bluuebunny/crossref_metadata_2025 huggingface dataset:
Comparison of febrile responsiveness of rats and rabbits to endogenous pyrogen
Authors: Stitt J. T. , Shimada S. G. , Bernheim H. A.
Published: December 2017

The fever responses of rats and rabbits were compared in detail using a single common source of semipurified endogenous pyrogen prepared from human monocytes. The characteristics and dynamics of the fever-response curves for each species were examined and their dose-response curves were determined and compared. The fevers displayed by rats were qualitatively similar to those of rabbits, but, typically, they developed and terminated more rapidly than those of rabbits. Rabbits were much more sensitive to the endogenous pyrogen than rats. The threshold dose of pyrogen required to elicit a fever was 5 times lower in the rabbit, and the slope of the rabbit's dose-response curve was 1.5 times steeper than that of the rat. The maximum fevers attainable in rabbits were approximately twice those attainable in rats. It was also shown that the more rapid febrile responses of the rat were not due to the 10-fold smaller mass of the rat; instead, we proposed that this difference was more likely due to a closer diffusional proximity of the pyrogen receptor sites to the circulation in rats. The lower sensitivity of the rat to endogenous pyrogen was attributed to a relative insensitivity of the pyrogen receptor sites in rats in the translation of the endogenous pyrogen stimulus into fever.
Respiratory impedance measured with head generator to minimize upper airway shunt
Authors: Peslin R. , Duvivier C. , Didelon J. , Gallina C.
Published: December 2017

A new method for measuring total respiratory input impedance (Zrs), which ensures minimal motion of extrathoracic airway walls, was tested over frequencies of 4–30 Hz in 14 normal subjects and 10 patients with airway obstruction. It consists of applying pressure variations around the head, rather than at the mouth, so that transmural pressure across upper airway walls is equal to the small pressure drop across the pneumotachograph. Compared with reference Zrs values obtained by directly measuring airway wall motion with a head plethysmograph and correcting the data for it, the investigated method provided similar values for respiratory resistance at all frequencies (30 Hz, 3.67 +/- 2.24 cmH2O X 1(-1) X s compared with 3.55 +/- 2.00) but slightly overestimated respiratory reactance at the largest frequencies (30 Hz, 2.82 +/- 1.28 cmH2O X 1(-1) X s compared with 2.52 +/- 1.22, P less than 0.01). In contrast, when the data were not corrected for airway wall motion, resistance was largely underestimated, especially in patients (-48% at 30 Hz, P less than 0.001), and the reactance-frequency curve was shifted to the right. The investigated method is almost as accurate as the reference method, provides equally reproducible data, and is much simpler.
Distribution of respiratory muscle and organ blood flow during endotoxic shock in dogs
Authors: Hussain S. N. , Roussos C.
Published: December 2017

Respiratory muscle blood flow and organ blood flow during endotoxic shock were studied in spontaneously breathing dogs (SB, n = 6) and mechanically ventilated dogs (MV, n = 5) with radiolabeled microspheres. Shock was produced by a 5-min intravenous injection of Escherichia coli endotoxin (0.55:B5, Difco, 10 mg/kg) suspended in saline. Mean arterial blood pressure and cardiac output in the SB group dropped to 59 and 45% of control values, respectively. There was a similar reduction in arterial blood pressure and cardiac output in the MV group. Total respiratory muscle blood flow in the SB group increased significantly from the control value of 51 +/- 4 ml/min (mean +/- SE) to 101 +/- 22 ml/min at 60 min of shock. In the MV group, respiratory muscle perfusion fell from control values of 43 +/- 12 ml/min to 25 +/- 3 ml/min at 60 min of shock. In the SB group, 8.8% of the cardiac output was received by the respiratory muscle during shock in comparison with 1.9% in the MV group. In both groups of dogs, blood flow to most organs was compromised during shock; however, blood flow to the brain, gut, and skeletal muscles was higher in the MV group than in the SB group. Thus by mechanical ventilation a fraction of the cardiac output used by the working respiratory muscles can be made available for perfusion of other organs during endotoxic shock.
Early increases in coronary vascular reserve in exercised rats are independent of cardiac hypertrophy
Authors: Buttrick P. M. , Levite H. A. , Schaible T. F. , Ciambrone G. , Scheuer J.
Published: December 2017

To evaluate the relationship between the physiological cardiac hypertrophy associated with physical training and the increases in vascular capacitance associated with this stimuli, male and female rats trained by a swimming program were studied. Both sexes were used so that the coronary vascular response to exercise could be studied in the presence (females) and absence (males) of cardiac hypertrophy. Coronary vascular reserve was assessed in isolated retrograde buffer-perfused hearts under conditions of minimal coronary resistance (15 microM adenosine or anoxia). Both groups demonstrated an increase in coronary vascular reserve after 8 wk of exercise swim training, male animals increasing flow (per g of myocardium) by 15% and females by 18%. When the time course of this response was compared in female animals with the time course of the development of myocardial hypertrophy, it was evident that the vascular changes occurred early, greater than 80% of the response was seen within the first 10 days of exercise, compared with an approximately 35% increase in cardiac mass. These data suggest that the vascular response to exercise swim training is independent of the hypertrophic response and further that the increase in coronary vascularity is an early event in the cardiac adaptation to a physiological load.
Influence of menstrual cycle on shivering, skin blood flow, and sweating responses measured at night
Authors: Hessemer V. , Bruck K.
Published: December 2017

In 10 women, external cold and heat exposures were performed both in the middle of luteal phase (L) and in the early follicular phase (F) of the menstrual cycle. Serum progesterone concentrations in L and F averaged 46.0 and 0.9 nmol X l-1, respectively. The experiments took place between 3:00 and 4:30 A.M., when the L-F core temperature difference is maximal. At neutral ambient temperature, esophageal (Tes), tympanic (Tty), rectal (Tre), and mean skin (Tsk) temperatures averaged 0.59 degrees C higher in L than in F. The thresholds for shivering, chest sweating, and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were increased in L by an average of 0.47 degrees C, related to mean body temperature [Tb(es) = 0.87Tes + 0.13 Tsk] and to Tes, Tty, Tre, or Tsk. The above-threshold chest sweat rate and cutaneous heat clearances at the thumb and forearm were also enhanced in L, when related to Tb(es) or time. The metabolic rate, arm blood flow, and heart rate at thermoneutral conditions were increased in L by 5.0%, 1.1 ml X 100 ml-1 X min-1, and 4.6 beats X min-1, respectively. The concomitant increase in threshold temperatures for all autonomic thermoregulatory responses in L supports the concept of a resetting of the set point underlying the basal body temperature elevation in L. The effects of the increased threshold temperatures are counteracted by enhanced heat loss responses.
Influence of menstrual cycle on thermoregulatory, metabolic, and heart rate responses to exercise at night
Authors: Hessemer V. , Bruck K.
Published: December 2017

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.
Leukotriene B4 induces airway hyperresponsiveness in dogs
Authors: O'Byrne P. M. , Leikauf G. D. , Aizawa H. , Bethel R. A. , Ueki I. F. , Holtzman M. J. , Nadel J. A.
Published: December 2017

We studied the effect of leukotriene B4 aerosols on airway responsiveness to inhaled acetylcholine aerosols and on the cellular components and cyclooxygenase metabolites in bronchoalveolar lavage fluid in dogs. Inhalation of leukotriene B4 aerosols had no effect on resting total pulmonary resistance but increased airway responsiveness, an effect that was maximum in 3 h and that returned to control levels within 1 wk. Three hours after leukotriene B4, the number of neutrophils and the concentration of thromboxane B2 recovered in lavage fluid increased markedly. Pretreatment with the thromboxane synthase inhibitor OKY-046 prevented the increases in airway responsiveness and in thromboxane B2 but did not alter neutrophil chemotaxis. Thus we speculate that leukotriene B4 causes neutrophil chemotaxis and release of thromboxane B2, which increases airway responsiveness.
Respiratory load compensation in chronic airway obstruction
Authors: Lopata M. , Onal E. , Cromydas G.
Published: December 2017

To assess respiratory neuromuscular function and load compensating ability in patients with chronic airway obstruction (CAO), we studied eight stable patients with irreversible airway obstruction during hyperoxic CO2 rebreathing with and without a 17 cmH2O X l-1 X s flow-resistive inspiratory load (IRL). Minute ventilation (VE), transdiaphragmatic pressure (Pdi), and diaphragmatic electromyogram (EMGdi) were monitored. Pdi and EMGdi were obtained via a single gastroesophageal catheter with EMGdi being quantitated as the average rate of rise of inspiratory (moving average) activity. Based on the effects of IRL on the Pdi response to CO2 [delta Pdi/delta arterial CO2 tension (PaCO2)] and the change in Pdi for a given change in EMGdi (delta Pdi/delta EMGdi) during rebreathing, two groups could be clearly identified. Four patients (group A) were able to increase delta Pdi/delta PaCO2 and delta Pdi/delta EMGdi, whereas in the other four (group B) the IRL responses decreased. All group B patients were hyperinflated having significantly greater functional residual capacity (FRC) and residual volume than group A. In addition the IRL induced percent change in delta Pdi/delta PaCO2, and delta VE/delta PaCO2 was negatively correlated with lung volume so that in the hyperinflated group B the higher the FRC the greater was the decrease in Pdi response due to IRL. In both groups the greater the FRC the greater was the decrease in the ventilatory response to loading. Patients with CAO, even with severe airways obstruction, can effect load compensation by increasing diaphragmatic force output, but the presence of increased lung volume with the associated shortened diaphragm prevents such load compensation.
Blood-gas equilibrium of carbon dioxide in lungs: a continuing controversy
Authors: Piiper J.
Published: December 2017

This review presents the experimental evidence that has been published in recent years both against and in support of the occurrence of negative blood-gas CO2 partial pressure differences (delta PCO2) in lungs in rebreathing equilibrium and during steady-state gas exchange in hypercapnia. Although some sources of potential experimental error can be pointed out, the reasons for the remarkably pronounced disagreement between the experimental data of the different studies cannot be definitely identified. Since a consistent and reproducible occurrence of negative blood-gas delta PCO2 in lungs in gas-blood equilibrium is not convincingly proved, it appears to be justified to continue accepting the validity of the conventional concept of equal PCO2 in blood and gas in equilibrium. Because the issue is of considerable importance in the analysis and understanding of alveolar gas exchange, pertinent evidence is expected from future work.
Beta-adrenoceptors and the regulation of blood pressure and plasma renin during exercise
Authors: Hespel P. , Lijnen P. , Vanhees L. , Fagard R. , Amery A.
Published: December 2017

The relative role of beta 1- and beta 2-adrenoceptors in the regulation of blood pressure and plasma renin at rest and during exercise was studied in 17 normal male volunteers. They performed, in a randomized order and according to a double-blind crossover study design, three graded and uninterrupted exercise tests until exhaustion after being pretreated during 3 consecutive days with a placebo, with a predominantly beta 1-blocker (atenolol, 50 mg once/day), or with a predominantly beta 2-blocker (ICI 118551, 20 mg 3 times/day). Both drugs caused a decrease of heart rate, but the reduction by ICI 118551 was less pronounced at rest and no additional decline occurred at exercise. ICI 118551 did not affect blood pressure at rest, but during exercise diastolic blood pressure was higher than after a placebo. Atenolol lowered systolic blood pressure at rest and suppressed the exercise-induced increase in systolic blood pressure. At rest and during exercise plasma renin activity was lowered by predominantly beta 1-blockade and unchanged during beta 2-antagonism. The exercise-induced increase in plasma renin was, however, not affected by the beta 1-blocker. After atenolol the urinary excretion of aldosterone was decreased but the plasma aldosterone concentration was not changed. ICI 118551 did not alter plasma or urinary aldosterone. Our results therefore provide further evidence that the adrenoceptors mediating the release of renin at rest and during exercise in humans are partially of the beta 1-subtype, whereas beta 2-adrenergic receptors probably play only a minor role in the control of renin secretion, especially at exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiorenal-endocrine responses to head-out immersion at night
Authors: Shiraki K. , Konda N. , Sagawa S. , Claybaugh J. R. , Hong S. K.
Published: December 2017

Cardiorenal-endocrine responses to 3-h head-out immersion (HOI) (water temperature = 34.5 +/- 0.5 degrees C) were studied during day (0900–1400 h) and night (2300–0400 h) in six hydropenic male human subjects. Although HOI induced a reversible increase in urine flow in all subjects, the response was faster and greater in magnitude during the day compared with night (P less than 0.05). Na excretion and osmolal clearance (Cosm) also followed the identical response pattern as urine flow, and in fact, the HOI-induced diuresis was entirely accounted for by the increased Cosm. Endogenous creatinine clearance was not different between the day and the night and remained unchanged during HOI. Both plasma renin activity and aldosterone concentration and urinary aldosterone excretion were nearly twofold greater during the day compared with night before HOI but decreased to the same level during HOI in both daytime and the nighttime series (P less than 0.05). There was no correlation between the Na excretion rate and renin-aldosterone levels either before or during HOI. Plasma antidiuretic hormone (ADH) level was comparable between day and night before HOI and decreased to a similar level during HOI in both daytime and nighttime series (P less than 0.05 for nighttime HOI). Cardiac output increased from 3.3 1/min before HOI to 5–6 1/min during HOI without showing any significant circadian difference. Hematocrit, hemoglobin, and plasma concentrations remained unchanged under all conditions. It is concluded that the renal response to HOI is subject to nocturnal inhibition, which cannot be attributed to circadian differences in the degree of HOI-induced central blood pooling, renin-aldosterone, or ADH responses.
Combined effects of hypertension and conditioning on coronary vascular reserve in rats
Authors: Buttrick P. M. , Schaible T. F. , Scheuer J.
Published: December 2017

To evaluate the combined effects of cardiac overload imposed by hypertension and chronic swim training on coronary vascularity, female rats were made hypertensive by unilateral renal artery stenoses and were exercised in an 8- to 10-wk swimming program. Maximal coronary flow was assessed in isolated retrograde buffer-perfused hearts under conditions of minimal coronary resistance (15 microM adenosine or anoxia). Sedentary normotensive animals, sedentary hypertensive animals, and normotensive animals exposed to a swimming program were also studied. Swimming was associated with an 18% increase in heart weight and with increases in both absolute (ml/min) and relative (ml X g-1 X min-1) maximal coronary flow. Hypertension was associated with a 32% increase in heart weight but with a decrease in absolute and relative coronary flow compared with controls. The combined stimuli resulted in a 63% myocardial hypertrophy and a 19% increase in absolute flow. Relative coronary flow (g tissue-1) was similar in hearts from hypertensive sedentary animals and hypertensive swimmers. These data indicate that the coronary vascular deficit that accompanies the cardiac hypertrophy of hypertension is not worsened by the superimposition of an exercise load that exaggerates the hypertrophy.
Effects of sulfur dioxide on pore populations of canine tracheal epithelium
Authors: Man S. F. , Hulbert W. C. , Mok K. , Ryan T. , Thomson A. B.
Published: December 2017

The bioelectric and barrier properties of the tracheal epithelium in nose-breathing dogs and in dogs that had been exposed for 75 min to compressed air or to two high concentrations of SO2 were measured and compared. We also studied tissues that had been treated with chloroform. Based on a model of restrictive diffusion we demonstrated heteropores (6 and 250 A) in the control tissues. Bioelectric changes due to 100-ppm SO2 were minimal. After exposure to 500 ppm SO2, adverse changes in the bioelectric properties were focal; they were marked in 8 out of 12 animals but were less striking in the other 4. Nonelectrolyte permeability increased with an increase in SO2 concentrations. Small pores were still present in the tissues severely affected by SO2 but they were absent in chloroform-treated tissues. Scanning electron microscopy of tissues from animals exposed to 500 ppm SO2 showed that in the same dog tissue appearance varied from normal to one of repair (normal bioelectric properties) or one of marked exfoliation of ciliated cells (abnormal bioelectric measurements).
Microvascular pressures measured by micropipettes in isolated edematous rabbit lungs
Authors: Raj J. U. , Bland R. D. , Lai-Fook S. J.
Published: December 2017

To study the mechanical effects of lung edema on the pulmonary circulation, we determined the longitudinal distribution of vascular resistance in the arteries, veins, and microvessels, and the distribution of blood flow in isolated blood-perfused rabbit lungs with varying degrees of edema. Active vasomotor changes were eliminated by adding papaverine to the perfusate. In three groups of lungs with either minimal [group I, mean wet-to-dry weight ratio (W/D) = 5.3 +/- 0.6 (SD), n = 7], moderate (group II, W/D = 8.5 +/- 1.2, n = 10), or severe (group III, W/D = 9.9 +/- 1.6, n = 5) edema, we measured by direct micropuncture the pressure in subpleural arterioles and venules (20–60 micron diam) and in the interstitium surrounding these vessels. We also measured pulmonary arterial and left atrial pressures and lung blood flow, and in four additional experiments we used radio-labeled microspheres to determine the distribution of blood flow during mild and severe pulmonary edema. In lungs with little or no edema (group I) we found that 33% of total vascular pressure drop was in arteries, 60% was in microvessels, and 7% was in veins. Moderate edema (group II) had no effect on total vascular resistance or on the vascular pressure profile, but severe edema (group III) did increase vascular resistance without changing the longitudinal distribution of vascular resistance in the subpleural microcirculation. Perivascular interstitial pressure relative to pleural pressure increased from 1 cmH2O in group I to 2 in group II to 4 in group III lungs.(ABSTRACT TRUNCATED AT 250 WORDS)
Hemodynamic effects of cardiac cycle-specific increases in intrathoracic pressure
Authors: Pinsky M. R. , Matuschak G. M. , Bernardi L. , Klain M.
Published: December 2017

Changes in intrathoracic pressure (ITP) can influence cardiac performance by affecting ventricular loading conditions. Because both systemic venous return and factors determining left ventricular (LV) ejection may vary over the cardiac cycle, phasic increases in ITP may differentially affect preload or afterload if delivered at specific points within the cardiac cycle. We studied the hemodynamic effects of cardiac cycle-specific increases in ITP (pulses) delivered by a high-frequency jet ventilator in an acute closed-chested canine model (n = 11), using electromagnetic flow probes to measure biventricular stroke volume. Measurements were taken during a control condition after the induction of acute ventricular failure (AVF) by propranolol hydrochloride and volume infusion. ITP was independently varied without changing lung volume by the inflation of thoracoabdominal binders. Although synchronous pulses had minimal hemodynamic effects in unbound controls, binding pulses timed to occur in early diastole resulted in decreases in LV filling pressure and left ventricular stroke volume (SVlv) (P less than 0.05). In the AVF condition, pulses increased LV performance, evidenced by increases in SVlv (P less than 0.01), despite decreases in LV filling pressure (P less than 0.05). This effect is maximized by binding and by timing the pulses to occur in systole. We conclude that cardiac cycle-specific increases in ITP can significantly affect cardiac performance. These effects appear to be related to the ability of such timed pulses to selectively affect LV preload and afterload.
Lung lymph flow during volume infusions
Authors: Gabel J. C. , Fallon K. D. , Laine G. A. , Drake R. E.
Published: December 2017

We investigated the effect of intravenous isotonic crystalloid solution infusion on lung lymph flow. Tracheobronchial lung lymph vessels were cannulated in 13 anesthetized dogs. The lymph flow rate was measured 1) with the lymph flowing against atmospheric pressure (QL), and 2) with the pressure at the outflow end of the lymph cannula equal to systemic venous pressure (QLV). QL and QLV were measured alternately in each lymph vessel. In one group of nine dogs, the base-line QL and QLV were 18 +/- 9 and 13 +/- 6 (SD) microliter/min, respectively (P less than 0.05). QL increased by 4.8 +/- 1.4-fold, and QLV increased by 3.5 +/- 2.1-fold during a 4-h infusion of 25 ml X kg-1 X h-1 of Ringer solution. QLV was significantly less than QL at all times. The increases in lymph flow were caused primarily by a reduction in the effective resistance of the lymph vessels with little rise in the pressure driving lymph from the lungs. Because QLV flowed against systemic venous pressure, the increase in QLV was blunted by a 3.1 +/- 2.3 cmH2O rise in venous pressure during the infusions. In the remaining four dogs, we infused Ringer solution rapidly in order to raise venous pressure to greater than 15 cmH2O. This caused QL to increase by 25 +/- 7-fold; however, QLV decreased to zero. We conclude that elevations in venous pressure which occur during volume infusions oppose lung lymph flow and lead to accumulation of excess fluid in the lungs.
Temporal pattern of arterial CO2 partial pressure during exercise in humans
Authors: Forster H. V. , Pan L. G. , Funahashi A.
Published: December 2017

The major objective of this study was to test the hypothesis that arterial CO2 partial pressure (PaCO2) does not change in transitions from rest to steady-state exercise and between two levels of exercise. Nine young adults exercised on a treadmill or a bicycle (sit or supine) for 5 min at a mild work load (heart rate = 90 beats X min-1) and then 3 min at a moderate work load (heart rate = 150 beats X min-1). In some studies the moderate work load preceded the mild work load. Arterial blood was sampled from a catheterized artery. During all exercise tasks isocapnia was not strictly maintained (F greater than 4.0, P less than 0.001). For example, a 1-to 2-Torr hypocapnia was the dominant trend during the first 15–45 s after increasing treadmill speed, and a transient hypercapnia was most prevalent when treadmill speed was decreased. During steady-state exercise PaCO2 did not deviate by more than 1–3 Torr from PaCO2 during any resting posture, and PaCO2 differences between exercise intensities and conditions did not exceed 1–2 Torr. A mouthpiece-breathing valve system was not used in most studies, but when this system was used, it did not consistently affect exercise PaCO2. Increasing inspired O2 to 40% likewise did not consistently alter exercise PaCO2. Failure to maintain isocapnia throughout exercise indicates that the matching of alveolar ventilation (VA) to lung CO2 delivery is not exquisitely precise. Accordingly it is inappropriate to base theories of the exercise hyperpnea on the heretofore contention of precise matching.(ABSTRACT TRUNCATED AT 250 WORDS)
An analysis of possible movements of human upper rib cage
Authors: Saumarez R. C.
Published: December 2017

A geometrically realistic mathematical model of the first six ribs and vertebrae of the human rib cage is described. Under the assumption that the individual elements of the rib cage do not deform significantly, the possible range of movements of the model are determined subject to the constraint that the joint surfaces remain in contact. It is shown that normal movements of the ribs cannot be described as a rotation about a single fixed axis. The possible movements of the ribs are analyzed in terms of the misfit incurred at the costovertebral joint surfaces. This analysis shows that there is a movement, corresponding to lateral expansion of the rib for an increase in anteroposterior diameter, in which the misfit at the joint is minimized and also that small deviations from this movement involve only very small degrees of misfit at the joint surfaces. It is concluded that many observed “deformations” of the chest wall can be explained by rigid ribs and normal movements at the costovertebral joints. The interaction between the ribs and the spine is analyzed. It is shown that there can be considerable independent movement of the sternum and the spine, thus allowing mobility of the spine without forcing concomitant movements of rib cage.
Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis
Authors: Bisgard G. E. , Busch M. A. , Forster H. V.
Published: December 2017

We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing cerebral vasoconstriction and brain lactic acidosis even though systemic arterial normoxia was maintained. In the present study we tested the hypothesis that hypocapnic alkalosis is a necessary component of VAH. Goats were prepared so that one carotid body could be perfused, from an extracorporeal circuit, with blood in which gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Using this preparation we carried out 4 h of hypoxic carotid body perfusion while maintaining systemic arterial (and brain) normoxia in awake goats. Expired minute ventilation (VE) was measured while CO2 was added to inspired air to maintain normocapnia. Carotid body PCO2 and PO2 were maintained near 40 Torr during the 4-h carotid body perfusion. Control mean VE was 8.65 +/- 0.48 l/min (mean +/- SE). With acute carotid body hypoxia (30 min) VE increased to 21.73 +/- 2.02 l/min (P less than 0.05); over the ensuing 3.5 h of carotid body hypoxia, VE progressively increased to 39.14 +/- 4.14 l/min (P less than 0.05). These data indicate that neither cerebral hypoxia nor hypocapnic alkalosis are required to produce VAH. After termination of the 4-h carotid body stimulation, hyperventilation was not maintained in these studies, i.e., there was no deacclimatization. This suggests that acclimatization and deacclimatization are produced by different mechanisms.
A general dimensionless equation of gas transport by high-frequency ventilation
Authors: Venegas J. G. , Hales C. A. , Strieder D. J.
Published: December 2017

To identify a general relationship between eucapnic oscillatory flow (Vosc) and frequency (f) in high-frequency ventilation (HFV), we searched the literature for eucapnic HFV data in different mammalian species. We found suitable results for rat, rabbit, monkey, dog, human, and horse, which we expressed in terms of two dimensionless variables, Q = Vosc/Va and F = f/(VA/VD), with VA the alveolar ventilation and VD the volume of the conducting airways. The experimental HFV data define the linear regression equation in Q = 0.54 In F + 0.92 (R = 0.94). Krogh's equation for conventional ventilation (CV), Vosc = VA + fVD, in dimensionless terms becomes Q = 1 + F, which is valid for low F. The intersection of the CV and HFV equations at F = 5.0 defines a transition frequency, ft = 5.0 (VA/VD). At that point the alveolar ventilation per breath, VA/f, represents 20% of VD, and tidal volume (VT) equals 1.20 VD. For eucapnia ft ranges from 5.9 Hz in the rat to 0.9 Hz in the dog. The dimensional form of our HFV equation, VA = 0.13 (VT/VD)1.2 (VTf) is very similar to other empirical equations reported for dogs in noneucapnic settings. Therefore the dimensionless equation should also be valid within a species at noneucapnic settings.
Remarkable metabolic availability of oral glucose during long-duration exercise in humans
Authors: Pallikarakis N. , Jandrain B. , Pirnay F. , Mosora F. , Lacroix M. , Luyckx A. S. , Lefebvre P. J.
Published: December 2017

It was reported previously that glucose ingestion prior to or at the beginning of muscular exercise was a readily available metabolic substrate. The aim of this study was to see what percentage of carbohydrate utilization can be covered by glucose ingested regularly during exercise. Male healthy volunteers exercised for 285 min at approximately 45% of their individual maximal O2 uptake on a 10% uphill treadmill. After 15 min adaptation to exercise they received either 200 g (group G 200) or 400 g (group G 400) glucose (0.25 g X ml H2O-1) orally in eight equal doses repeated every 30 min (G 200 = 8 X 25 g, n = 4; G 400 = 8 X 50 g, n = 4). Indirect calorimetry was used to evaluate carbohydrate and lipid oxidation. Naturally labeled [13C]glucose was used to follow the oxidation of the exogenous glucose. Total carbohydrate oxidation was 341 +/- 22 and 332 +/- 32 g, lipid oxidation was 119 +/- 8 and 105 +/- 5 g, and exogenous glucose oxidation was 137 +/- 4 and 227 +/- 13 g (P less than 0.005) in groups G 200 and G 400, respectively. Endogenous glucose oxidation was about half in G 400 of what it was in G 200: 106 +/- 27 vs. 204 +/- 24 g (P less than 0.02). During the last hour of exercise, exogenous oxidation represented 55.3 and 87.5% of total carbohydrate oxidation for groups G 200 and G 400, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Energy balance in exercise-trained rats acclimated at two environmental temperatures
Authors: Richard D. , Arnold J. , Leblanc J.
Published: December 2017

The present study was carried out to investigate the effects of exercise training on energy balance in male rats acclimated at two different environmental temperatures. Sedimentary and exercised rats were housed and trained at either 24 or 4 degrees C, with the training program consisting of running on a motor-driven treadmill within their respective environments. After 45 days, energy, protein, and fat contents of rats were determined together with the energy content of food and feces. The results show that metabolizable energy intake was reduced by 10% in exercise-trained groups. Substantial differences in energy gains were observed between sedentary and trained rats; sedentary rats showed almost three times more energy gain than trained rats. Carcass analysis revealed the energy gain differences to be mainly due to varied amounts of fat deposition. Energy expenditure (kJ) excluding the cost of exercise training was corrected for metabolic body size (BW 0.75), which in turn showed no significant differences between trained rats and their respective sedentary controls. The present results suggested that exercise training in rats leads to neither increase nor decrease in energy expenditure through components additional to physical activity. The present results also indicated that brown adipose tissue thermogenesis, as assessed through mitochondrial guanosine 5′-diphosphate binding, was not significantly modified by exercise training, regardless of the temperature at which the rats were housed and trained.
Density dependence of maximal expiratory flow before and during tracheal constriction in dogs
Authors: Castile R. G. , Pedersen O. F. , Drazen J. M. , Ingram R. H.
Published: December 2017

The effect of carbachol-induced central bronchoconstriction on density dependence of maximal expiratory flow (MEF) was assessed in five dogs. MEFs were measured on air and an 80% He-20% O2 mixture before and after local application of carbachol to the trachea. Airway pressures were measured using a pitot-static probe, from which central airway areas were estimated. At lower concentrations of carbachol the flow-limiting site remained in the trachea over most of the vital capacity (VC), and tracheal area and compliance decreased in all five dogs. In four dogs, decreases in choke point area predominated and produced decreases in flows. In one dog the increase in airway “stiffness” apparently offset the fall in area to account for an increase in MEF. Density dependence measured as the ratio of MEF on HeO2 to MEF on air at 50% of VC increased in all five dogs. Increases in density dependence appeared to be related to increases in airway stiffness at the choke point rather than decreases in gas-related airway pressure differences. Lower concentrations produced a localized decrease in tracheal area and extended the plateau of the flow-volume curve to lower lung volumes. Higher concentrations caused further reductions in tracheal area and greater longitudinal extension of bronchoconstriction, resulting in upstream movement of the site of flow limitation at higher lung volumes. Density dependence increased if the flow-limiting sites remained in the trachea at mid-VC but fell if the flow-limiting site had moved upstream by that volume.
Unique spectral peak in phrenic nerve activity characterizes gasps in decerebrate cats
Authors: Richardson C. A.
Published: December 2017

The respiratory pattern of gasping has been characterized on the phrenic nerve as rapidonset, rapid-rise, large-amplitude bursts of neural activity. Furthermore, medullary sites critical for the neurogenesis of gasping have been identified and are not the sites of identified respiratory neurons, such as the dorsal and ventral respiratory groups. I classified envelopes of phrenic nerve activity as eupneic breaths, or gasps based on the time-domain features of duration, shape, and amplitude. Gasps were elicited by hypoxia and low blood pressure in 9 of 12 decerebrate cats. Inspiratory times were 1.15 +/- 0.43 (SD) for eupneic breaths and 0.55 +/- 0.18s for gasps. The high-frequency peaks in the power spectra of phrenic nerve activity were at 80 +/- 13 Hz for eupneic breaths and at 120 +/- 21 Hz for gasps. Three of the 12 cats developed a breathing pattern that began as a normal breath and terminated in a gasp. Power spectra of the normal portion had eupneic spectral peaks (75 +/- 24 Hz); power spectra of the gasp portion had the high peaks at 110 +/- 23 Hz, a value 1.5 times higher than that for the normal peaks. Although this analysis of peripheral nerve activity cannot distinguish between two central pattern generators at two distinct anatomical sites or one pattern generator operating in two distinct modes, the fact that gasps were much shorter in duration and had markedly higher spectral peaks than control breaths supports the idea that the central pattern generator for gasping is not the central pattern generator for eupnea.
Suppression of pulmonary and systemic vascular histamine H2-receptors in allergic sheep
Authors: Ahmed T. , King M.
Published: December 2017

We have previously demonstrated a depression of airway H2-receptor function in sheep allergic to Ascaris suum antigen. To investigate whether this is a generalized defect, we studied the H1- and H2- histamine receptor functions in the pulmonary and systemic circulations of allergic and nonallergic sheep. Pulmonary arterial pressure, and cardiac output were measured for calculation of pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) before and immediately after a rapid intrapulmonary infusion of histamine (10 micrograms/kg), with and without pretreatment with H1- (chlorpheniramine) and H2- (metiamide) antagonists. Histamine alone increased mean PVR to 435 and 401% of base line and decreased mean SVR by 51 and 54% in the nonallergic and allergic sheep, respectively (P less than 0.001). In the nonallergic sheep following pretreatment with chlorpheniramine (selective H2 stimulation) or metiamide (selective H1 stimulation), histamine decreased SVR by 18 and 36%, respectively, suggesting that approximately two-thirds of the vasodepressor response was mediated by H1-receptors and one-third by H2-receptors. Combined H1- and H2-antagonists completely blocked the histamine response. In allergic sheep the histamine-induced decrease in SVR was primarily mediated by H1-receptors, because the response was blocked by H1-antagonist, chlorpheniramine, and the H2-antagonist, metiamide, had no effect. In the pulmonary circulation selective H1-stimulation caused a similar increase in PVR in allergic (365%) and nonallergic sheep (424%), whereas selective H2-stimulation caused a significant decrease in PVR in the nonallergic group (14%) but not in the allergic group.(ABSTRACT TRUNCATED AT 250 WORDS)
Determinants of behavioral response with ozone exposure
Authors: Tepper J. S. , Weiss B.
Published: December 2017

Three separate experiments were performed to evaluate how the topography of a behavioral response and its consequences influence the behavioral effects produced by ozone (O3) exposure. The first experiment measured the responding of food-deprived rats working to obtain intermittent delivery of small pellets of food by completing an active response, wheel running. Low O3 concentrations (0.12 ppm) reduced the frequency of running responses maintained by this fixed-interval 10-min schedule of food delivery. The second experiment examined the effects of O2 on food-deprived rats performing a response (nose poking) that required minimal physical effort to produce deliveries of food pellets. Rats in this situation began to show reductions in responding at 0.5 ppm O3. A third experiment showed that responses requiring minimal physical effort, such as lever pressing, can be a sensitive index of O3 exposure if the response provides access to wheel running. We concluded that increased physical activity during exposure appeared to be an important variable in determining sensitivity to O3 exposure.
Mucus transport in the airways by two-phase gas-liquid flow mechanism: continuous flow model
Authors: Kim C. S. , Greene M. A. , Sankaran S. , Sackner M. A.
Published: December 2017

Mucus transport speed induced by two-phase gas-liquid interaction was measured in the continuous two-phase annular flow tube models, and factors influencing the transport speed were assessed in conjunction with rheological properties of mucus. The flow model was made with 1.0-cm-ID glass tubes and positioned either vertically or horizontally. During a continuous passage of airflow through the model tube, mucus stimulants were supplied into the tube at a rate of 0.5–2.0 ml/min. The advancing speed of the leading edge of the mucous layer and mean mucous layer thickness were then measured. The transport speed in the vertical tube model ranged from 1.1 to 3.1 cm/min with a mucus feed rate of 0.5 ml/min at airflow rates of 0.33–1.17 l/s and increased with increasing airflow rates but decreased rapidly with increasing viscosity of mucus. The transport speed increased almost proportionally with increasing mucus feed rate. Elasticity of mucus did not affect the transport speed itself. However, more elastic mucus caused lower flow resistance and thereby could be transported with a much reduced work load. The transport speed in the horizontal tube model was 5–60% faster than that in the vertical tube model. The mean mucous layer thickness in the vertical tube model was found to be in the range of 0.5–1.5 mm in the experimental conditions used, and decreased rapidly with increasing airflow rate and decreasing viscosity of mucus. From these data the transport speed could be functionally related to airway diameter, mucous layer thickness, and mucus production rate.
Effects of 0.5 ppm ozone on glycoprotein secretion, ion and water fluxes in sheep trachea
Authors: Phipps R. J. , Denas S. M. , Sielczak M. W. , Wanner A.
Published: December 2017

We studied the effects of ozone (O3) exposure on airway mucus secretion. Sheep were exposed in vivo to 0.5 ppm O3, 4 h/day for 2 days (acute, n = 6), 6 wks (chronic, n = 6) or 6 wks + 1 wk recovery (chronic + recovery, n = 6). Secretion of glycoproteins (radiolabeled with 35SO4 and [3H]threonine), and transepithelial fluxes of Cl-, Na+ and water were subsequently measured in tracheal tissues in vitro, and were compared with values from control, unexposed sheep (n = 8). Acute O3 exposure increased basal secretion of sulfated glycoproteins (P less than 0.05), but had no effect on ion fluxes. Chronic exposure reduced basal glycoprotein secretion, but increased net Cl- secretion. Under open-circuit conditions, chronic exposure also induced net water secretion (P less than 0.05). With 7 days recovery, basal glycoprotein secretion (predominantly sulfated) was greatly increased above control, while the increased net secretion of Cl- and of water persisted (P less than 0.05). Histology of the airways indicated that acute exposure induced moderate hypertrophy of submucosal glands in the lower trachea (P less than 0.05), while chronic exposure (with and without recovery) induced a large hypertrophy of submucosal glands in both upper and lower trachea (P less than 0.05). Without recovery, however, the gland cells were devoid of secretory material, whereas with recovery they were full of secretory material. This suggests that the decreased glycoprotein secretion with chronic exposure alone resulted from incomplete replenishment of intracellular stores after 6 wks of stimulation. We conclude that both short- and long-term O3 exposure causes airway-mucus hypersecretion.
Three degree of freedom description of movement of the human chest wall
Authors: Smith J. C. , Mead J.
Published: December 2017

A three degree of freedom description of movement of the human chest wall is presented. In addition to the standard variables representing surface displacements of the rib cage and abdominal wall in transverse planes, the description includes a variable representing axial displacements of the chest wall associated with postural movements of the spine and pelvis. A simple technique was developed for quantifying the axial displacements using a single measurement by magnetometry of changes in the distance between a point on the anterior surface of the rib cage near the xiphisternum and a point on the abdominal surface near the pubic symphysis. It was found that axial displacements produced by either flexion-extension of the spine or rotation of the pelvis in the standing postures can be treated as a single degree of freedom. The chest wall displacements induced over the range of axial displacement examined were as large as those normally accompanying a change in lung volume on the order of 30–50% of the vital capacity. It is concluded, however, that although this additional degree of freedom can cause large chest wall displacements, it probably cannot independently change lung volume. This implies that the system is constrained so that there are only a limited number of independent modes of chest wall movement that are capable of producing significant changes in lung volume. It also suggests that the system is constructed so that lung volume can be relatively independent of certain postural distortions of the chest wall.
Pulmonary vascular tone is increased by a voltage-dependent calcium channel potentiator
Authors: Tolins M. , Weir E. K. , Chesler E. , Nelson D. P. , From A. H.
Published: December 2017

The mechanism of hypoxia-induced pulmonary vasoconstriction remains unknown. To explore the possible dependence of the hypoxic response on voltage-activated calcium (Ca2+) channels, the effects of BAY K 8644 (BAY), a voltage-dependent Ca2+ channel potentiator, were observed on the pulmonary vascular response to hypoxia of both the intact anesthetized dog and the perfused isolated rat lung. In six rat lungs given BAY (1 X 10(-6)M), hypoxia increased mean pulmonary arterial pressure (Ppa) to 30.5 +/- 1.7 (SEM) Torr compared with 14.8 +/- 1.2 Torr for six untreated rat lungs (P less than 0.01). After nifedipine, the maximum Ppa during hypoxia fell 14.1 +/- 2.4 Torr from the previous hypoxic challenge in the BAY-stimulated rats (P less than 0.01). BAY (1.2 X 10(-7) mol/kg) given during normoxia in seven dogs increased pulmonary vascular resistance 2.5 +/- 0.3 to 5.0 +/- 1.2 Torr X 1(-1) X min (P less than 0.05), and systemic vascular resistance 55 +/- 4.9 to 126 +/- 20.7 Torr X 1(-1) X min (P less than 0.05). Systemic mean arterial pressure rose 68 Torr, whereas Ppa remained unchanged. Administration of BAY during hypoxia produced an increase in Ppa: 28 +/- 1.5 to 33 +/- 1.9 Torr (P less than 0.05). Thus BAY, a Ca2+ channel potentiator, enhances the hypoxic pulmonary response in vitro and in vivo. This, together with the effect of nifedipine on BAY potentiation, suggests that increased Ca2+ channel activity may be important in the mechanism of hypoxic pulmonary vasoconstriction.