Drugs online research references
Clin Sci (Lond). 1994 May;86(5):531-5.
Analysis of vagal effects on ventricular rhythm in patients with atrial fibrillation.
van den Berg MP, Crijns HJ, Haaksma J, Brouwer J, Lie KI.
Department of Cardiology, Thoraxcentre, University Hospital Groningen, The Netherlands.
1. Animal studies suggest that the heart-rate-lowering effect of vagal stimulation during atrial fibrillation is due to: (1) a direct depressant effect on atrioventricular node conductivity, (2) enhancement of concealed atrioventricular nodal conduction of atrial impulses through augmenting fibrillatory activity, thereby indirectly prolonging atrioventricular nodal refractoriness. The purpose of the present study was to analyse these effects in man. 2. Sixteen patients with chronic atrial fibrillation were studied. After administration of propranolol (0.2 mg/kg intravenously) baseline ventricular rhythm was recorded (500 R-R intervals). Recordings were repeated after methylatropine (0.02 mg/kg intravenously). The shortest R-R interval was taken to represent atrioventricular nodal refractoriness. The ratio of the longest to the shortest R-R interval and the coefficient of variation of R-R intervals were used as parameters of concealed conduction. 3. Methylatropine foremost shortened long R-R intervals: values for the mean, shortest and longest R-R intervals decreased from 834 to 685 ms (-18%) (P < 0.001), 573 to 498 ms (-13%) (P < 0.001) and 1228 to 924 ms (-25%) (P < 0.001), respectively. Accordingly, the ratio of the longest to the shortest R-R interval decreased: 2.12 to 1.89 (-11%) (P < 0.05). Also, the coefficient of variation decreased: 0.24 to 0.20 (-17%) (P < 0.05). 4. This study supports the contention that vagal stimulation lowers ventricular rate during atrial fibrillation both by exerting a direct effect on the atrioventricular node and by augmenting concealed conduction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8033507&dopt=Abstract
J Neuroimmunol. 1994 Jul;52(2):165-73.
Inhibition of murine splenic T lymphocyte proliferation by 2-deoxy-D-glucose-induced metabolic stress.
Miller ES, Klinger JC, Akin C, Koebel DA, Sonnenfeld G.
Department of Microbiology and Immunology, School of Medicine, University of Louisville, KY 40292.
Female Swiss-Webster mice were injected with the glucose analogue 2-deoxy-D-glucose (2-DG), which when administered to rodents induces acute periods of metabolic stress. A single or multiple injections of 2-DG invoked a stress response, as evidenced by increases in serum corticosterone levels. The influence of this metabolic stressor on the blastogenic potential of splenic T lymphocytes was then examined. It was found that one, two, or three injections of 2-DG resulted in depressed T cell proliferative responses, with an attenuation of the effect occurring by the fifth injection. The 2-DG-induced inhibition of T cell proliferation was not attributable to 2-DG-induced cytolysis, as in vitro incubation of naive T cells with varying concentrations of 2-DG did not result in a reduction in cell number or viability, and flow cytometric analysis demonstrated that percentages of CD3, CD4, and CD8 splenic T cells were not altered as a result of 2-DG-induced stress. Incubating naive T cells in varying concentrations of 2-DG resulted in a dose-dependent inhibition of T cell blastogenic potential. Following in vivo exposure to 2-DG, T cell proliferation did not return to normal levels until 3 days after the cessation of 2-DG injections. Administering the beta-adrenergic receptor antagonist propranolol did not reverse the inhibited lymphoproliferation in 2-DG-treated mice. The inhibition in T cell proliferation was not observed, however, in mice that had been adrenalectomized or hypophysectomized and injected with 2-DG.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8034756&dopt=Abstract
Ann Thorac Surg. 1994 Jul;58(1):128-34.
Long-term effects of dynamic aortomyoplasty.
Chachques JC, Haab F, Cron C, Fischer EC, Grandjean P, Bruneval P, Acar C, Jebara VA, Fontaliran F, Carpentier AF.
Department of Cardiovascular Surgery, Broussais Hospital, Paris, France.
Aortomyoplasty consists of wrapping the latissimus dorsi muscle (LDM) around the ascending aorta and electrostimulating it during diastole. The ascending aorta will act as an ectopic neo-ventricle compressed during diastole, thus reproducing the effects of long-term diastolic counterpulsation. In 5 goats, the right LDM was transferred to the thoracic cavity after removal of the second rib. The ascending aorta was enlarged by a pericardial patch and wrapped with the LDM. Postoperative electrostimulation was delivered in a counterpulsating manner. Hemodynamic studies were performed at 12 and 24 months postoperatively. Percent increase in the subendocardial viability index (diastolic pressure-time index/systolic tension-time index) was calculated using unassisted and assisted cardiac cycles with the stimulator off versus the stimulator on at a 1:1 ratio in the basal state and after acute heart failure was induced by the administration of high doses of propranolol hydrochloride. Diastolic counterpulsation of the ascending aorta resulted in significant improvement in the subendocardial viability index long term, both in basal state conditions and after induced cardiac failure. During heart failure, aortomyoplasty increased the cardiac output and decreased systemic vascular resistance. Histopathologic studies up to 24 months showed preservation of the histologic structure of the aortic wall and no evidence of thromboembolism. Tight adhesions developed between the aortic wall (including the pericardial patch) and the LDM. The diameters of the enlarged aortas showed no significant differences compared with diameters immediately postoperatively. In conclusion, aortomyoplasty produces chronic diastolic augmentation with preservation of aortic structure. After induction of heart failure, aortomyoplasty offers efficient circulatory support.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8037510&dopt=Abstract
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