were smallest at 4 and greatest at 8 atm absolute. In IX-sectioned rats the rates of rise of VT at 4, 6 and 8 atm absolute and off at 4 atm absolute were similar to those of intact rats. At 6 atm absolute and even more so at 8 atm absolute, however, f decreased. Hence the slope of FE in IX-sectioned compared with intact rats was similar at 4 atm absolute but smaller at 6 and 8 atm absolute. In fact at 8 atm absolute F'E remained constant in IX-sectioned rats.3. Since the slope of VE versus time in intact rats was steeper the greater the pressure and since the removal of carotid bodies in IX-sectioned rats reduced the G'E slope at 6 and 8 atm absolute, the stimulus to the hyperventilation induced by o.h.p. cannot be an accumulation of CO2 in the brain resulting from the lack Of 02 desaturation of haemoglobin. This theory would predict that PE should be identical at all pressures above 3-5 atm absolute.4. The findings in the IX-sectioned rats indicate a major contribution of the carotid bodies to the f increase in o.h.p. They may be stimulated by a histotoxic hypoxia induced by early 02 poisoning. Since the VT increase on exposure to o.h.p.was both large and fairly similar in intact and IX-sectioned rats, it is suggested that a large part ofthe VT increase was caused by stimulation ofthe central chemoreceptors by lactic acidosis induced by an o.h.p.-induced histotoxic hypoxia of the brain.
1. Ventilation ( V(E)), tidal volume (V(T)), respiratory frequency (f) and arterial and end-tidal gas tensions were measured in seventy-one tracheostomized New Zealand white rats ( approximately 405 g) anaesthetized with an initial dose of pentobarbitone followed by repeated small doses to ensure that a weak limb-withdrawal reflex remained.2. O(2) consumption (1.2 ml (s.t.p.d.) min(-1) 100 g(-1)), CO(2) production (1.0 ml (s.t.p.d.) min(-1) 100 g(-1)), heart rate (357 min(-1)), V(E) (43 ml min(-1) 100 g(-1)), P(a,CO2) (34 mmHg) and P(a,O2) (84 mmHg) in the control periods did not change significantly during the course of the experiment.3. Inspirates of 21% O(2) with 2-10% CO(2), 15, 10 or 7.5% O(2) with either no or sufficient CO(2) to maintain normocapnia and 15 or 10% O(2) with 4, 6 or 8% CO(2) were tested. Steady-state responses were measured after 2 min of exposure.4. Hypoxic-hypercapnic interaction on V(E), V(T) and f determined by a three-inspirate test ((i) hypoxia alone, (ii) hypercapnia and (iii) these hypoxic and hypercapnic levels combined) yielded various conclusions depending on the level of asphyxia examined. Essentially, the milder the asphyxia the more the interaction appeared additive or even multiplicative and the stronger the asphyxia the more the interaction appeared occlusive. However, this test is unsuitable for accurately showing interactions because the P(a,O2) achieved in asphyxia was higher than in hypoxia and the asphyxial P(a,CO2) was lower than in hypercapnia.5. For isoxic conditions (P(a,O2) = 97, 77 and 51 mmHg), V(E) and V(T) were related linearly to P(a,CO2) whilst f was related hyperbolically with convexity upwards (P(a,O2) 97 mmHg) or downwards (P(a,O2) 77 and 51 mmHg).6. For isocapnic conditions (P(a,CO2) = 33, 40 and 48 mmHg), V(E) and V(T) were inversely related to P(a,O2) with a hyperbolic curve (convexity downwards) whilst f was inversely and linearly related (P(a,CO2) 33 mmHg) or constant (P(a,CO2) 40 and 48 mmHg).7. Multivariate analyses showed that the hypoxic-hypercapnic interaction was additive for V(T) but occlusive for V(E) and f and the occlusion was more severe in the latter. This was illustrated graphically for the variable plotted against P(a,CO2) or P(a,O2) as parallel shifts in regression lines for V(T), flatter regression lines for V(E) during asphyxia and a virtually constant f during asphyxia.8. V(E) responses and sensitivities to hypoxia and hypercapnia, the shape of V(E), V(T) and f regression lines against P(a,O2) and P(a,CO2) and the type of hypoxic-hypercapnic interaction on each variable in the rat were compared with other species.9. Possible causes of the occlusive hypoxic-hypercapnic interaction in the rat were considered.
2. In all 'free-breathing' tests ventilation decreased significantly after a mean latency of 5-2 sec; the average lung-ear circulation time was 4 9 sec. HR increased slightly above pre-test levels in eighty-one of one hundred and four tests of all types, the changes being significant after a latency identical to that of the ventilatory changes. Except in the 'controlled-breathing' CO2 tests this early tachycardia was followed by a decrease in HR within the following 5-6 sec.3. These findings indicate that the primary effect of withdrawal of arterial chemoreceptor stimulation in conscious man as in the anesthetized animal is tachycardia. The secondary development of bradycardia in 'free-breathing' CO2 tests is probably due to the operation of a lung reflex sensing changes in ventilation. The absence of bradycardia in ' controlled-breathing' CO2 tests and its presence in 'controlled-breathing' 02 tests, finally, suggest that relief of systemic hypoxia causes a slowing of the heart not due to lung reflexes but to some other mechanism which operates with a latency nearly twice as long as the arterial chemoreflex.
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