Respiration physiology
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Respiration physiology · Jun 1995
Hypoxic ventilatory response predicts the extent of maximal breath-holds in man.
To understand the factors influencing breath-holding performance, we tested whether the hypoxic (HVR) and hypercapnic ventilatory responses (HCVR) were predictors of the extent of maximal breath-holds as measured by breath-hold duration, the lowest oxyhemoglobin saturation (SpO2min), lowest calculated PaO2 (PaO2min) and highest end-tidal PCO2 (PETCO2max) reached. Steady state isocapnic HVR and hyperoxic HCVR were measured in 17 human volunteers. Breath-holds were made at total lung capacity (TLC), at TLC following hyperventilation, at functional residual capacity, and at TLC with FIO2 = 0.15. ⋯ HVR and forced vital capacity were predictors of breath-hold duration by multiple linear regression. HCVR had no significant predictive value. We conclude that HVR, but not HCVR, is a significant predictor of breath-holding performance.
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Isolated rabbit lungs were buffer-perfused under constant flow-conditions with separate control of alveolar (PAO2) and mixed venous (PvO2) O2 tension. Alveolar hypoxia caused an increase in pulmonary artery pressure (PAP) with sigmoidal dose-dependency. Erythrocytes increased the strength of the hypoxic pulmonary vasoconstriction (HPV). ⋯ In contrast, changes in PvO2, both in the absence and presence of erythrocytes, did neither provoke any pressor response nor amplify the response to concomitant alveolar hypoxia. Repeatedly performed HPV manoeuvres revealed excellent reproducibility, and long-term alveolar hypoxia (90 min) provoked a biphasic pressor response. We conclude that the isolated rabbit lung is a feasible model for the characterization of hypoxic vasoconstriction, with specific features hitherto not described for perfused lungs of other species.
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Respiration physiology · Aug 1994
Effects of inhaled nitric oxide in rats with chemically induced pulmonary hypertension.
To determine the model animal with pulmonary hypertension in which nitric oxide (NO) inhalation reduces pulmonary arterial pressure (PAP), we examined the inhalation of 20-100 ppm NO gas on normal rats and rats with monocrotaline induced pulmonary hypertension. In the control group, mean PAP showed no change after spontaneous breathing of NO at the concentration of 20 to 100 ppm for 5 min. On the contrary, in both the severe (mean PAP > 40 mmHg) and moderate (mean PAP < 40 mmHg) pulmonary hypertensive groups, NO inhalation produced a prompt reduction of the mean PAP which had been elevated by monocrotaline. 20 ppm NO inhalation reduced mean PAP from 64.4 +/- 3.7 mmHg to 56.2 +/- 4.4 mmHg (mean +/- SEM, P < 0.01) in the severe pulmonary hypertensive group, from 31.0 +/- 2.0 mmHg to 24.2 +/- 0.9 mmHg in the moderate pulmonary hypertensive group (mean +/- SEM, P < 0.05). The onset of the reduction of mean PAP occurred within 30 sec after the start of NO inhalation and maximum reduction occurred within 4 min. 20 ppm NO inhalation significantly reduced mean PAP, and mean PAP was reduced dose-dependently at the concentration of 20 to 60 ppm and reaction to NO was almost constant at the concentrations of over 60 ppm.
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Respiration physiology · May 1994
The dose-response relationship for hypoxic pulmonary vasoconstriction.
In 12 pentobarbital anesthetized dogs the lungs were independently ventilated with a double piston ventilator. The right lung was ventilated throughout with 100% oxygen. Blood was drawn from the right atrium and pumped through a bubble oxygenator to a cannula in the ligated left main pulmonary artery. ⋯ From the combined data a three dimensional response surface for hypoxic pulmonary vasoconstriction was derived. The maximum increase of pulmonary vascular resistance (r%PVRmax) was defined at a stimulus oxygen tension (PSO2) of 10 mmHg amounting to a 3.15 +/- (0.18)-fold increase of the vascular resistance on "100%" oxygen. The stimulus oxygen tension was shown to be PSO2 = PVO2(0.41) x PAO2(0.59) and the dose-response sigmoid for hypoxic pulmonary vasoconstriction in canine lungs was derived as r%PVRmax = 100 (PSO2(-2.616))/(6.683 x 10(-5) + PSO2(-2.616)) These results appear to reconcile observations from a number of laboratories and to be of quite general application.
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Respiration physiology · Feb 1994
Transfer of gas from the acinus during continuous flow and intermittent positive pressure ventilation.
We used a technique of measuring Xenon133 washout (XeW) from the alveolar space to evaluate transfer of gas from the acinus (Mackenzie et al., J. Appl. Physiol. 68: 2013-2018, 1990) during 2 min of apnea, 2 min of tracheal insufflation with oxygen (TRIO) and 90 sec of intermittent positive pressure ventilation (IPPV) in 6 anesthetized and paralyzed dogs. ⋯ This was not different (P > 0.05) with TRIO (0.29 +/- 0.04). With IPPV, the rate constant increased to 3.49 +/- 0.39, faster than with either apnea or TRIO (P < 0.001). We conclude that: (1) TRIO does not increase convective gas transfer from the acini compared to apnea; and (2) transfer of gas out of the acini due to cardiogenic oscillations is a very small portion of the total gas eliminated during IPPV.