Journal of applied physiology: respiratory, environmental and exercise physiology最新文献

The objective of this study was to determine whether changes in limb motion per se influence arterial CO2 partial pressure (PaCO2) during muscular exercise in ponies. Fifteen ponies were studied at rest and during 8 min of treadmill exercise when the work load was constant or when the work load was increased after the 4th min. Five different treadmill settings were selected to provide for a range of metabolic rate achieved with primary changes in either speed or grade (1.8 mph at 3, 8, and 15% grade; or 3 and 6 mph at 3% grade). The ponies exercised either on all four legs or on only the hindlegs. Step frequencies were 49, 66, and 99 at 1.8, 3, and 6 mph, respectively. During all work tasks PaCO2 decreased maximally 30-60 s after the work task was initiated from rest or from a less intense level of exercise. This nadir in PaCO2 was followed by some recovery with a stable level of mild hypocapnia (delta PaCO2) maintained after 3-4 min. The delta PaCO2 was directly related to O2 consumption (VO2) (P less than 0.01). The delta PaCO2-VO2 regression slopes did not differ between speed and grade VO2 changes nor between four- and two-legged exercise (P greater than 0.10). These data suggest that neither frequency of limb movement nor the number of limbs moving are major factors in the PaCO2 (and alveolar ventilation) response to exercise in ponies. We conclude that the apparent difference in PaCO2 regulation during exercise between ponies (hypocapnia) and humans (isocapnia during walking and bicycling) is not related to a species difference in the number of limbs employed in the exercise task.

Recording from pulmonary stretch receptors in the intact cervical vagus nerve revealed a novel interaction between stretch receptors and smooth muscle in the lungs of anesthetized paralyzed cats. Firing rates of pulmonary stretch receptors were modulated in step with the inflation-deflation cycle of the mechanical respirator, as expected. Firing rates of most slowly adapting receptors, but not rapidly adapting receptors, were also strongly modulated in step with the phrenic nerve activity even when the respirator was turned off and the cat motionless. The modulation of some receptors' firing rates by the inspiratory motor output was as great as the change in firing-rate in response to a lung inflation of 20 ml of air (one tidal volume). Atropine blocked the inspiratory-related modulation of slowly adapting/receptor firing rates; it did not block the inflation-related modulation. Pulmonary resistance was modulated in step with the inspiratory activity on the phrenic nerve. Hyperventilation to neural apnea (no phrenic nerve activity) reduced pulmonary resistance to its lowest level, a level equal to that produced by an injection of isoproterenol or atropine. Hypoxia during hypocapnic apnea caused bursts of inspiratory activity on the phrenic nerve accompanied by one-to-one increases in airway resistance. We conclude that the intrathoracic airway smooth muscle contracts with each neural inspiration, that the modulation of the pulmonary stretch receptors is due to a mechanical interaction with the intrathoracic airway smooth muscle, and that through the mechanical link with airway smooth muscle, stretch receptor sensitivity depends on inspiratory output, a closed loop.

An apparatus and method for rearing neonatal rabbits in hypoxia is described. This technique relies on the use of hypoxia chambers that need to be serviced once a day for approximately 1 h. By use of the apparatus and procedures outlined, rabbits that exhibit standard clinical signs of hypoxemia (cyanosis and elevated hematocrit) can be reliably reared and maintained for long periods of time.

To investigate the effect of different levels of central blood volume on cardiac performance during exercise, M-mode echocardiography was utilized to determine left ventricular size and performance during cycling exercise in the upright posture (UP), supine posture (SP), and head-out water immersion (WI). At submaximal work loads requiring a mean O2 consumption (Vo2) of 1.2 1/min and 1.5 1/min, mean left ventricular end-diastolic and end-systolic dimensions were significantly greater (P less than 0.05) with WI than UP. In the SP during exercise, left ventricular dimensions were intermediate between UP and WI. Heart rate did not differ significantly among the three conditions at rest and at submaximal exercise up to a mean Vo2 of 1.8 1/min. However, at a mean Vo2 of 2.4 1/min, heart rate in the UP was significantly greater than WI (P less than 0.01) and the SP (P less than 0.05). Maximal Vo2 did not differ statistically in the three conditions. These data indicate that a change in central blood volume results in alterations in left ventricular end-diastolic and end-systolic dimensions during moderate levels of exercise and a change in heart rate at heavy levels of exercise.

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)

In rabbits exposed to 100% O2 at 1 ATA from 48 to 72 h, we measured the accumulation of intravenously injected 125I-bovine albumin, [57Co]cyanocobalamin, and 51Cr-erythrocytes in the intestine, skeletal muscle, heart, and lungs. From these data, we calculated the extravascular albumin and cyanocobalamin spaces (EVAS, EVECS) and the partition of water among vascular, interstitial, and cellular compartments in these organs. All variables remained at their base-line levels at 48 h in O2. At 64-66 h, the lung EVECS remained unchanged, but its EVAS increased by 210%. This change occurred after the previously documented increase of the alveolar epithelial permeability to solute and of the pulmonary conductance to water but before the appearance of pulmonary edema and arterial hypoxemia. The only change in the systemic circulation was a 17% increase of the heart EVAS. The increased heart and lung EVAS values, in the absence of any fluid volume shifts, are consistent with damage to the tissue polysaccharides of these organs by the toxic O2 species.

The effect of peak airway pressure (Paw) on vascular permeability and the "safety factor" against edema formation was determined in isolated blood-perfused lower lobes of dog lungs. Microvascular permeability was evaluated using the measured filtration coefficient (Kf,C), isogravimetric capillary pressure (Pc,i), and critical capillary pressure (Pcrit) for exhaustion of tissue safety factors. Airway pressure was maintained constant at -3 cmH2O except for the test period of 20 min when the lungs were ventilated at 6/min with sufficient volume to generate a peak inflation pressure ranging from 5 to 60 cmH2O. Mean Kf,C (in ml X min-1 X cmH2O X 100 g-1) were measured before and immediately after the period of peak airway pressures. Kf,C was significantly increased in all lungs where Paw exceeded 42 cmH2O, but in only two experiments at a lower Paw. Mean Pc,i was significantly reduced from control in the 45-55 and 55-65 cmH2O Paw groups, and both Pc,i and Pcrit were found to be inversely related to Kf,C measured after Paw ventilation. These data indicate that ventilation with Paw above 42 cmH2O (30.9 Torr) and in some cases lower pressures for 20 min significantly increased capillary hydraulic conductivity, reduced the effective osmotic effect of plasma proteins at the capillary wall, and reduced the total tissue safety factor against edema formation.

Pulmonary surfactant research is considered from the perspective of interdisciplinary correlations based on information acquired from biophysics and physical chemistry, biochemistry, cell biology, physiology, and medicine. Current views of the important molecular constituents of the pulmonary surfactant system are described and related to the biophysical surface properties necessary to generate appropriate effects on respiratory physiology. The fundamental importance of multidisciplinary characterizations of lung surfactant, together with correlations between these descriptions, is stressed throughout. The primary advantage of such an approach is that it provides broad but coordinated principles and data with which to test hypotheses of lung surfactant function and roles in respiratory physiology and pathophysiology. This perspective is used to examine available information about the functional composition of lung surfactant, its surface tension-lowering properties at physiological temperature and humidity, and considerations relevant to the formulation of effective exogenous surface-active mixtures in the treatment of surfactant-deficient states. Also discussed is the biophysical state in vivo of pulmonary surfactant at the alveolar level, including current knowledge of the alveolar hypophase as well as the concept of functional surfactant acting in predominantly dry alveoli in the normal lung.

We examined the effect of acute pulmonary vascular congestion on bronchial reactivity in dogs in a standard challenge protocol. Airway responsiveness to histamine whose concentration was varied in a stepwise incremental fashion was assessed from changes in pulmonary resistance (RL) and dynamic compliance (Cdyn) in 10 anesthetized dogs. Brief acute pulmonary congestion was created by inflating a balloon placed in the left atrium to raise left atrial pressure to 20-30 cmH2O for 1 min. Pulmonary congestion did not change RL in the control condition. However, after histamine inhalation, RL was further increased by pulmonary congestion, making the two effects synergistic. This phenomenon could not be observed with vagi cut. Pulmonary congestion decreased Cdyn in all dogs regardless of histamine concentration, with or without vagotomy. We conclude that pulmonary vascular congestion makes the bronchi hyperreactive through vagal reflexes. The reduction in Cdyn caused by pulmonary congestion appears to stem mainly from the narrowing of peripheral airways by adjacent vascular engorgement.

We looked for evidence of changes in lung elastic recoil and of inspiratory muscle fatigue at maximal exercise in seven normal subjects. Esophageal pressure, flow, and volume were measured during spontaneous breathing at increasing levels of cycle exercise to maximum. Total lung capacity (TLC) was determined at rest and immediately before exercise termination using a N2-washout technique. Maximal inspiratory pressure and inspiratory capacity were measured at 1-min intervals. The time course of instantaneous dynamic pressure of respiratory muscles (Pmus) was calculated for the spontaneous breaths immediately preceding exercise termination. TLC volume and lung elastic recoil at TLC were the same at the end of exercise as at rest. Maximum static inspiratory pressures at exercise termination were not reduced. However, mean Pmus of spontaneous breaths at end exercise exceeded 15% of maximum inspiratory pressure in five of the subjects. We conclude that lung elastic recoil is unchanged even at maximal exercise and that, while inspiratory muscles operate within a potentially fatiguing range, the high levels of ventilation observed during maximal exercise are not maintained for a sufficient time to result in mechanical fatigue.