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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



this capacity for vasoconstriction is actually used by 

 the intact animal under natural conditions: the 

 strength of such a decision depends on the degree to 

 which all conceivable passive influences on the pulmo- 

 nary circulation have to be appraised and found 

 wanting. And the list of potential passive influences 

 is apt to be longer for experiments performed under 

 natural conditions than under contrived experimental 

 conditions (387). 



Recognizing that final proof of the operation of 

 pulmonary vasomotor activity under natural condi- 

 tions is difficult to obtain, there is, nonetheless, 

 reasonable evidence to indicate that it does occur; 

 this evidence is of two types: /) the response of the 

 pulmonary circulation to acute hypoxia and to acute 

 acidosis and 2) the occurrence of pulmonary vaso- 

 motor reflex activity. More uncertain is the occurrence 

 of pulmonary vasomotor waves. 



Respiratory Gases 



The first experiments devoted to the effects of the 

 respiratory gases on the pulmonary circulation were 

 concerned with asphyxia. Although these experiments 

 did show that asphyxia elicited pulmonary hyperten- 

 sion, they made no attempt to distinguish which of 

 the respiratory gases was responsible for the rise in 

 pressure. Thirty years later, acute hypoxia, per se, 

 was shown to be capable of eliciting pulmonary 

 hypertension in the anesthetized dog (132). There- 

 after, interest in the respiratory gases was episodic 

 until 1946, when Euler and Liljestrand demonstrated 

 that acute hypoxia and acute hypercapnia evoked an 

 increase in pulmonary arterial pressure in the anesthe- 

 tized cat and that this pressor response occurred in 

 the face of an unchanged or a decreased left atrial 

 pressure (125, 268). Although these experiments were 

 inconclusive in some respects — e.g., the lack of meas- 



urement of pulmonary blood flow or peripheral 

 arterial oxygen saturation or pH — they constituted 

 a landmark in the study of the pulmonary circulation 

 because of the clairvoyant hypothesis which they sug- 

 gested and the subsequent work which they stimu- 

 lated. The hypothesis consisted of three parts: /) that 

 a change in the composition of the inspired gas is 

 capable of eliciting an increase in resistance and that 

 this increase in resistance stems, in turn, from pulmo- 

 nary vasoconstriction; 2) that this vasoconstriction is 

 mediated by local vasomotor responses rather than 

 by reflexes involving the extrapulmonary portions of 

 the autonomic nervous system; and 3) that the vaso- 

 motor effects of the respiratory gases serve to adjust 

 alveolar perfusion to alveolar ventilation. Subsequent 

 experiences have done more to supply and clarify 

 details than to alter the general structure of the hy- 

 pothesis; in particular, they have distinguished be- 

 tween the effects of acute hypoxia, acute hypercapnia, 

 and respiratory acidosis on the pulmonary circulation. 



Acute Hypoxia 



A reduction in the fraction of oxygen in the inspired 

 air — generally below 1 2 per cent — has elicited an in- 

 crease in pulmonary arterial pressure in every species 

 in which it has been tested (132). In the intact, un- 

 anesthetized animal and man this pressor response 

 generally occurs when the oxygen saturation of 

 peripheral arterial blood drops below 80 per cent 

 (136). The associated increase in mean pressure is of 

 the order of 4 to 8 mm Hg (fig. 43) (300). Only a 

 small part of this increase in pressure is attributable to 

 an increase in pulmonary blood flow: during the 

 breathing of a 10 per cent oxygen mixture the in- 

 crease in flow rarely exceeds 30 per cent (132). Since 

 the usual passive determinants of pulmonary vascular 

 pressure — pulmonary blood volume (154), ventila- 



fic. 43. Effect of acute hypoxia on 

 pulmonary arterial pressure. During 

 acute hypoxia, the systolic, diastolic, 

 and mean blood pressures increase. The 

 heart rate also increases and respiratory 

 fluctuations in the luminal pressures 

 (referred to atmosphere) become more 

 marked. 



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