Hemodynamic Effects Of Acute Administration Research Articles

Hemodynamic Effects of Acute Administration of Atomoxetine and Methylphenidate

The Journal of Clinical PharmacologyVolume 45, Issue 7 p. 851-855 Hemodynamic Effects of Acute Administration of Atomoxetine and Methylphenidate Dr Ronan P. Kelly MRCP, Corresponding Author Dr Ronan P. Kelly MRCP Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeAddress for reprints: Ronan P. Kelly, Lilly-NUS Centre for Clinical Pharmacology, Level 6 Clinical Research Centre (MD11), National University of Singapore, 10 Medical Drive, Singapore 117597.Search for more papers by this authorDr Kwee Poo Yeo PhD, Dr Kwee Poo Yeo PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Choo-Hua Teng PhD, Dr Choo-Hua Teng PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Brian P. Smith PhD, Dr Brian P. Smith PhD Eli Lilly and Company, Indianapolis, IndianaSearch for more papers by this authorDr Stephen Lowe PhD, Dr Stephen Lowe PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Danny Soon MD, Dr Danny Soon MD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Holly A. Read MD, Dr Holly A. Read MD Eli Lilly and Company, Indianapolis, IndianaSearch for more papers by this authorDr Stephen D. Wise FRCP, Dr Stephen D. Wise FRCP Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this author Dr Ronan P. Kelly MRCP, Corresponding Author Dr Ronan P. Kelly MRCP Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeAddress for reprints: Ronan P. Kelly, Lilly-NUS Centre for Clinical Pharmacology, Level 6 Clinical Research Centre (MD11), National University of Singapore, 10 Medical Drive, Singapore 117597.Search for more papers by this authorDr Kwee Poo Yeo PhD, Dr Kwee Poo Yeo PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Choo-Hua Teng PhD, Dr Choo-Hua Teng PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Brian P. Smith PhD, Dr Brian P. Smith PhD Eli Lilly and Company, Indianapolis, IndianaSearch for more papers by this authorDr Stephen Lowe PhD, Dr Stephen Lowe PhD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Danny Soon MD, Dr Danny Soon MD Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this authorDr Holly A. Read MD, Dr Holly A. Read MD Eli Lilly and Company, Indianapolis, IndianaSearch for more papers by this authorDr Stephen D. Wise FRCP, Dr Stephen D. Wise FRCP Lilly-NUS Centre for Clinical Pharmacology, National University of SingaporeSearch for more papers by this author First published: 25 March 2013 https://doi.org/10.1177/0091270005276737Citations: 17Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume45, Issue7July 2005Pages 851-855 RelatedInformation

Dose-dependent biphasic effect of ethanol on 24-h blood pressure in normotensive subjects

The vasodilation that follows acute alcohol intake is hard to conciliate with the high prevalence of hypertension detected in those persons who consume regular amounts of alcohol. In this experiment we examined early and late hemodynamic effects of acute administration of water and of 15 g, 30 g, and 60 g of alcohol in 40 normal men, aged 19 to 30 years, using 24-h ambulatory blood pressure monitoring (ABPM). Mean systolic and diastolic blood pressures were each approximately 4 mm Hg lower during the period immediately after ingestion of 60 g ( v 0 g) of ethanol, and were 7 and 4 mm Hg higher, respectively, at night. The day minus night differences displayed a dose-response curve both for systolic ( P < .001) and diastolic blood pressure ( P = .045). Three subjects in the 60-g group had more than 50% of nightly blood pressure loads in the hypertensive range against none in the remaining groups ( P < .01). In conclusion, our findings suggest that acute alcohol intake elicits a biphasic hemodynamic response, causing, first, vasodilatation and, later, a pressor effect. The higher prevalence of hypertension in alcohol abusers seen in epidemiological surveys may be, in part, a result of measurements done in the period of transiently increased blood pressure during ethanol washout.

Hemodynamic effects of terlipressin and octreotide administration alone or in combination in portal hypertensive rats

Background/Aims: The action sites and kinetic effects of octreotide and terlipressin may be different. Therefore, we studied the hemodynamic effects of acute administration of these drugs alone or in combination in rats with portal hypertension due to portal vein ligation. Methods: In a first study performed in anesthetized rats, hemodynamics were measured before and after drug administration (placebo, octreotide: 8 μg·kg −1·h −1 for 30 min, terlipressin: 50 μg/kg bolus, terlipressin + octreotide at the same doses). The second study, performed in conscious rats, included the same groups and drug doses; hemodynamics were measured every 10 min for 1 h. The third study tested the effect of preinfusion of octreotide on responsiveneness to terlipressin. Results: Terlipressin produced more marked systemic effects than octreotide by decreasing heart rate and cardiac output and increasing mean arterial pressure. Terlipressin produced a greater decrease in portal pressure than octreotide: placebo: −3±5%, terlipressin: −42±8%, octreotide: −16±10%, combination: −44±8% (conscious rats at 20 min, p<10 −4). The decrease in portal pressure was immediate and lasted at least 60 min with both drugs. Octreotide significantly decreased spleno-renal shunt blood flow (% variation): placebo: −6±8, terlipressin: −15.5±20, octreotide: −22.5±20, combination: −27±10 ( p<10 −2). Octreotide preinfusion significantly increased the responsiveness of arterial pressure and heart rate to terlipressin. Conclusions: Terlipressin decreases portal pressure significantly more than octreotide, while only octreotide significantly decreases collateral blood flow. Simultaneous administration of these drugs does not have significant additive effects but has complementary effects. The preadministration of octreotide alters systemic reponse to terlipressin.

Attenuation of myocardial ischaemic injury 24 h after diacylglycerol treatment in vivo.

Previous work suggests that delayed protection against infarction following ischaemic preconditioning of rabbit myocardium may involve the activation of protein kinase C (PKC). Preconditioning in the presence of chelerythrine, an inhibitor of PKC, abolished the late anti-infarct effect of preconditioning. In the studies described here, we tested the hypothesis that direct PKC activation with an analogue of diacylglycerol, the physiological activator of PKC, would invoke an adaptive mechanism leading to enhanced myocardial tolerance to ischaemia 24 h later. Rabbits were treated with i.v. injections of 1,2-dioctanoyl-sn-glycerol (DiC8) 5 mg/kg or 15 mg/kg or an equivalent volume of vehicle solution. Twenty-four h after pretreatment, the animals were anaesthetised and underwent 30 min coronary artery occlusion with 120 min reperfusion. Infarct size was determined by triphenyltetrazolium staining. In vehicle pretreated rabbits, infarct-risk zone ratio was 32.8+/-2.6%. Pretreatment with DiC8 5 mg/kg did not significantly affect infarct size (26.3+/-4.0%), but pretreatment with DiC8 15 mg/kg resulted in a marked reduction in infarct size (18.0+/-3.4%, P<0.05, 1-way ANOVA). Reduction in infarct size with the higher dose of DiC8 was independent of myocardial risk zone size and systemic haemodynamic parameters during coronary occlusion. The haemodynamic effects of acute administration of DiC8 15 mg/kg were examined in a separate cohort of pentobarbitone-anaesthetised rabbits. The compound was found not to affect systolic blood pressure or heart rate under these conditions. We examined the possibility that increased ischaemic tolerance might be due to induction of the 27 and 72 kDa heat shock proteins (hsp27 and hsp70i) which are known to be cytoprotective and are upregulated by ischaemia and other stressful stimuli. Western blot analysis of left ventricular tissue revealed that neither protein was induced 24 h after treatment with DiC8 15 mg/kg. Thus, infarct limitation 24 h after DiC8 treatment did not appear to be due to increased tissue content of these proteins. The mechanisms of DiC8-induced delayed myocardial protection remain unclear. However, these data are compatible with the hypothesis that activation of PKC isoenzymes is an important intermediate signal of sub-acute cellular adaptation, and results in enhanced tolerance to ischaemia-reperfusion injury in myocardium many hours later.

Hemodynamic effects of acute administration of furosemide in patients with cirrhosis receiving β-adrenergic antagonists

In patients with cirrhosis, both beta-blockers and diuretics decrease the degree of portal hypertension. Since their mechanisms of action differ, the combination of these two substances should induce a more pronounced effect on portal pressure than one of these substances alone. Thus, the hemodynamic effects of furosemide were evaluated in ten patients with cirrhosis receiving beta-blockers. One hour after furosemide (0.75 mg/kg intravenously) administration, cardiac output decreased significantly from 6.2 +/- 0.6 to 5.2 +/- 0.3 l/min and blood volume from 8.0 +/- 1.6 to 5.3 +/- 0.5 l. Mean arterial pressure was not affected. Wedged and free hepatic venous pressures did not change significantly; nor did the hepatic venous pressure gradient (19.6 +/- 1.7 to 18.6 +/- 1.5 mmHg). Azygos blood flow was not affected (0.46 +/- 0.05 to 0.50 +/- 0.07 l/min). In conclusion, this study did not demonstrate that the addition of furosemide to propranolol further decreased portal pressure in patients with cirrhosis. The long-term effects of this combination are unknown and should be tested.

Hemodynamic Effects of Acute Administration of Slow-Release Nifedipine in Elderly Patients with Systolic Hypertension

Hemodynamic Effects of Acute Administration of Slow-Release Nifedipine in Elderly Patients with Systolic Hypertension