Recovery of the ventilatory response to hypoxia in normal adults.

Recovery of the initial ventilatory response to hypoxia was examined after the ventilatory response had declined during sustained hypoxia. Normal young adults were exposed to two consecutive 25-min periods of sustained isocapnic hypoxia (80% O2 saturation in arterial blood), separated by varying interludes of room air breathing or an increased inspired O2 fraction (FIO2). The decline in the hypoxic ventilatory response during the 1st 25 min of hypoxia was not restored after a 7-min interlude of room air breathing; inspired ventilation (VI) at the end of the first hypoxic period was not different from VI at the beginning and end of the second hypoxic period. After a 15-min interlude of room air breathing, the hypoxic ventilatory response had begun to recover. With a 60-min interlude of room air breathing, recovery was complete; VI during the second hypoxic exposure matched VI during the first hypoxic period. Ventilatory recovery was accelerated by breathing supplemental O2. With a 15-min interlude of 0.3 FIO2 or 7 min of 1.0 FIO2, VI of the first and second hypoxic periods were equivalent. Both the decline and recovery of the hypoxic ventilatory response were related to alterations in tidal volume and mean inspiratory flow (VT/TI), with little alteration in respiratory timing. We conclude that the mechanism of the decline in the ventilatory response with sustained hypoxia may require up to 1 h for complete reversal and that the restoration is O2 sensitive.

Ventilatory response to sustained hypoxia in normal adults.

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.

Treatment of canine low pressure pulmonary edema. Nitroprusside versus hydralazine.

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of different doses of nitroprusside and compared the results with those obtained after intravenously administered hydralazine. Oleic acid increased (p less than 0.05) intrapulmonary shunt (Qs/Qt), increased (p less than 0.01) systemic vascular resistance (SVR), and reduced (p less than 0.05) cardiac output (CO). In the presence of low-pressure pulmonary edema, low-dose nitroprusside (NP1) reduced (p less than 0.01) mean blood pressure (BP) approximately 8%, but with the exception of a small fall in ventricular filling pressure, other parameters remained constant. Compared with control values, a higher dose of nitroprusside (NP2) reduced mean BP 20%, and despite a fall (p less than 0.01) in pulmonary capillary wedge pressure, CO increased (p less than 0.05) 20%. Corresponding to the increase in flow, mean Qs/Qt increased (p less than 0.05) from 26 to 36% with NP2 and arterial O2 tension fell (186 to 166 mmHg, p less than 0.05). Compared with NP2, intravenously administered hydralazine caused a larger (p less than 0.01) change in CO. Despite increased CO and increased (p less than 0.01) mixed venous O2 tension, there was no deterioration in gas exchange with hydralazine. Mean Qs/Qt remained constant and arterial O2 tension, (PaO2) increased (p less than 0.05) from 174 mmHg to 217 mmHg. The increased CO with NP2 and hydralazine is probably explained by the large reduction in systemic vascular resistance. Because Qs/Qt remained constant with hydralazine, the increase in PaO2 is most likely due to the increase in PvO2, which increased because CO increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of previous volume history on airway closure.

We studied the effect of volume history on airway closure in six healthy males ranging from 32 to 67 yr of age. The method used was to compare the regional distribution of 133Xe boluses distributed according to N2O uptake during open-glottis breath-hold maneuvers with the regional distribution of boluses of intravenously injected 133Xe. Measurements were made at two lung volumes, one close to residual volume (RV) and the other just below closing volume. The required volume was reached either by expiring from total lung capacity or by inspiring from RV. Although there was considerable airway closure in the basal regions of the lungs at both lung volumes studied, the degree of airway closure was not dependent on the previous volume history. We conclude that the airways concerned with closure have a volume-pressure hysteresis similar to that of the lung parenchyma. Furthermore in normal humans the volume-pressure hysteresis of the lung is not secondary to airway closure.