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This Article Full Text Full Text (PDF) All Versions of this Article: 91/5/915    most recent expphysiol.2006.033480v1 Alert me when this article is cited Alert me if a correction is posted 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 Fernández, N. Articles by Diéguez, G. Search for Related Content PubMed PubMed Citation Articles by Fernández, N. Articles by Diéguez, G. Related Collections Vascular

¹ Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain

To study the effects of arterial pressure on coronary reactive hyperaemia, left circumflex coronary artery flow was measured, and reactive hyperaemia was determined after 5, 10 or 20 s of occlusion of this artery in anaesthetized goats during normotension, hypertension and hypotension. During hypertension induced by aortic constriction (mean arterial pressure, MAP = 140 ± 6 mmHg) coronary vascular resistance (CVR), reactive hyperaemia (ratio of peak in hyperaemic flow to control flow and ratio of repayment to debt) and the decrease in CVR during the peak in hyperaemic flow were comparable to those during normotension. During hypertension induced by noradrenaline (MAP = 144 ± 6 mmHg) CVR was 16% lower (P < 0.05), reactive hyperaemia was reduced by 14–25% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was lower than the values of these parameters during normotension. During hypotension induced by constriction of the caudal vena cava (MAP = 40 ± 4 mmHg) CVR was 22% lower (P < 0.05), reactive hyperaemia was reduced by 25–65% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was less compared to the values of these parameters during normotension. During hypotension induced by isoprenaline (MAP = 45 ± 4 mmHg) CVR was 59% lower, reactive hyperaemia was reduced by 55–100% (P < 0.01) and the decrease in CVR during the peak in hyperaemic flow was less compared to the values of these parameters during normotension. Arterial pressure is a main determinant of coronary reactive hyperaemia after brief periods of ischaemia, and the relationship between arterial pressure and reactive hyperaemia may depend in part on changes in CVR after variations in arterial pressure. These changes in CVR may be related to the action on coronary vessels of myocardial factors and vascular myogenic mechanisms.

(Received 9 February 2006; accepted after revision 12 June 2006; first published online 15 June 2006)
Corresponding author G. Diéguez: Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo 2, 28029 Madrid, Spain. Email: gdieguez{at}uam.es