Release of epinephrine during carotid artery occlusion following vagotomy in dogs

Abstract

The blood pressure (BP), serum norepinephrine (NE), and epinephrine (E) responses to carotid artery occlusion (CAO) were examined in three different groups of anesthetized dogs. The response was first examined under control conditions in the three groups and then following vagotomy and adrenalectomy in the first group, following adrenalectomy and vagotomy in the second group, and following atropine administration and vagotomy in the third group. The results obtained in these three groups of dogs during the control period demonstrate that CAO produces significant increases in BP (from 144 ± 5 to 182 ± 8, 154 ± 7 to 202 ± 9, and 143 ± 3 to 185 ± 2 mmHg, respectively) (1 mmHg = 133.322 Pa) and in NE serum level (from 218 ± 36 to 337 ± 45, 215 ± 51 to 275 ± 46, and from 163 ± 23 to 247 ± 22 pg/mL, respectively), thus confirming previous studies. No rise in E serum level occurred in these three conditions (226 ± 100 vs. 275 ± 87, 280 ± 161 vs. 205 ± 88, and 183 ± 75 vs. 157 ± 46 pg/mL, respectively), as also previously reported. The first series of experiments demonstrated that following vagotomy, CAO induced a marked elevation of E serum levels from 275 ± 87 to 1145 ± 274 pg/mL (P < 0.005). These CAO-induced changes in E were abolished by previous (group 2) or subsequent (group 1) adrenalectomy which also attenuated BP and NE elevations, although these remained significant. By comparison with these changes, vagotomy only had a modest effect on BP and serum NE increase following CAO. These results demonstrate that vagal inhibition upon vasomotor tone was most important in controlling the adrenal release of catecholamines (CA), particularly E. In the third series of dogs atropine sulfate could not reproduce the BP, NE, and E changes observed after vagotomy, as the results were comparable to those observed under control conditions. Subsequent vagotomy produced results analogous to those observed in the first group of animals and confirmed that vagal afferent fibers are responsible for tonic inhibition of vasomotor centers.