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J Physiol. 2000 Oct 15;528 Pt 2:349-58.

Reflex effects of independent stimulation of coronary and left ventricular mechanoreceptors in anaesthetised dogs.

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The Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK.


Previous studies which have indicated that the stimulation of ventricular mechanoreceptors induces significant reflex responses can be criticised because of the likelihood of concomitant stimulation of coronary arterial baroreceptors. We therefore undertook this investigation to examine the coronary and ventricular mechanoreflexes in a preparation in which the pressure stimuli to each region were effectively separated. Dogs were anaesthetised, artificially ventilated and placed on cardiopulmonary bypass. A balloon at the ventricular outflow separated pressure in the left ventricle from that perfusing the coronary arteries. Ventricular pressures were changed by varying inflow and outflow of blood entering and leaving the ventricle through an apical cannula, and coronary pressure by changing pressure in a reservoir connected to a cannula tied in the aortic root. Pressures distending carotid and aortic baroreceptors were controlled. Changes in descending aortic perfusion pressure (flow constant) were used to assess systemic vascular responses. Large changes in carotid sinus and coronary pressures decreased vascular resistance by 35+/-1.9 and 40+/-2.5%, respectively. Intracoronary injections of veratridine (30-60 microg) decreased vascular resistance by 31+/-2.5%. However, large increases in ventricular pressure decreased resistance by only 9+/-2.2%. Significant changes in vascular resistance were obtained with increases in coronary arterial pressure from 60 to 90 mmHg. However, ventricular pressures had to increase to 152/18 mmHg (systolic/end-diastolic) before there was a significant response. These results show that coronary mechanoreceptors are likely to play an important role in cardiovascular control. If ventricular receptors have any function at all, it is as a protective mechanism during gross distension, possibly associated with myocardial ischaemia.

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