Drugs online research references
Nihon Kyobu Shikkan Gakkai Zasshi. 1993 Feb;31(2):206-13.
[Pulmonary hemodynamic effects of cold pressor test in patients with chronic lung disease]
[Article in Japanese]
Okada O, Naitou T, Katou K, Tanabe N, Kouchi F, Yamagishi F, Sugita T, Kuriyama T, Watanabe S.
Department of Chest Medicine, Chiba University School of Medicine, Japan.
Cold Pressor Test (CPT) was applied to patients with chronic lung disease, including primary pulmonary hypertension, and the effects on pulmonary circulation were compared to those on systemic circulation. HR PPA, and TPR showed maximum values at the end of CPT (Time = 0) and recovered to baseline values 5 min after CPT. CO, however, did not change significantly after CPT. PPA and PAR showed maximum values at the end of CPT and then gradually decreased, but still were significantly higher than baseline values at 5 min after CPT. Nifedipine (NFP) reduced the maximum values of both TPR and PAR at the end of CPT. There was significant correlation between PPA change after CPT and baseline PPA value, and NFP decreased the slope of the regression line. These results indicate that cold stimulation induces both systemic and pulmonary vasoconstriction in patients with chronic lung disease, and this pulmonary vasoconstriction was correlated to the baseline pulmonary vascular tone. Moreover, nifedipine may reduce this cold stimulation-induced pulmonary vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8515600&dopt=Abstract
Arch Int Pharmacodyn Ther. 1995 Mar-Apr;329(2):245-54.
Central cardiovascular effects of CPU-23, a substituted tetrahydroisoquinoline, in rats.
Dong H, Lee CM, Ng KW, Wong TM.
Department of Biophysics, School of Basic Medical Sciences, Shanghai Medical University, P.R.C.
The cardiovascular effects of intracerebroventricular (i.c.v.) injections of low doses of CPU-23, a substituted tetrahydroisoquinoline, were investigated and compared with those of nifedipine in pentobarbital-anaesthetized Sprague-Dawley rats. CPU-23, in doses of 0.2 to 0.5 mg/kg (i.c.v.), which did not elicit any significant cardiovascular responses when injected intravenously, caused a clear-cut and long-lasting decrease of mean arterial pressure (MAP) and heart rate (HR) in a dose-dependent manner. The effects of CPU-23, in a dose of 0.05 mg/kg, were similar to those of nifedipine, a prototype L-type calcium antagonist. The hypotensive effects of CPU-23 were significantly attenuated by bilateral cervical vagotomy. The results strongly suggest that a central component may be involved in the cardiovascular effects of CPU-23 and that dihydropyridine receptor sites in the brain may be involved in the central control of cardiovascular functions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8540764&dopt=Abstract
Cardiovasc Drugs Ther. 1992 Apr;6(2):183-6.
Long-term hemodynamic effects of nifedipine on congenital heart disease with Eisenmenger's mechanism in children.
Wimmer M, Schlemmer M.
Department of Pediatrics, University of Vienna, Austria.
The hemodynamic effect of long-term nifedipine medication was studied in 10 children, 3-12 years of age, five with ventricular septal defect and five with complete atrioventricular septal defect; all had Eisenmenger's reaction, seven also had Down's syndrome. They underwent heart catheterization prior to and during 1-4 years of nifedipine therapy. Fick's principle was used to calculate the ratio of pulmonary arterial pressure to aortic pressure (PAP/PAO), the ratio of pulmonary flow to aortic flow (QP/QS), as well as the ratio of pulmonary vascular resistance to aortic vascular resistance (RP/RS). In the seven children under 8.8 years, nifedipine caused a significant drop in PAP/PAO (p less than 0.004), a slight increase in arterial O2 saturation, a significant increase in QP/QS (p less than 0.02), and a decrease in RP/RS (p less than 0.02). The nifedipine effect was age related. On nifedipine, breathing oxygen resulted in, independent of age, a significant increase in QP/QS (p less than 0.003) and a significant decrease in PAP/PAO (p less than 0.04) and in RP/RS (p less than 0.003). Direct O2 consumption measurements before and during oxygen breathing in six patients demonstrated no significant change in RP, RS, QP, or QS indices. Nifedipine had a relaxing effect on the pulmonary vascular bed, especially in the younger child with Eisenmenger's mechanism. On nifedipine therapy, O2 produced a more complex hemodynamic reaction that was not restricted to the pulmonary circulation alone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1390332&dopt=Abstract
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