Drugs online research references
Circulation. 1996 Aug 1;94(3):340-5.
Negative chronotropic effect of beta-blockade therapy reduces myocardial oxygen expenditure for nonmechanical work.
Yamakawa H, Takeuchi M, Takaoka H, Hata K, Mori M, Yokoyama M.
First Department of Internal Medicine, Kobe University School of Medicine, Japan.
BACKGROUND: The negative chronotropic effect of beta-blocking agents is likely to provide hemodynamic and energetic advantages. However, the negative chronotropic effect on cardiac energetics observed on the initiation of beta-blockade therapy has not been fully elucidated. METHODS AND RESULTS: In 18 patients with heart failure, left ventricular pressure and volume, external work (EW), myocardial oxygen consumption per beat (total Vo2), mechanical efficiency (EW/total Vo2), and Vo2 for nonmechanical work (total Vo2-2.EW) were measured with the use of conductance catheter and Webster catheter at the following three states: under control conditions and after beta-blockade (0.15 +/- 0.07 mg/kg propranolol IV) with and without atrial pacing to keep the heart rate at control levels. Heart rate decreased after atrial pacing was stopped. EW decreased during beta-blockade with pacing and returned to the control level after pacing was stopped. Total Vo2 did not change during beta-blockade with or without pacing, whereas Vo2 for nonmechanical work increased with pacing and returned to the control level after pacing was stopped. As a result, mechanical efficiency decreased during beta-blockade with pacing and returned to the control level after pacing was stopped. CONCLUSIONS: The negative chronotropic effect of a beta-blocking agent may offset the mechanoenergetical deterioration resulting from its negative inotropic effect through a reduction in oxygen expenditure for nonmechanical work. These findings suggest that the negative chronotropic effect is an important aspect of beta-blockade therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8759074&dopt=Abstract
Am J Physiol. 1996 Aug;271(2 Pt 2):R311-9.
Autoregulation of myocardial glycogen concentration during intermittent hypoxia.
McNulty PH, Ng C, Liu WX, Jagasia D, Letsou GV, Baldwin JC, Soufer R.
Department of Internal Medicine, Veterans Affairs Medical Center, West Haven, Connecticut, USA.
During hypoxia, the heart consumes glycogen to generate ATP. Tolerance of repetitive hypoxia logically requires prompt replenishment of glycogen, a process whose regulation is not fully understood. To examine this, we imposed a defined hypoxic stimulus on the rat heart while varying its workload. In intact rats, hypoxia reduced myocardial glycogen approximately 30% and increased both the fraction of glycogen synthase in its physiologically active (GS I) form (from 0.24 +/- 0.06 to 0.82 +/- 0.07; P < 0.005) and glycogen synthesis (from 0.087 +/- 0.011 to 0.375 +/- 0.046 mumol.g-1.min-1; P < 0.005). Reducing cardiac work (with propranolol or heterotopic transplantation) reduced glycogen breakdown, glycogen synthase activation, and glycogen synthesis in parallel, stepwise fashion in intact rats. Correspondingly, hypoxia increased GS I activity in the perfused heart in vitro, but only under conditions where glycogen was consumed. This suggests myocardial glycogen synthase is activated by systemic hypoxia and catalyzes rapid posthypoxic glycogen synthesis. Hypoxic glycogen synthase activation appears to be a proportionate, wholly intrinsic response to local glycogenolysis, operating to preserve myocardial glycogen stores independent of any extracardiac mediator of carbohydrate metabolism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8770128&dopt=Abstract
Boll Soc Ital Biol Sper. 1996 Mar-Apr;72(3-4):71-7.
Determination of the optimal conditions to study DNA synthesis in cultures of mouse hepatocytes.
Basso A, Rossolini G, Piantanelli L.
Centre of Biochemistry, Gerontologic Research Department, INRCA, Ancona.
Mouse hepatocytes undergo profound changes during aging, such as increased nuclear volume, occurrence of tetraploid nuclei and impaired DNA synthesis following in vivo adrenergic stimulation. These alterations have been found reversible by implanting a neonatal thymus into old animals. In the present paper we studied the optimal experimental conditions in order to investigate the mechanisms of such actions in vitro. Unfortunately, in fact, most of data in the field comes from experiments on rats. Thus, we examined DNA synthesis of hepatocytes from mice cultivated in presence of neonatal calf serum only, or after the addition of the beta-adrenergic agonist isoproterenol or the beta-adrenergic antagonist propranolol. DNA synthesis in hepatocytes from young Balb/c-nu mice shows a peak between 36 and 48 h even in the absence of any specific stimulation other than newborn calf serum. The addition of isoproterenol does not modify the DNA synthetic pattern, while propranolol causes a slight but statistically significant decrease in 3H-thymidine incorporation. Results are compared with those obtained from other authors in rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8771906&dopt=Abstract
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