To gain insight into the differences in antiarrhythmic potential of right vs left stellate ganglionectomy, 72 dogs were randomized to either unilateral stellectomy or second intercostal space thoracotomy and left circumflex coronary arteriovenous pedicle occlusion was performed, without vagotomy, a mean of 8 weeks later under anesthesia. The type and timing of ventricular ectopic beats, including both nonsustained and sustained ventricular tachycardia and ventricular fibrillation, were investigated. Several covariates, including postischemic electrocardiographic changes, were considered. Both right and left stellate ganglionectomy reduced the incidence of early (0 to 10 min) (p = .004 and p = .001, respectively) and total (0 to 60 min) (p = .009 and p = .008, respectively) ischemia-induced ventricular fibrillation, and improved outcome (p = .0013 and p = .0012, respectively). Early sustained ventricular tachycardia was similarly reduced (p = .02) in both stellectomized groups. By contrast, neither the type nor the time distribution of the other forms of ventricular arrhythmias differed significantly among the randomized groups. The multivariate Cox's regression model showed that ST segment elevation at 3 min postocclusion, unilateral stellate ganglionectomy (either right or left), sex, and weight were significant independent predictors of the incidence of ventricular fibrillation during the occlusion period. Lower ST segment elevation and reduced incidence of sustained ventricular tachycardia in the early postischemic period might explain improved outcome in stellectomized dogs by Cox analysis. The side of intervention (either stellectomy or sham operation) did not influence survival; however, left-sided interventions were more effective than right-sided ones. These results confirm the previously reported antifibrillatory effect of left and indicate like effects of right stellate ganglionectomy in a randomized experimental study. Circulation 77, No. 4, 935-946, 1988. IT IS generally believed that increased sympathetic tone at the onset of acute myocardial ischemia contributes to life-threatening arrhythmias in a variety of animal preparations, including anesthetized, morphine-sedated, and conscious ones.
Prostacyclin (PGI 2 ) and prostaglandin E 2 (PGE 2 ) production was Investigated in human aortas (five controls and 27 with atherosclerotic lesions). The specific activities of PGI 2 and PGE 2 synthetase were studied using radioimmunoassays of PGE 2 and 6-keto-PGE 1( , of aortic microsomes incubated in the presence of additional substrate and cofactors. The atherosclerotic lesions were examined under the light microscope and were classified as Stage 1 when the disease was restricted to the intima and as Stages 2 and 3 when there were moderate or advanced lesions. Prostaglandin production for the control group (n = 5), Stage 1 (n = 7), Stage 2 (n = 10), and Stage 3 (n = 10) were as follows: 454 ± 15, 162 ± 81, 92 ± 90, and 65 ± 61 pmol 6-K-PGF 1u /50 mg proteln/10 minutes; and 15 ± 12, 399 ± 406, 227 ± 174, and 366 ± 362 pmol PGEj/50 mg protein/10 minutes (mean ± SD) respectively. We conclude that: 1) In normal aortas, PGE 2 production was low, while PGI 2 synthesis activity was elevated. The reverse situation was observed In aortas with atherosclerosis lesions (p < 0.05). 2) There was an inverse relationship between PGE 2 and PGI, production (p < 0.05).3) There was a direct hlstologlc relationship between lower PGI 2 production and atherosclerosis progression. A decided decline In 6-K-PGF,,, production was detected in aortas In the early stages (65% of control values). 4) By contrast, a progressive increase In PGE 2 production was found In Stage 2 and Stage 3 groups (p < 0.05). These results demonstrate that there are correlations between the changes In prostaglandin production and the morphological features of atherosclerosis development. Because of the pharmacologlc properties of prostaglandins, these changes in prostaglandin production may promote the development of atherosclerosis. (Arteriosclerosis 4:70-78, January/February 1984)
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