaphragmatic O2 consumption (VO2phr). Diaphragmatic energy demands were varied by using three inspiratory resistances (R1, R2, and R3), which increased peak transdiaphragmatic pressure two-, three-, and fourfold, respectively. During quiet breathing, Qphr was independent of Pa between Pa of 90 and 120 mmHg (i.e., plateau of pressure-flow relation), but at lower Pa, Qphr was directly related to Pa. During inspiratory loading, the Qphr plateau ended at a higher Pa than with quiet breathing, but within the normal ranges of Pa there still was a plateau. VO2phr at a given work load was constant between Pa of 70 and 120 mmHg, but at Pa of 50-55 mmHg, VO2phr declined with all work loads. We conclude that in spontaneously breathing dogs 1) Qphr is autoregulated over the normal range of blood pressures and 2) VO2phr is maintained over wider ranges of Pa than Qphr.
Breathing strategy of the adult horse (Equus caballus) at rest
Authors: Koterba A. M. , Kosch P. C. , Beech J. , Whitlock T.
Published: December 2017

To investigate the mechanism underlying the polyphasic airflow pattern of the equine species, we recorded airflow, tidal volum, rib cage and abdominal motion, and the sequence of activation of the diaphragm, intercostal, and abdominal muscles during quiet breathing in nine adult horses standing at rest. In addition, esophageal, abdominal, and transdiaphragmatic pressures were simultaneously recorded using balloon-tipped catheters. Analysis of tidal flow-volume loops showed that, unlike humans, the horse at rest breathes around, rather than from, the relaxed volume of the respiratory system (Vrx). Analysis of the pattern of electromyographic activities and changes in generated pressures during the breathing cycle indicate that the first part of expiration is passive, as in humans, with deflation toward Vrx, but subsequent abdominal activity is responsible for a second phase of expiration: active deflation to below Vrx. From this end-expiratory volume, passive inflation occurs toward Vrx, followed by a second phase of inspiration: active inflation to above Vrx, brought about by inspiratory muscle contraction. Under these conditions the abdominal muscles appear to share the principal pumping duties with the diaphragm. Adoption of this breathing strategy by the horse may relate to its peculiar thoracoabdominal anatomic arrangement and to its very low passive chest wall compliance. We conclude that there is a passive and active phase to both inspiration and expiration due to the coordinated action of the respiratory pump muscles responsible for the resting adult horse's biphasic inspiratory and expiratory airflow pattern. This unique breathing pattern perhaps represents a strategy of minimizing the high elastic work of breathing in this species, at least at resting breathing frequencies.
Effects of nasal cold receptors on pattern of breathing
Authors: Burgess K. R. , Whitelaw W. A.
Published: December 2017

To investigate the effect on the pattern of breathing of cooling receptors in the nose, eight normal male volunteers underwent a steady-state CO2 stimulation by nasal inhalation. The inhaled gas temperature was randomly switched between "warm" (32 degrees C) and "cold" (2 degrees C) at each of three levels of inspired CO2 fraction (FICO2). Breathing cold air through the nose reduced the mean slope of the ventilatory response to CO2 by 27% (P less than 0.05) and the mean intercept at PCO2 of 45 Torr by 6.6 l/min (P less than 0.01). This was due mainly to a reduction in tidal volume (VT). Analysis of the breathing pattern recorded at a high level of minute ventilation (VE) (end-tidal partial pressure of CO2 approximately 52 Torr) showed a reduction of VE that was due almost entirely to a reduction in VT (P less than 0.05) associated with a reduction in inspiratory time (TI) as a fraction of total respiratory cycle time (P less than 0.05) but little change in VT/TI. In a separate experiment conducted with five subjects, there was no significant difference in inspired nasal resistance between warm and cold runs during CO2-stimulated breathing. The results confirm the previous observation that cold air breathed through the nose inhibits ventilation in normal subjects and show that this is not related to an increase in flow resistance. The reduction in ventilation is due to reduction in VT associated with shortening of the duty cycle.
Role of barometric pressure in pulmonary fluid balance and oxygen transport
Authors: Levine B. D. , Kubo K. , Kobayashi T. , Fukushima M. , Shibamoto T. , Ueda G.
Published: December 2017

To examine the role of barometric pressure in high-altitude pulmonary edema, we randomly exposed five unanesthetized chronically instrumented sheep with lung lymph fistulas in a decompression chamber to each of three separate conditions: hypobaric hypoxia, normobaric hypoxia, and normoxic hypobaria. A combination of slow decompression and/or simultaneous adjustment of inspired PO2 provided three successive stages of simulated altitudes of 2,600, 4,600, and 6,600 m during which hemodynamics and lymph flow were monitored. Under both hypoxic conditions we noted significant and equivalent elevations in pulmonary arterial pressure (Ppa), cardiac output, and heart rate, with left atrial and systemic pressures remaining fairly constant. Normoxic hypobaria was also accompanied by a smaller but significant rise in Ppa. Lymph flow increased to a highly significant maximum of 73% above base line, accompanied by a slight but significant decrease in lung lymph-to-plasma protein ratio, only under conditions of combined hypobaric hypoxia but not under equivalent degrees of alveolar hypoxia or hypobaria alone. Arterial hypoxemia was noted under all three conditions, with arterial PO2 being uniformly lower under hypobaric conditions than when identical amounts of inspired PO2 were delivered at normal atmospheric pressure. We therefore hypothesize that alveolar pressure significantly alters the Starling forces governing transcapillary fluid flux in the lung and may affect the alveolar-arterial gradient for O2 as well.
Causes of error of respiratory pressure-volume curves in paralyzed subjects
Authors: Dall'ava-Santucci J. , Armaganidis A. , Brunet F. , Dhainaut J. F. , Chelucci G. L. , Monsallier J. F. , Lockhart A.
Published: December 2017

Respiratory pressure-volume (PV) curves are commonly obtained in paralyzed patients by relating airway pressure to volume changes of a syringe (Vsyr). This is based on the implicit assumption that changes in thoracic volume (Vtho) and Vsyr are equal. We undertook to verify this assumption through simultaneous measurements of Vtho by respiratory inductive plethysmography and Vsyr in six comatose, paralyzed, intubated patients. At any constant Vsyr, Vtho fell and was smaller on deflation than on inflation during inflation-deflation (ID) cycle. The rate of fall was 110 +/- 64 (SD) ml/min. During ID cycles lasting 76 +/- 7 s, thoracic PV curves showed less hysteresis and a larger compliance on deflation than PVsyr curves (12 +/- 2 vs. 18 +/- 6% and 73 +/- 13 vs. 67 +/- 12 ml/cmH2O, P less than 0.05). With PVsyr curves, hysteresis increased and compliance on deflation decreased with increasing rate of fall of Vtho. We submit that the difference between changes in Vsyr and Vtho is best explained by gas exchange and should be taken into account when performing PV curves with a syringe in paralyzed patients.
Flow and volume dependence of pulmonary mechanics in anesthetized cats
Authors: Kochi T. , Okubo S. , Zin W. A. , Milic-Emili J.
Published: December 2017

The effects of inspiratory flow rate and inflation volume on pulmonary mechanics were investigated in six anesthetized-paralyzed cats ventilated by constant-flow inflation. Pulmonary mechanics were assessed using the technique of rapid airway occlusion during constant-flow inflation which allows measurement of the intrinsic pulmonary resistance (RLmin) and of the overall "pulmonary flow resistance" (RLmax), which includes the additional pulmonary pressure losses due to time constant inequalities within the lung and/or stress adaptation. We observed that, at fixed inflation volume, 1) RLmin fitted Rohrer's equation, 2) RLmax was higher at low than intermediate flows, and 3) RLmax-RLmin decreased progressively with increasing flow. At fixed flow, RLmax increased, whereas RLmin decreased with increasing volume. We conclude that during eupneic breathing in cats, the pulmonary flow resistance as conventionally measured includes a significant component reflecting stress adaptation.
Carotid body excision significantly changes ventilatory control in awake rats
Authors: Olson E. B. , Vidruk E. H. , Dempsey J. A.
Published: December 2017

We determined the effects of carotid body excision (CBX) on eupneic ventilation and the ventilatory responses to acute hypoxia, hyperoxia, and chronic hypoxia in unanesthetized rats. Arterial PCO2 (PaCO2) and calculated minute alveolar ventilation to minute metabolic CO2 production (VA/VCO2) ratio were used to determine the ventilatory responses. The effects of CBX and sham operation were compared with intact controls (PaCO2 = 40.0 +/- 0.1 Torr, mean +/- 95% confidence limits, and VA/VCO2 = 21.6 +/- 0.1). CBX rats showed 1) chronic hypoventilation with respiratory acidosis, which was maintained for at least 75 days after surgery (PaCO2 = 48.4 +/- 1.1 Torr and VA/VCO2 = 17.9 +/- 0.4), 2) hyperventilation in response to acute hyperoxia vs. hypoventilation in intact rats, 3) an attenuated increase in VA/VCO2 in acute hypoxemia (arterial PO2 approximately equal to 49 Torr), which was 31% of the 8.7 +/- 0.3 increase in VA/VCO2 observed in control rats, 4) no ventilatory acclimatization between 1 and 24 h hypoxia, whereas intact rats had a further 7.5 +/- 1.5 increase in VA/VCO2, 5) a decreased PaCO2 upon acute restoration of normoxia after 24 h hypoxia in contrast to an increased PaCO2 in controls. We conclude that in rats carotid body chemoreceptors are essential to maintain normal eupneic ventilation and to the process of ventilatory acclimatization to chronic hypoxia.
Reductions in blood pressure after acute exercise by hypertensive rats
Authors: Overton J. M. , Joyner M. J. , Tipton C. M.
Published: December 2017

Postexercise reductions in blood pressure at rest have been reported for hypertensive subjects. To determine whether post-exercise hypotension would occur in spontaneously hypertensive rats and to test the hypothesis that any reductions would result because of decreases in regional vascular resistances, hypertensive rats (n = 19) were instrumented with indwelling arterial catheters and Doppler probes to measure regional blood flows from the iliac, superior mesenteric, and renal arteries. Data were collected from animals who performed a 20- and a 40-min treadmill test at between 60 and 70% of their maximum O2 uptake. When the animals ran for 20 min, there was a pre- to postexercise drop in mean arterial pressure (MAP) from 158 +/- 3.6 to 150 +/- 3.6 mmHg (P less than 0.05), which was recorded 30 min after the exercise had ceased. The pre- to postexercise reduction in MAP after 40 min of treadmill running was from 154 +/- 3.1 to 138 +/- 3.0 mmHg (P less than 0.05) as recorded 30 min postexercise. Postexercise heart rate was significantly lower after the 40-min exercise bout, from a preexercise mean of 351 +/- 3 beats/min to 324 +/- 5 beats/min 30 min after the treadmill had stopped. Surprisingly, marked pre- to postexercise reductions in regional vascular resistance were not observed in either the iliac, superior mesenteric, or renal vascular beds. These data demonstrated the existence of postexercise hypotension in genetic hypertensive rats and suggested that reductions in cardiac output were the primary hemodynamic mechanism for this finding.
Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses
Authors: Rose R. J. , Hodgson D. R. , Kelso T. B. , McCutcheon L. J. , Reid T. A. , Bayly W. M. , Gollnick P. D.
Published: December 2017

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
Thermoregulatory, cardiovascular, and muscular factors related to exercise after precooling
Authors: Olschewski H. , Bruck K.
Published: December 2017

The effect of slightly lowered body temperature on endurance time and possibly related physiological factors was studied in seven male volunteers exercising on a cycle ergometer at an ambient temperature (Ta) of 18 degrees C. Work load was increased to 40% in a stepwise manner (phase I, min 0–16) followed by a period at 80% of peak oxygen consumption (VO2) sustained to exhaustion. On one day, exercise was preceded by a double cold exposure (precooling test, PRET), resulting in a 204-kJ/m2 negative heat storage and a 4 and 0.2 degrees C lower mean skin and core temperature at the start of exercise compared with the control test (CONT). Core temperature dropped further during exercise in PRET. Endurance time at 80% of peak VO2 was increased by 12% (P less than 0.05) in PRET. Heart rate (HR) was decreased throughout PRET (P less than 0.05); oxygen pulse and arteriovenous O2 difference were significantly increased in phase I of PRET, whereas the PRET-CONT differences in stroke volume and cardiac output were not significant. In phase II of PRET (min 16–28, heavy exercise) sweat rate (SR) and heat conductivity, indicating forearm blood flow, were lower (-39%, P less than 0.001; -37%). Pedal rate (PR) was 9% lower (P less than 0.01) in phase II of PRET. At the termination of exercise, PRET-CONT differences in HR, SR, and PR had disappeared.
Effect of exercise on nonspecific airway reactivity in asthmatics
Authors: Zawadski D. K. , Lenner K. A. , McFadden E. R.
Published: December 2017

To investigate whether exercise increases the responsivity of the tracheobronchial tree to nonspecific stimuli, 11 atopic asthmatics underwent serial challenges with aerosolized methacholine before and 4 and 24 h after an asthma attack induced by cycle ergometry while breathing cold air (mean +/- SE = -11 +/- 1 degree C). Bronchodilator therapy was withheld the day before and throughout each study day. There were no significant differences in base-line lung function before exercise or any of the three methacholine bronchoprovocations. Exercise produced a 25 +/- 3% maximal fall in 1-s forced expiratory volume (FEV1) within 15 min. This attack was not associated with either an immediate or a delayed increase in methacholine sensitivity. The provocation concentration of methacholine required to reduce the FEV1 20% from saline control at base line and 4 and 24 h after exercise were 0.8 +/- 0.5, 0.9 +/- 0.5, and 1.1 +/- 0.8 mg/ml, respectively. This was not significant by a one-way analysis of variance (F = 0.078, P = NS). These data demonstrate that exercise-induced asthma does not produce an increase in nonspecific bronchial reactivity. Hence, if mediators are elaborated with exercise as has been suggested, they appear to function differently than when released by antigen.
Effects of exercise on cardiac myosin isozyme composition during the aging process
Authors: Farrar R. P. , Starnes J. W. , Cartee G. D. , Oh P. Y. , Sweeney H. L.
Published: December 2017

The effects of aging and exercise on isoforms of cardiac myosin and Ca2+-activated actomyosin adenosinetriphosphatase (ATPase) activity were examined in Fischer 344 rats. Rats were divided into running (R) and age-matched sedentary (S) groups. The groups initiated their exercise program at either 3, 4, or 18 mo of age. Rats were killed at 10, 12, 24, or 27 mo of age. ATPase activity decreased 25% in the S group and 28% in the R group from 12 to 27 mo of age. The myosin isozyme patterns shifted in both S and R groups from a predominantly V1 isozyme form (63.8%) at 10 mo of age to a more equal distribution of isozyme forms at 24 mo (V1, V2, and V3 comprising 40.0, 27.8, and 31.9%, respectively). Age-related shifts in myosin composition occurred despite chronic endurance training at an intensity of approximately 75% maximum O2 consumption. Improvement of cardiac performance through training during aging is not accompanied by attenuating shifts in myosin isozyme composition.
Brain stem extracellular fluid pH and respiratory drive during hypoxia in newborn pigs
Authors: Brown D. L. , Lawson E. E.
Published: December 2017

In response to moderate hypoxia many newborn animals are capable of increasing ventilation only transiently. To examine the hypothesis that changes in brain stem extracellular fluid (ECF) pH explain this transient ventilatory response, we measured brain stem ECF pH and respiratory drive during hypoxia in newborn pigs. The animals were anesthetized with alpha-chloralose-urethan, paralyzed, vagotomized, and mechanically ventilated with a servo-controlled ventilator to regulate end-tidal CO2. Hypoxic ventilation for 6 min was achieved by changing inspired gas from 100% to 10-15% O2. Respiration, measured as integrated phrenic nerve activity, showed a range of responses. In 13 trials increased phrenic activity early in the hypoxic period was sustained or further augmented for the duration of the period. In contrast, in eight other trials phrenic activity increased and then declined. Regardless of the respiratory response, ECF pH (measured with a flat-surface electrode) increased slightly (0.009 ±0.002 U) during the first 2.5 min of hypoxia and then declined 0.061 ± 0.017 U by the 6th min. This acidotic shift in ECF pH is inconsistent with the hypothesis that an alkalotic shift causes the nonsustained respiratory response of newborn pigs.
Functional and structural adaptations in skeletal muscle of trained athletes
Authors: Alway S. E. , MacDougall J. D. , Sale D. G. , Sutton J. R. , McComas A. J.
Published: December 2017

Twitch contractile and ultrastructural characteristics of the human triceps surae were determined in six male strength-trained athletes, six endurance-trained athletes, six active controls, and seven sedentary controls of similar height and age. Twitch contraction time in the triceps surae complex was 20% longer in strength-trained and sedentary groups than in endurance-trained or active control groups. In the 15 subjects peak twitch torque and one-half relation time in the triceps surae were 22.6 ± 7.9 N.m and 91.1 ± 18.3 ms, respectively. Mean fiber area in the gastrocnemius was approximately 1.6-, 1.7-, and 2.5-fold greater in the active control, endurance-trained, and strength-trained groups, respectively, relative to the sedentary group. Despite these large differences in fiber areas, the fiber fractional volume of the sarcoplasmic reticulum-transverse tubule network averaged 3.38 ± 0.86% and 5.50 ± 0.94% in type I and type II fibers, respectively, in all subjects. The fractional fiber volume of cytoplasm and lipid were similar for all four groups. However, mitochondrial volume was approximately 30% lower in both fiber types of the strength-trained group relative to the other groups. This implies that with exercise-induced hypertrophy, the sarcoplasmic reticulum, cytoplasm, and lipid components increase proportionately with contractile protein, whereas the mitochondrial fraction does not. The proportion of type I fibers in the soleus, medial gastrocnemius, and lateral gastrocnemius was 75.2 ± 8.3, 58.5 ± 6.1, and 52.4 ± 4.2%, respectively, and was similar in all subject groups. The results demonstrate that twitch duration is prolonged in strength-trained athletes relative to endurance athletes.(ABSTRACT TRUNCATED AT 250 WORDS)