Drugs online research references
Z Gastroenterol. 1990 Jul;28(7):343-7.
[Effect of enalapril on heart rate, arterial blood pressure and exocrine pancreatic secretion in the alert dog]
[Article in German]
Teyssen S, Tarnarzewski M, Haurand C, Bretschneider S, Singer MV.
Abteilung fur Gastroenterologie, Universitatsklinikum Essen.
A changed exocrine pancreatic secretion could be a pathogenetic factor of an acute pancreatitis after administration of angiotensin-converting enzyme (ace) inhibitors. In six conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous (iv.) bolus injection of 10 mg enalaprilat, an intraduodenal (id.) bolus injection of 20 and 40 mg enalapril (e.), and 0.15 M NaCl (20 ml iv., resp., id.) on pancreatic bicarbonate- and protein output in response to secretin (20.5 pmol/kg bw/h and caerulein (29.6 pmol/kg bw/h). Arterial blood pressure and heart rate we also measured. The iv. and id. injection of enalapril(at) significantly increased heart rate by 28% after 10 mg of e. iv. [peak 101 +/- 11 beats/min, N = 6, X +/- SEM] and by 13 resp. 37% after 20 resp. 40 mg e. id. [peak 89 +/- 4, resp., 108 +/- 7 beats/min] as compared to control [peak 79 +/- 5 beats/min]. Systolic blood pressure was significantly decreased by 6% after 10 mg e. iv. [lowest value 121 +/- 2 mm Hg] and by 8% and 9% after 20 and 40 mg e. id., respectively, [lowest value 119 +/- 2, resp., 118 +/- 1 mm Hg] as compared to control [lowest value 129 +/- 1 mm Hg]. The applied enalapril(at) doses had no significant effect on hormonal stimulated pancreatic bicarbonate- and protein output. The results confirmed the well known effects of enalapril(at) on heart rate and on arterial blood pressure. Beyond that the results exposed that therapeutical doses of enalapril(at) had no significant effect on exocrine pancreatic secretion. Conclusion of this study is that a pathogenetic role of pancreatic exocrine secretion in the ace-inhibitors and the acute pancreatitis induced by ace-inhibitors is unlikely.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2238764&dopt=Abstract
Am J Physiol. 1988 Oct;255(4 Pt 2):F690-8.
Influence of kinins and angiotensin II on the regulation of papillary blood flow.
Roman RJ, Kaldunski ML, Scicli AG, Carretero OA.
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226.
The influence of kinins and angiotensin II on the regulation of renal cortical and papillary blood flow and sodium and water excretion was examined in rats. Superficial cortical and papillary blood flows were measured using a laser-Doppler flowmeter. Papillary blood flow increased 50% after enalaprilat (60 micrograms/kg) and phosphoramidon (5.5 micrograms.kg-1.min-1) were given along with 0.3 M sodium bicarbonate solution to inhibit degradation of kinins and enhance urinary kallikrein activity. Infusion of a kinin antagonist, D-Arg-Hyp-Thi-D-Phe-bradykinin (5 micrograms/min), returned papillary blood flow to control levels. Urine flow and sodium excretion increased after the administration of the kininase inhibitors and sodium bicarbonate, while glomerular filtration rate (GFR) and outer cortical blood flow were unaltered. The kinin antagonist did not alter sodium and water excretion in rats receiving the kininase inhibitors and bicarbonate. Administration of the kinin antagonist alone lowered papillary blood flow by 20%, without affecting outer cortical blood flow or GFR. Urine flow decreased and urine osmolality increased after the rats received the kinin antagonist, but sodium excretion remained unaltered. To assess the role of angiotensin II in the control of papillary blood flow, kinin receptors were blocked by infusion of an antagonist, and the effects of enalaprilat and saralasin were studied. Papillary blood flow increased after blockade of the angiotensin II system in rats receiving the kinin antagonist. These results indicate that the kallikrein-kinin and renin-angiotensin systems participate in the regulation of papillary blood flow.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2845811&dopt=Abstract
Int J Cardiol. 1986 Apr;11(1):37-51.
Enalapril in congestive heart failure: acute and chronic invasive hemodynamic evaluation.
Gomez HJ, Cirillo VJ, Davies RO, Bolognese JA, Walker JF.
Following hemodynamic evaluation using invasive and noninvasive methods, 73 patients were treated in an open, uncontrolled, multicenter study with single oral doses of enalapril maleate 1.25 to 40 mg until the optimal dose for each patient (based upon hemodynamic response) was achieved. Diuretics were withheld and reinstituted only if necessary. Hemodynamic measurements were made at 0 (predrug), 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours postdrug. Patients were discharged on their optimal dose, treated 1 to 4 months and then rehospitalized for repeat hemodynamic measurements. The optimal enalapril single dose was associated with the following mean peak responses: increased cardiac index 42% (SE = 6) and decreased pulmonary capillary wedge pressure 40% (SE = 3), systemic vascular resistance 39% (SE = 2), and mean arterial pressure 23% (SE = 1.5). These changes persisted during chronic therapy. Chronic treatment with enalapril also improved exercise capacity 40% (P less than 0.01), ejection fraction 18% (P less than 0.05) and clinical status (N.Y.H.A. functional class, P less than 0.01). Ten and 20 mg/day, taken as once- or twice-daily regimens, were the most commonly effective doses.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3007379&dopt=Abstract
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