Inversion of cardiac inotropism response to carotid arteries occlusion in dogs treated with propranolol.

The effect of beta-adrenergic blockade achieved by propranolol (0.5-1.0 mg/kg) on the inotropic alterations induced by adrenergic hyperactivity resulting from bilateral carotid occlusion (BCO) was analysed in 25 dogs anesthetized with morphine (2 mg/kg) and sodium pentobarbital (20 mg/kg). The heart rate was kept unchanged by means of a pace-maker. The first derivative of ventricular pressure (dp/dt) was considered as contractility index. Because BCO is followed by increase of left ventricle end-diastolic pressure (LVEDP) and of blood pressure (BP), to avoid the influence of these variables on dp/dt, we have reduced preload and afterload by means of hemorrhage (group A) and alpha-adrenergic blocker administration--phentolamine (group B). The carotid occlusion promoted similar variations in hemodynamic parameters in the two groups--there was a significant increase of blood pressure and LVEDP. BCO did not produce alteration in dp/dt values in both groups; when BP and LVEDP in group A were reduced, there was a significant reduction of dp/dt (2 927 +/- 139 to 2 066 +/- 95 mmHg/s; p less than 0.01). However there was no dp/dt alteration in group B (2 559 +/- 239 to 2 512 +/- 285 mmHg/s). These results suggest that during increase of sympathetic activity, anesthetized dogs under beta-adrenergic blockade show contractility depression. This could be related to secondary myocardic hypoxia and coronary vasoconstriction due to coronary alpha-adrenergic hyperactivity, once cardiac inotropism response can be alleviated by alpha-adrenergic blockers.