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

Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.

We produced pulmonary fibrin microembolism using an infusion of a prothrombin activator (Echis carinatus venom, 30 min, 0.5 NIH thrombin equivalent units/kg) in open-chest mongrel dogs. To determine the nonclotting effects of this venom on edemagenesis we infused an irreversible thrombin inhibitor, D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK, 57 nmol X kg-1 X min-1 for 120 min), alone (n = 5) or with venom (Echis + PPACK, n = 5). The control group (n = 5) was given 1 ml of 0.9% NaCl. A decline in left atrial pressure (means +/- SE, 5.3 +/- 0.4 to 4.0 +/- 0.5 mmHg, P less than 0.05) and cardiac index (149 +/- 10 to 82 +/- 13 ml X min-1 X kg-1, P less than 0.01) in association with a marked increase in pulmonary arterial pressure (14.5 +/- 0.6 to 26.6 +/- 2.5 mmHg, P less than 0.001) and pulmonary vascular resistance (64 +/- 5 to 304 +/- 42 mmHg X ml-1 X min-1 X kg-1, P less than 0.001) was observed after 20 min of venom infusion. During this interval, pulmonary artery wedge pressure increased (4 +/- 1 to 12 +/- 4 mmHg, P less than 0.01) in four of eight animals. Fibrinogen declined below measurable levels and fibrin microemboli were seen in many pulmonary arterioles. These changes were not observed in the Echis + PPACK, PPACK, or control groups. Leukopenia and thrombocytopenia were observed in the Echis and Echis + PPACK groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Female rats were exercised by swimming up to 4 h/day either 2, 4, or 6 days/wk. After 7 wk they continued to train at these frequencies or had their training reduced from 6 to 4, 2, or 0 days/wk for an additional 9 wk. Ventricular weights and maximum O2 uptake (VO2max) were increased by 5-10% after training 2 days/wk, 15-17% after 4 days/wk, and 25-30% after 6 days/wk. Following reduced training, VO2max was similar when the 4- or 2-day/wk reduced training groups are compared with their 4- or 2-day/wk continued training counterparts. In contrast, VO2max was greater in the 0-day reduced than in the sedentary control group. No differences in mitochondrial markers or myoglobin content in red or mixed skeletal muscles were found between training 2 or 4 days/wk vs. reduced training at comparable frequencies. O2 uptake capacity of plantaris muscles and myoglobin concentration in fast-twitch red vastus lateralis muscles were greater in the 0-day reduced group than in the sedentary controls. These data show that VO2max and certain markers of aerobic metabolism in skeletal muscles of rats are lost at a slower rate than their rate of increase from the untrained state. However, a reduction of swimming frequency from 6 to 4 or 2 days/wk is not a sufficient stimulus to maintain VO2max, cardiac enlargement, or the increased aerobic potential of skeletal muscle at the 6-day/wk levels.(ABSTRACT TRUNCATED AT 250 WORDS)

The pressure swings under the costal (Pcos) and crural diaphragms (Pcru) and between the intestinal loops (Pint) were compared with the swings in gastric pressure (Pga) in 13 supine anesthetized dogs. Pcos, Pcru, and Pint were measured with air-filled latex balloons in eight dogs and saline-filled catheters in five. Pga was measured with an air-filled balloon in all dogs. During quiet breathing differences were often present, the directions of which were variable from animal to animal. During mechanical ventilation, all pressures increased, but both Pcos and Pcru increased more than Pga, whereas only a small change was observed in Pint. During bilateral stimulation of the costal diaphragm, Pcos invariably increased more than Pga and Pint, whereas almost no change was observed in Pcru. During bilateral stimulation of the crural diaphragm, Pcru invariably increased more than Pga, Pint, and Pcos. During abdominal muscle stimulation as during external abdominal compression, Pint always increased more than Pcos and Pcru. During lower rib cage compression, Pga, Pcos, and Pcru increased more than Pint. During sternocleidomastoid stimulation, all pressure swings were negative, but the change in Pint was always smaller than in Pcos, Pcru, or Pga. Inhomogeneities observed with balloons and saline-filled catheters were similar. After the abdomen was filled with 2 liters of saline all pressure swings became much more homogeneous.

Previously we observed what appeared to be augmented D-glucose transport across the pulmonary epithelium. To investigate this phenomenon we placed fluid containing L-[3H]glucose and D-[U-14C]glucose in the alveoli of isolated Ringer-perfused lungs from 4-wk-old rabbits. The appearance of radioactivity in recirculating glucose-free perfusate was measured. 3H appearing in the perfusate was associated with L-glucose. 14C, however, was associated with three compounds, with approximate molecular weights of 180 (glucose), 300, and 560. The nonglucose species were not identified. This 14C movement was inhibited by phlorizin, but not phloretin, in the alveolar fluid. A similar pattern of 14C movement occurred when D-[U-14C]glucose was replaced with 2-deoxy-D-[U14C]-glucose, but not with methyl-alpha-D-[U-14C]glucopyranoside. The activation energy of the 14C metabolism-transport process was found to be 34 kcal/mol, and L-glucose transport showed an unusual temperature dependence, with maximum conductance at 15 degrees C. It appears that some D-glucose crosses the pulmonary epithelium as does L-glucose. However, most enters epithelial cells and is incorporated into larger molecules which enter the vascular but not the alveolar space.

We administered antifibrotic agent beta-aminopropionitrile (BAPN) to rats exposed to 10% O2-90% N2 for 3 wk to prevent excess vascular collagen accumulation. Groups of Sprague-Dawley rats studied were air breathing, hypoxic, and hypoxic treated with BAPN, 150 mg/kg twice daily intraperitoneally. After the 3-wk period, we measured mean right ventricular pressure (RVP), the ratio of weight of right ventricle to left ventricle plus septum (RV/LV + S), and hydroxyproline content of the main pulmonary artery (PA) trunk. Hypoxia increased RVP from 14 to 29 mmHg; RVP was 21 mmHg in hypoxic BAPN-treated animals. Hypoxia increased the RV/LV + S ratio from 0.28 to 0.41; the ratio was 0.32 in hypoxic BAPN-treated animals. Hypoxia increased PA hydroxyproline from 20 to 239 micrograms/artery; hydroxyproline was 179 micrograms/artery in hypoxic BAPN-treated animals. Thus BAPN prevented pulmonary hypertension, right ventricular hypertrophy, and excess vascular collagen produced by hypoxia. We conclude that vascular collagen contributes to the maintenance of chronic hypoxic pulmonary hypertension.

The response of colonic and tail-skin temperatures to treadmill exercise was assessed in female Sprague-Dawley rats using incremental and single-stage exercise protocols to investigate the relationship between deep body temperature and work rate. O2 uptake (VO2) was measured by flow-through technique to evaluate the exercise intensity. Experiments were performed in ambient temperatures below (22-25 degrees C) and above (33-35 degrees C) the thermoneutral zone of the rat. During graded incremental exercise there was a linear relationship between colonic temperature (Tco) and VO2 in both the cooler and warmer ambient temperatures. However, Tco and tail-skin temperature (Tsk) at comparable work rates in the cooler and warmer environments were 40.22 +/- 0.59, 34.84 +/- 1.10 degrees C and 42.04 +/- 0.57, 38.39 +/- 1.54 degrees C, indicating that the rise in Tco was unrelated to the severity of exercise. During single-stage exercise the rats were able to achieve thermal equilibrium but only at low work rates and in the cool environment (22-25 degrees C). There were no significant differences in Tco at the first three levels of single-stage exercise (stage 1, 39.63 +/- 0.34 degrees C; stage 2, 39.67 +/- 0.49 degrees C; stage 3, 39.75 +/- 0.50 degrees C) despite significant differences in VO2 (stage 1, 4.3 +/- 0.7 ml X min-1 X 100 g-1; stage 2, 5.3 +/- 0.6 ml X min X 100 g-1; stage 3, 7.6 +/- 1.2 ml X min-1 X 100 g-1). This demonstrates that there was no relationship between the level of Tco maintained during exercise and the work intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies using tissue homogenates have demonstrated an increase in pulmonary beta-receptors during development. However, techniques using disrupted tissue have not permitted the precise anatomic localization of pulmonary beta-receptors or identification of structures where increases occur. Using L-[3H]dihydroalprenolol, beta-receptors were radioautographically localized and quantitated in sections of newborn (NB) and adult (A) guinea pig lung. Scatchard analysis showed a single class of binding sites with a maximum binding capacity of 189 +/- 3 (NB) and 305 +/- 37 (A) fmol X mg-1 protein (P less than 0.02). Binding was of high affinity with the dissociation constant (Kd) = 1.46 +/- 0.2 (NB) and 1.26 +/- 0.3 (A) nM (NS). The majority of beta-receptors were localized in alveolar wall and airway epithelia (alveolar much greater than bronchiolar greater than bronchial) (P less than 0.0001). Airway and vascular smooth muscle had significantly fewer demonstrable beta-receptors. The increased number of beta-receptors in the adult appeared to be due primarily to a 2.0 +/- 0.12-fold increase in alveolar wall and airway epithelia as opposed to only a 1.3 +/- 0.18-fold increase in the already low number in airway and vascular smooth muscle (P less than 0.05). While apparent receptor density may not necessarily correlate with physiological response or importance, radioautographic localization of pulmonary beta-receptors may significantly enhance our understanding of their role in normal and pathologic states.

To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.

Spacelab is a cylindrical pressurized laboratory (approximately 7 m long and 4 m in diameter) that is part of the payload of the Space Shuttle. It provides an orbiting "shirtsleeves" environment for laboratory experiments on the physiological effects of weightlessness. The first Spacelab flew in November 1983 with great success. Of special interest to physiologists is Spacelab 4, which is scheduled for early 1986 and will be the first dedicated to life sciences. It will contain 24 experiments covering the area of vestibular, cardiovascular, pulmonary, renal, endocrine, blood, bone, and muscle physiology, with additional experiments in gravitational biology. Opportunities for research on subsequent life science Spacelabs have recently been announced, and this is therefore an opportune time to review progress to date in the field of space physiology and to point to some of the challenges of this emerging discipline.