α-Adrenoceptor Control of Norepinephrine Release from Acutely Ischaemic Myocardium

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Abstract
We studied the effects of yohimbine, an α-adrenoceptor blocker with selectivity for the α2-subtype, on myocardial norepinephrine (NE) overflow, regional myocardial blood flow (RMBF), and patterns of epicardial conduction abnormalities during occlusion of the proximal left anterior coronary artery in an open-chest anaesthetised dog model. With a 12-min period of coronary occlusion (n = 9), spontaneous overflow of NE into ischaemic venous effluent was not observed either before or after yohimbine (1 mg/kg i.v.), but the drug significantly potentiated the enhanced NE overflow during supramaximal stimulation of the left stellate ganglion at low (1 Hz) and high (10 Hz) frequency [peak NE 4.3 ± 0.4 pmol/ml control; 11.8 ± 5.4 pmol/ml yohimbine (p < 0.005)] with a delayed return towards prestimulation levels. Myocardial NE overflow on coronary reperfusion was also enhanced. Yohimbine increased arterial epinephrine two- to threefold but did not substantially alter myocardial lactate overflow during coronary occlusion. RMBF was reduced 24 and 36% to ischaemic endocardium and epicardium, respectively (p < 0.01, compared with control occlusion). This contrasted with a 9 and 6% decrease in flow to the respective nonischaemic areas (p = NS, compared with control occlusion). Spontaneous ventricular fibrillation and the area and magnitude of epicardial conduction abnormalities in the ischaemic myocardium were both increased compared with the control occlusion. Thus, α-blockers with selectivity for the α2-adrenoceptor may be detrimental to acutely ischaemic myocardium, presumably through increased local catecholamine release at the nerve terminal.

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