Coronary reactive hyperaemia and arterial pressure in anaesthetized goats.
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.
Fernández
N
N
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo 2, 28029 Madrid, Spain.
Monge
L
L
García-Villalón
A L
AL
Diéguez
G
G
D000318:Adrenergic beta-Agonists; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D003331:Coronary Vessels / Q000502:physiology*; D005260:Female; D006041:Goats; D006321:Heart / Q000502:physiology*; D006940:Hyperemia / Q000503:physiopathology*; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology; D007545:Isoproterenol; D009638:Norepinephrine; D012039:Regional Blood Flow / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014662:Vasoconstrictor Agents
D000318:Adrenergic beta-Agonists; D014662:Vasoconstrictor Agents; D007545:Isoproterenol; D009638:Norepinephrine