Drugs online research references
Int J Clin Monit Comput. 1995 May;12(2):77-83.
In vivo comparison between two tip pressure transducer systems.
Aubert AE, Vrolix M, De Geest H, Van de Werf F.
Department of Cardiology, University Hospital Gasthuisberg, Catholic University Leuven, Belgium.
Experimental findings are presented of an in vivo comparison between a Sentron catheter and another tip transducer manometer: a Millar microtip catheter. Both catheters have been used simultaneously in the left ventricle of dogs. Pressure variations were elicited by drug infusion. Pressure values and derivatives obtained from both systems were compared. A cross correlation between episodes of the two pressures was computed. Results from this study showed good correlation between left ventricular systolic pressure measured with both manometers (R = 0.992, p < 0.0001), end-diastolic pressure (R = 0.809, p < 0.0001) and between first derivatives: positive derivative (R = 0.993, p < 0.0001) and negative (R = 0.634, p < 0.0001). The mean cross correlation between both pressure signals was 0.61 +/- 0.04. In the frequency domain no statistical difference was found between the location of the maxima of the peaks. It is concluded that a Sentron manometer can be a valid alternative, at a reasonable price, to a cheaper, though less accurate fluid filled catheter and a more expensive 'golden standard' microtip catheter.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8847469&dopt=Abstract
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Cardiovasc Res. 1996 Jan;31(1):117-23.
Cocaine-stimulated endothelin-1 release is decreased by angiotensin-converting enzyme inhibitors in cultured endothelial cells.
Hendricks-Munoz KD, Gerrets RP, Higgins RD, Munoz JL, Caines VV.
Neonatal Program, Department of Pediatrics, New York University Medical Center, NY 10016, USA.
OBJECTIVE: The primary aim was to determine the action of pathophysiologically relevant cocaine concentrations (10(-7)-10(-5) M) on endothelin-1 (ET-1) release from cultured endothelial cells under various cellular conditions. Further aims were to evaluate the effect of angiotensin-converting enzyme inhibitors on cocaine-treated endothelial cells, to assess their potential for inhibition of ET-1-stimulated release. METHODS: Endothelin-1 release into the media was evaluated by radioimmunoassay under basal conditions and after 24 h treatment of endothelial cells with cocaine hydrochloride (HCl), or cocaine HCl and ACE inhibitors, captopril and lisinopril. The effect of serum and plasma under these conditions was also investigated. RESULTS: Cocaine HCl stimulated ET-1 release in a dose response fashion that was independent of plasma or serum factors. Furthermore, cocaine-stimulated ET-1 release was inhibited by administration of angiotensin-converting enzyme inhibitors captopril and lisinopril. CONCLUSIONS: These findings suggest that cocaine can directly stimulate endothelial cells to release ET-1 and that the observed increase is independent of serum or plasma factors. Furthermore, cocaine-stimulated endothelin-1 release appears to be mediated at least in part by the angiotensin system. These observations provide a framework for understanding the cellular mechanisms involved in cocaine-induced vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8849595&dopt=Abstract
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Physiol Res. 2000;49(1):183-8.
Long-term lisinopril dihydrate application decreases plasma noradrenaline but not adrenaline levels in chickens.
Ozdemir HS, Aksulu HE, Karatas F, Ustundag B, Bingol I.
Department of Pharmacology, Faculty of Medicine, University of Firat, Elazig, Turkey.
Little is known about the effect of chronic angiotensin-converting enzyme inhibition on the catecholamine levels in fowls. In this study, we investigated the effects of chronic lisinopril dihydrate (Ld) application on the plasma levels of adrenaline and noradrenaline and on the blood pressure. Lisinopril was given in different concentrations (25, 75 and 250 mg/l drinking water) to the white Leghorn chickens for 9 weeks, while the control group drank tap water only. Twenty-eight hours after the last lisinopril application, arterial blood pressure (BP), plasma adrenaline and noradrenaline levels, plasma renin (PRA) and plasma angiotensin-converting enzyme (ACE) activities were determined. In all concentrations, lisinopril significantly increased PRA and decreased ACE activities. Arterial BP was decreased only in the group receiving high lisinopril concentration (Controls 119+/-10.27, Ld3 98+/-5.4 mm Hg). However, the lower lisinopril concentrations did not alter arterial BP compared to the control group. Plasma noradrenaline levels were decreased in a concentration-dependent manner (47-58%), but plasma adrenaline levels remained unchanged. The heart weight/body weight ratio was not changed in any of the lisinopril-treated groups. The persistent decrease in the blood pressure after lisinopril treatment was not directly related to a decrease of plasma ACE activity or plasma noradrenaline levels. Its mechanism still remains to be elucidated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10805421&dopt=Abstract
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