Drugs online research references
Am Heart J. 1982 Nov;104(5 Pt 2):1154-9.
Variable clinical response to long-term angiotensin inhibition in severe heart failure: demonstration of additive benefits of alpha-receptor blockade.
Kugler J, Maskin CS, Frishman W, Sonnenblick EH, LeJemtel TH.
The effects of long-term therapy with captopril (CPT) were studied in 11 patients with severe chronic congestive heart failure (CHF). At initiation of therapy, cardiac index increased from 1.88 +/- 0.56 to 2.12 +/- L/min/m2 (p less than 0.05), while pulmonary capillary wedge pressure decreased from 27.9 +/- 7.2 to 17.8 +/- 7.6 mm Hg (p less than 0.01). This improvement in resting cardiac performance was maintained during maximal exercise; however, maximal oxygen uptake was not acutely increased by CPT. During chronic therapy, 6 of 11 patients showed symptomatic improvements; however, only three of these six patients demonstrated an increase in maximal oxygen uptake, which was measured at an average of 13.2 weeks following initiation of therapy. Five patients did not improve clinically during chronic therapy. In these patients, hemodynamic measurements that had improved initially after CPT returned to baseline values during chronic therapy. The addition of prazosin to chronic CPT therapy elicited a beneficial hemodynamic response in all five patients. Thus, the results of long-term therapy with CPT are variable in patients with severe CHF, and symptomatic improvement does not always correlate with objective measurement of exercise capacity. Combined alpha-adrenergic blockade and angiotensin-converting enzyme inhibition appears safe in patients who failed to exhibit a sustained improvement on CPT alone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6127943&dopt=Abstract
Zhonghua Yi Xue Za Zhi. 1993 Jul;73(7):416-9, 448.
[Anoxia-reperfusion injury to endothelial cells: mechanism and protection]
[Article in Chinese]
Yu S.
Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xian.
Endothelial cells in the aortic walls of inbred SD rats were cultured in MEM culture medium containing 10% calf serum, and an anoxia-reperfusion injury model was established. The effect of anoxia-reperfusion injury on cultured endothelial cells was studied by measurements of membrane fluidity, intracellular Ca content, the release rate of 51Cr and the uptake rate of trypan-blue. The effect of fructose 1-6 diphosphate (FDP) and captopril (Cap) on cultured endothelial cells was also investigated. The findings indicated that the two drugs might protect cultured endothelial cells from anoxia-reperfusion injury. The mechanism of anoxia-reperfusion injury and the protective effect of the two drugs on cultured endothelial cells were briefly discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8293345&dopt=Abstract
Hypertension. 1993 Jun;21(6 Pt 2):1030-4.
Angiotensinogen is cleaved to angiotensin in isolated rat blood vessels.
Hilgers KF, Hilgenfeldt U, Veelken R, Muley T, Ganten D, Luft FC, Mann JF.
Department of Medicine-Nephrology, University of Erlangen, FRG.
The cleavage of synthetic tetradecapeptide renin substrate has been used to infer the presence of renin in the walls of isolated blood vessels; however, the conversion of natural angiotensinogen to angiotensin in isolated blood vessels has not been reported. We studied the release of angiotensinogen and the formation of angiotensins in a bloodless, perfused, isolated hind limb preparation of the rat. Perfusion with a modified Tyrode's solution resulted in spontaneous release of 4.7 +/- 1.5 pmol per 30 minutes of angiotensinogen as measured directly by radioimmunoassay. Western blot further identified the released material as angiotensinogen. Spontaneous release of angiotensins I and II was demonstrated by high performance liquid chromatography and radioimmunoassay. When highly purified rat angiotensinogen was added to the perfusate, release of angiotensin II was increased 14-fold compared with saline infusion. Captopril (10 mumol/L) inhibited angiotensinogen-induced angiotensin II release by 67% and led to an increase in angiotensin I release by 301%. Bilateral nephrectomy 24 hours before the experiments reduced basal angiotensin release below the detection limit and blunted angiotensinogen-induced angiotensin II formation by 95%. We conclude that active renin is present in the vessel wall and interacts with its natural substrate to form angiotensin peptides. Our data support the notion that the bulk of vascular renin is taken up from the circulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8505088&dopt=Abstract
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