[Abnormal vasomotor response of the forearm due to propranolol-induced loss of cardiopulmonary baroreflex sensitivity: experience with seven cases of recent myocardial infarct].

In 7 patients suffering from acute myocardial infarction (AMI) occurring in the previous 30 days, we investigated forearm vascular reactivity to lower body negative pressure (LBNP), by the strain gauge plethysmography with simultaneous administration of negative pressure around the lower limbs. This manoeuvre has then been repeated after 10 days of oral beta-blocker therapy (propanolol 160 mg/die). A significant flow reduction derived from LBNP associated to plethysmography with respect to plethysmography alone, but this significant difference was suppressed by propranolol treatment, that prevented the reflex decrease in forearm blood flow, (forearm blood flow from 5.97 to 3.85 ml/min/100 ml in wash-out vs 5.64 to 5.75 ml/min/100 ml during propranolol treatment). We hypothesize that this phenomenon is due to the desensitizing effect of propranolol on cardiopulmonary mechanoreceptors (CPB), with the consequent loss or reduction of their functional inhibition for the efferent sympathetic outflow towards resistance vessels in skeletal muscle. Therefore, LBNP does not elicit forearm reflex sympathetic vasoconstriction, because pressure unloading of CPB areas is no longer able to modify sympathetic discharge, since the influence on it of baroreceptor activity has already been weakened by prolonged beta-blockade. Thus, the LBNP low levels, by ruling out and/or by removing the CPB activity are theorically able to elicit sympathetic "disinhibition", and to exercise, consequently, a reflex, vasoconstrictor influence upon the forearm vascular bed, whereas the same reflex behaviour by forearm resistance vessels does not appear feasible if the CPB activity has been preventively minimized by prolonged, chronic beta-blockade.