HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hainsworth, R Articles by Soladoye, A O Search for Related Content PubMed PubMed Citation Articles by Hainsworth, R Articles by Soladoye, A O

Dogs were anaesthetized with chloralose and the cephalic circulation was perfused, through the brachiocephalic and left subclavian arteries, with blood equilibrated with various tensions of CO2. The vascularly isolated carotid bifurcations were perfused at a constant pressure with either arterial or venous blood. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with heart rate and aortic pressure held constant. Stimulation of carotid chemoreceptors with venous blood, at all values of cephalic PCO2, always resulted in a decrease in dP/dt max. An increase in cephalic PCO2, during arterial perfusion of chemoreceptors, resulted in an increase in dP/dt max and the response to chemoreceptor stimulation was enhanced. Graded changes in cephalic PCO2 resulted in graded changes in dP/dt max during arterial perfusion of chemoreceptors. However, the value of dP/dt max during venous perfusion was not significantly affected by increases in cephalic PCO2 above normal but it did decrease significantly during cephalic hypocapnia. These results confirm that an increase in cephalic PCO2 and stimulation of carotid chemoreceptors result in opposite responses of the cardiac inotropic state. The responses to chemoreceptor stimulation were enhanced by cephalic hypercapnia but the responses to cephalic hypercapnia, although not to hypocapnia, were suppressed by chemoreceptor stimulation.