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Biomedical subjects

R J Peters

Publications and source records attributed to R J Peters.

6 recordsLinked to original sources

Frequency of myocardial indium-111 antimyosin uptake after uncomplicated coronary artery bypass grafting.

The reported incidence of myocardial damage after coronary artery bypass grafting (CABG) is highly related to the methods used. Since indium-111 monoclonal antimyosin antibody scintigraphy has been shown to be highly specific and sensitive for myocardial necrosis, even in small lesions, uptake of this radiotracer was evaluated after CABG. In 23 consecutive patients without previous myocardial infarction who underwent CABG for stable angina, 80 MBq indium-111 antimyosin was injected on the third postoperative day. Planar images were obtained 48 hours later and analyzed for myocardial uptake of indium-111 antimyosin. Scintigraphic results were related to creatine kinase MB levels, duration of both aortic cross-clamping and cardiopulmonary bypass, and electrocardiographic changes. In all patients surgical procedure and postoperative course was uncomplicated. Indium-111 antimyosin uptake was present in 19 of 23 patients (82%). It was diffused in 7 patients and localized in 12. No pathologic Q waves occurred postoperatively. Fourteen patients exhibited ST-segment changes. No good relation was found among indium-111 antimyosin uptake and creatine kinase MB levels, duration of cross-clamping or bypass, and ST-T changes. It is concluded that some degree of myocardial damage, though silent, is common after CABG.

Antibodies, Monoclonal

Catecholamine release and potassium accumulation in the isolated globally ischemic rabbit heart.

The relation between the release of endogenous catecholamines and the rise in extracellular potassium concentration [( K+]0) was studied during global ischemia in the isolated perfused rabbit heart. An increase in release of catecholamines was observed only after ischemic periods longer than 10 min. In agreement with other studies, [K+]0 initially rose until a plateau phase was established after 8 min. During this phase [K+]0 actually decreased in several hearts. In these hearts, lactate release was larger (116.9 +/- 22.4 mumol/g dry wt, n = 5) than in hearts in which no decrease in [K+]0 was observed (83.3 +/- 16.0 mumol/g dry wt, n = 6). Blockade of the alpha- and beta-adrenoceptors by phentolamine (5 x 10(-6) M) and propranolol (10(-6) M), respectively, prevented the decrease in [K+]0. These findings show that the secondary decrease in [K+]0 is associated with increased glycolytic flux. Moreover, catecholamines are a prerequisite for this decrease and are frequently observed between 8 and 15 min of ischemia.

Animals

Effects of unilateral stellate ganglion stimulation and ablation on electrophysiologic changes induced by acute myocardial ischemia in dogs.

We recorded direct-current extracellular electrograms simultaneously from 60 left ventricular epicardial sites in 38 alpha-chloralose-anesthetized dogs during repeated, 5 min coronary arterial occlusions. In each dog recordings made during control occlusions were compared with those made in occlusions after, or during, the following interventions on the sympathetic nervous system: left stellate ganglion stimulation, left stellectomy, right stellectomy, and clamping the abdominal aorta with intact sympathetic nerves to induce a rise of blood pressure equal to that present during left stellate stimulation. Heart rate was kept constant. Measurements included determination of TQ segment potentials and times of local activation. After 2 min of ischemia, the degree of TQ segment depression was increased by left stellate ganglion stimulation and was decreased by both left stellectomy and clamping the aorta. Also, the area showing negative TQ potentials, indicating decreased resting membrane potentials, was enlarged by both left stellate stimulation and right stellectomy and reduced by left stellectomy. No differences were found in the results of experiments in which the left anterior descending coronary artery was occluded and those in which the circumflex branch was occluded. Left stellate stimulation significantly improved conduction within the ischemic zone. No evidence was found to suggest that the arrhythmogenic effects of left stellate stimulation and of right stellectomy, confirmed in the present study, resulted from an increased likelihood for reentry in the subepicardium of the ischemic zone.

Animals