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

Nine puppies underwent left pneumonectomy at 10 wk of age while nine sex-matched littermates had a sham operation, and all animals were studied at 25 wk of age. Postpneumonectomy dogs demonstrated compensatory growth in that lung weight and total lung capacity (TLC) were the same as those of control animals when normalized for body weight. In postpneumonectomy dogs all lobes of the remaining right lung increased in weight, but this was most notable in the cardiac lobe which grew across the mediastinum. Subdivisions of lung volume were normal in postpneumonectomy animals except for residual volume (RV): RV/TLC was increased when compared with control animals. In intact dogs static pressure-volume curves of the lung and respiratory system did not differ between groups, and the static pressure-volume curves of excised lungs were closely similar. Maximum expiratory flow was sharply reduced in postpneumonectomy dogs, averaging 40% of flow in control dogs over the lower 50% of the vital capacity. In both groups the fractional increase in maximal expiratory flow during HeO2 breathing was substantial and similar. Regional compliances, resistances, and perfusion distribution were examined using 133Xe. Regional compliance and perfusion were reduced in the left hemithorax of postpneumonectomy dogs while regional resistances were increased.

We hypothesize that training results in a faster and greater repletion of glycogen in skeletal muscles of normal and diabetic rats. Normal male Sprague-Dawley rats (100-140 g) were divided into two groups--one to train by treadmill running for 10 wk and the other to remain sedentary. Forty-eight hours after the last training session the rats of both groups were exercised to exhaustion. One subgroup of each was fed oral glucose (3 g/kg) at exhaustion and killed 60 min later. The other was killed at exhaustion. The glycogen concentration of soleus, plantaris, and red and white gastrocnemius was determined in all rats. The trained group had higher glycogen levels after glucose feeding in all muscles (P less than 0.002) and repleted their muscle glycogen more rapidly (P less than 0.05). However, in diabetic rats (45 mg streptozotocin/kg body wt) the trained and sedentary rats have similar glycogen levels and glycogen repletion rates in all muscles. Compared with the normal trained rats, the diabetic trained rats had slower glycogen repletion rates (P less than 0.05).

The contractile effects of substance P (SP) were studied in isolated rabbit tracheal smooth muscle (TSM) segments in vitro. Noncumulative administration of SP produced dose-dependent increases in TSM tension. The mean (+/- SE) peak isometric tension (Tmax) with SP was 35.7 (+/- 6.2%) of the corresponding Tmax response to methacholine. The dose of agonist producing 50% of Tmax (ED50) was significantly lower for SP, averaging 1.8 (+/- 0.4) X 10(-7) M, vs. 1.7 (+/- 0.32) X 10(-6) M for methacholine. Blockade of both parasympathetic ganglia with hexamethonium (10(-4) M) and neural transmission with tetrodotoxin (1 microgram/ml) had no effect on the TSM response to SP. On the other hand, TSM contraction to an ED50 dose of SP was 1) augmented by a mean (+/- SE) of 470 (+/- 110%) following pretreatment with the cholinesterase inhibitor, neostigmine (10(-6) M);2) inhibited by a mean (+/- SE) of 35 (+/- 15%) with the cholinergic antagonist, atropine (10(-4) M); and 3) also inhibited by a mean (+/- SE) of 45 (+/- 11%) following inhibition of acetylcholine synthesis with hemicholinium-3 (10(-4) M). Antagonists to 5-hydroxytryptamine, alpha 1-adrenergic, and histamine receptor binding had no effect on TSM contraction with SP. In contrast, the SP antagonist, D-Pro2,D-Trp7,9-SP, markedly inhibited TSM contraction to SP. Our findings indicate that rabbit TSM is sensitive to SP and its contraction is in part mediated by a peripheral cholinergic action, likely involving the accelerated release of acetylcholine at the airway neuromuscular junction.

Because the pulmonary endothelium is sensitive to O2-induced damage, we studied in vivo angiotensin-converting enzyme (ACE) activity in the lungs of 14 catheterized unanesthetized dogs exposed either to air or continuous 100% O2 at 1 ATA. For 5 days, or until the dog died, we measured physiological variables and lung ACE activity. The metabolic data were analyzed with a model that accounted for the effect of changes in cardiac output. Nine dogs breathing O2 lived 88 +/- 21.8 (SD) h and except for blood O2 tensions were indistinguishible from controls until development of a terminal response lasting only a few hours. Hemodynamic instability preceded a precipitous terminal change in blood gas tensions which resulted in impairment of arterial oxygenation, hypercapnia, and acidosis. Plasma renin activity increased. The metabolic capacity of the pulmonary endothelium of O2-exposed animals decreased with time so that after 96 h it was 50% of the control. That of five control animals did not change with time. Thus changes in lung ACE activity preceded alterations in hemodynamics or gas exchange, and the contributions of each are discussed.

To determine if neural control of the crural diaphragm is similar to that of the costal diaphragm, electrical activity was recorded from these two parts of the diaphragm in 10 anesthetized dogs during resting O2 breathing and during progressive hyperoxic hypercapnia. Within a breath, the onset of crural diaphragm inspiratory activity started significantly earlier than that of the costal diaphragm under both resting and CO2 stimulated conditions, although the relative delay in costal diaphragm activity was smaller during hypercapnia than during resting O2 breathing. Following hyperventilation to apnea, both parts of the diaphragm resumed activity on the same breath. During CO2 rebreathing, the maximal increase in crural diaphragm peak electrical activity was significantly greater than that of the costal diaphragm. We also examined the effects of histamine-induced bronchoconstriction on diaphragm activity. Following administration of histamine aerosol there was a transient of irregular breathing during which in three animals costal diaphragm activity became nearly quiet, although there was continued activity of the crural diaphragm. Once breathing became more regular, there was a significantly greater stimulation of crural diaphragm than costal diaphragm activity; this difference persisted for 15 min after histamine inhalation. These results support the concept that electrical activity can be distributed nonuniformly to the costal and crural diaphragm and demonstrate that the crural diaphragm has a greater gain with hypercapnia and bronchoconstriction than does the costal diaphragm.

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.

A decrease in functional residual capacity (FRC) during sleep could result in worsening of ventilation distribution contributing to sleep hypoxemia. Therefore the purpose of this study was to determine whether FRC does decrease and to what extent it decreases in normal humans during sleep. Using helium dilution in a closed system we measured FRC in 10 healthy males during wakefulness, stage 2, stages 3-4, and rapid-eye-movement (REM) sleep. Mean FRC decreased from 3.14 +/- 0.01 (SE) liters during wakefulness to 2.95 +/- 0.01 liters in stage 2 sleep. Lowest sleep values were 2.86 +/- 0.01 liters in stages 3-4 and 2.83 +/- 0.01 liters in REM sleep (P less than 0.05 from wakefulness). Although the amount of the decrease in FRC identified during sleep was surely not large enough to impair ventilation distribution in normal humans, this degree of decrease might contribute to the hypoxemia seen in patients with severe airflow limitation.

We measured K, an index of interdependence in sublobar segments of both intact and excised calf lungs. In excised and intact lungs, segment volume was held constant while the lung was inflated. K in excised lungs was of small magnitude but was greater in caudal than in cranial and middle lobes. When isolated segments in a variety of regions and with a variety of shapes were studied, K was positively correlated with the interface area between the segment and the remainder of the lung, was negatively correlated with the pleural surface area of the segment, but was not correlated with segment volume. In a given region of lung, however, small segments had a greater interdependence than large segments. In intact lungs of anesthetized calves, K was an order of magnitude greater than in excised lungs, confirming that the chest wall is the major determinant of interdependence. There were no lobar differences in K in intact lungs.

The purpose of this study was to determine the effects of bed-rest-induced deconditioning on changes in O2 uptake (VO2) kinetics, O2 deficit, steady-state VO2, and recovery VO2 during the performance of constant-load exercise. Five male subjects (36-40 yr) underwent 7 days of continuous bed rest (BR) in the head-down (-6 degrees) position. Two days before (pre) and the day after (post) BR each subject performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min of rest, 5 min of cycle ergometer exercise at 700 kg.m/min, and 10 min of recovery from exercise. VO2 was measured continuously in all tests from 2-liter aliquot gas samples collected every 30 s. Following BR steady-state VO2 was unchanged in supine and upright exercise. In the supine position BR did not change total exercise VO2, O2 deficit, or total recovery VO2. However, compared with pre-BR, total exercise VO2 decreased (P less than 0.05) from 7.41 +/- 0.11 to 7.23 +/- 0.17 liters, O2 deficit increased (P less than 0.05) from 1.15 +/- 0.05 to 1.41 +/- 0.07 liters, and total recovery VO2 increased (P less than 0.05) from 5.17 +/- 0.11 to 5.47 +/- 0.17 liters during the post-BR upright test. Despite the ability to attain similar steady-state VO2 within 5 min, bed-rest-induced deconditioning resulted in a reduction of total VO2 capacity and an increase in the O2 deficit during submaximal constant-load exercise. This change in VO2 kinetics is found only with exercise in the upright rather than supine position implicating orthostatic mechanisms in the delayed response to submaximal exercise.

We have examined the effects of changes in functional residual capacity (FRC), determined by positive and negative body surface pressures, on the breathing pattern of intact newborn rats, before and after barbiturate anesthesia. With distending pressures (between 1 and 4 cmH2O) minute ventilation decreased mainly due to a prolongation of the expiratory time. This response was more marked after anesthesia and accompanied by a fall in tidal volume. The time of peak expiratory flow (TE'), an index of expiratory flow resistance, was not changed before anesthesia and only slightly decreased after anesthesia. With collapsing pressures between 1 and 2 cmH2O only small changes in breathing pattern occurred, whereas the TE' increased in all cases and the flow profile indicated a maintenance of lung volume during expiration. These data indicate that tonic vagal information is present in the newborn rat and is substantially enhanced after barbiturates. The result that changes in breathing pattern are not fully matched by the changes in TE' and expiratory flow profile may indicate that the receptors which control the respiratory pattern are not the same as those involved in the regulation of the expiratory flow. The pressure-volume curve of the respiratory system was similar before and after anesthesia, and the intercept was close to the zero pressure value, indicating that the FRC of the newborn rat, differently from the human baby, is not actively maintained above the resting volume of the system.