The identification of specific brain nuclei in which catecholamine turnover is increased by left ventricular receptors during acute myocardial infarction in the rat.

Central catecholaminergic nerves have been shown to participate in the integration of cardio-cardiac reflexes induced by coronary artery ligation in the rat. In this study we measured the turnover of dopamine, norepinephrine and epinephrine in microdissected brain regions to identify some of the specific neural loci involved in this integration. Three groups of rats, treated with alpha-methyltyrosine, an inhibitor of catecholamine biosynthesis were examined: left coronary artery ligation, left coronary artery ligation with the left ventricle painted with lidocaine, and sham operation. An untreated group of resting rats was also examined. Dopamine, norepinephrine and epinephrine turnover was increased in ligated rats in nucleus tractus solitarius (right and left), nucleus commissuralis, A1-region, locus coeruleus, nucleus cuneatus, and area postrema in the pons-medulla and nucleus dorsomedialis in the hypothalamus. Norepinephrine and dopamine (but not epinephrine) turnover was increased in nucleus ambiguus in the brain stem and nucleus paraventricularis in the hypothalamus. A ligation-induced increase in norepinephrine turnover, alone, was exhibited by the A2-region and nucleus gigantocellularis in the medulla and nucleus supraopticus and nucleus hypothalamicus posterior in the hypothalamus. Dopaminergic nerves to the nucleus gigantocellularis appeared to be inhibited following coronary ligation. The catecholamine stores of 11 nuclear regions were not influenced by coronary artery occlusion. Topical lidocaine, applied to the ischemic left ventricle, only, of ligated rats, completely restored regional brain catecholamine turnover to that found in sham-operated animals. In conclusion, we have identified discrete loci in the brain in which catecholamine turnover (as measured by alpha-methyltyrosine induced disappearance) is increased by the stimulation of left ventricular receptors during acute myocardial ischemia in the rat.