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Biomedical subjects

R Corbalan

Publications and source records attributed to R Corbalan.

12 recordsLinked to original sources
PubMed1990

[Beta adrenergic receptors in circulating lymphocytes of patients with chronic heart failure].

Severe decompensated chronic heart failure is associated to increased levels of circulating catecholamines and decreased density of myocardial beta-adrenergic receptors. In 14 patients with stable, class II-III heart failure we studied circulating lymphocytes to determine the number of beta adrenergic receptors, the dissociation constant of 3H dihydroalprenolol (kd) and the intracellular content of cyclic AMP (AMPc). Results (mean +/- SEM) were compared to those obtained in 10 healthy controls. The number of beta receptors was significantly decreased (105 +/- 16 vs 185 +/- 24, fmol/mg of membrane protein, p less than 0.01). No differences were found in Kd (1.65 +/- 0.2 vs. 1.36 +/- 0.28 nm) nor the level of AMPc (7.9 +/- 2.1 vs 7.1 +/- 2.9 pmol/mg protein), respectively. The decreased number of beta adrenergic receptors in the circulating lymphocytes may be related to the increased level of circulating catecholamines that have been shown to be present during exercise in these patients.

Adult↗
PubMed1981

Effect of a calcium inhibitor, nifedipine, on exercise tolerance in patients with angina pectoris: a double-blind study.

The effect of nifedipine on exercise tolerance was studied in 30 patients with stable angina and positive graded exercise testing. Treadmill exercise testing was performed on each of five consecutive days. Placebo or nifedipine, 10 mg sublingually, was given 30 minutes before exercise on the third day. The following day the intervention was reversed in a double-blind manner. Angina was abolished by nifedipine but not by placebo in 12 patients (40 percent). The time to onset of angina in the remaining patients increased from 4.1 +/- 0.4 (SEM) to 6.7 +/- 0.6 min (p less than .001). Time to ST depression greater than or equal to 2 mm increased from 4.0 +/- 0.3 to 5.4 +/- 0.5 min, while duration of exercise increased from 6.3 +/- 0.3 to 8.2 +/- 0.4 min (p less than .001). The maximum heart rate was 145 +/- 3.3 with nifedipine and 122 +/- 3.8 min-1 with placebo (p less than .01). Resting systolic blood pressure decreased 30 min after nifedipine administration from 131 +/- 3.4 to 106 +/- 2.9 mm Hg (p less than .01). Maximal systolic blood pressure during exercise was lower with nifedipine (127 +/- 4.8 mm Hg) than with placebo (155 +/- 5.6 mm Hg, p less than .01). We conclude that nifedipine significantly improves the exercise tolerance of patients with stable angina pectoris by decreasing peripheral vascular resistance and myocardial oxygen demand.

Adult↗
PubMed1976

Differing mechanisms for ventricular vulnerability during coronary artery occlusion and release.

The time course and mechanism of vulnerability to ventricular fibrillation (VF) a 10-minute occlusion of the left anterior descending coronary artery and following its release were studied in 48 dogs. VF threshold was determined by inducing a sequence of three extrasystoles (sequential R/T pulsing). Within 1 minute of occlusion, the fibrillation current decreased to the level required for eliciting a propagated diastolic response. This state of enhanced vulnerability lasted for approximately 6 minutes, after which the VF threshold returned to preocclusion values. The vulnerability changes upon reperfusion, by comparison, occurred within seconds of release and persisted only transiently. Three minutes of occlusion was the minimal time which resulted in a reduction in VF threshold after release. Alpha and beta-adrenergic blockade with phentolamine and propranolol, respectively, prevented the decrease in VF threshold during occlusion but were without effect upon threshold changes during coronary artery release. Lidocaine failed to alter the pattern of vulnerability. It is concluded that adrenergic mechanisms play a key role in the increased susceptibility to VF associated with acute myocardial ischemia, whereas the changes in VF threshold following reperfusion may be due to washout products of cellular ischemia. These findings support the view that protection against VF during coronary artery occlusion and release may require different antiarrhythmic measures.

Animals↗