Evaluation of the isolated perfused heart of mice, with special reference to vasoconstriction caused by intracoronary acetylcholine.
A perfusion model of isolated hearts (left in situ) was developed in mice. The heart was perfused retrogradely, according to the Langendorff technique, under a fixed flow rate of about 4 ml/min with physiological saline solution. Left ventricular (LV) cavity pressure, LV dP/dt max, heart rate, and arterial perfusion pressure were measured. Stable levels of mechanical parameters were reached within 30 min following the start of perfusion and were maintained for more than three hours. Single doses of acetylcholine (ACh, 0.003-1 microgram) administered into the coronary perfusion system elicited a dose-dependent increase (vasoconstriction) followed by a decrease (vasodilation) in perfusion pressure. Coronary vasoconstriction in response to ACh was especially prominent. LV systolic pressure, LVdP/dt max, and heart rate resulted in a decrease followed by an increase. A single injection of atropine (10 micrograms) antagonized both cardiac and vascular (vasoconstrictor and dilator) effects of ACh. The present studies substantiate the validity of this experimental model for the assessment of the action of drugs on the heart and coronary vasculature.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D003331:Coronary Vessels / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D051379:Mice; D010477:Perfusion; D014661:Vasoconstriction / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
D001285:Atropine; D000109:Acetylcholine