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Hemodynamic Effects (hemodynamic + effects)

Distribution by Scientific Domains

Medical Sciences	93%
2 Other Domains	7%

Selected Abstracts

Hemodynamic Effects of Nesiritide and Dopamine in Cardiovascular Collapse Assessed Via Impedance Cardiography

CONGESTIVE HEART FAILURE, Issue 1 2007
Joe Witten DO
First page of article [source]

Clinical and Hemodynamic Effects of Nesiritide (B-Type Natriuretic Peptide) in Patients With Decompensated Heart Failure Receiving , Blockers

CONGESTIVE HEART FAILURE, Issue 2 2005
William T. Abraham MD
The use of , blockers in congestive heart failure presents a therapeutic challenge for patients with acute episodes of decompensation. Such patients may be less responsive to positive inotropic agents, whereas the beneficial effects of nesiritide, which are not dependent on the ,-adrenergic receptor signal-transduction pathway, may be preserved. This analysis of the Vasodilation in the Management of Acute CHF trial evaluated the safety and efficacy of nesiritide in decompensated congestive heart failure patients receiving , blockers. The Vasodilation in the Management of Acute CHF trial was a multicenter, randomized, controlled evaluation of nesiritide in 489 hospitalized patients with decompensated congestive heart failure. One hundred twenty-three patients were on chronic ,-blocker therapy at enrollment (31 randomized to placebo, 50 to nesiritide, and 42 to nitroglycerin). Primary end points included pulmonary capillary wedge pressure and dyspnea evaluation at 3 hours. Patients receiving nesiritide, but not IV nitroglycerin, had significantly reduced pulmonary capillary wedge pressure vs. placebo at 3 hours regardless of ,-blocker use. The use of , blockers did not alter the beneficial effects of nesiritide on systemic blood pressure, heart rate, or dyspnea evaluation. In nesiritide-treated subjects, safety profiles were similar regardless of ,-blocker use. Thus, the clinical and hemodynamic benefits and safety of nesiritide are preserved in decompensated congestive heart failure patients receiving chronic , blockade. [source]

Hemodynamic Effects of Innominate Artery Occlusive Disease on Anterior Cerebral Artery

JOURNAL OF NEUROIMAGING, Issue 1 2002
Teng-Yeow Tan MD
Stenoses of the innominate artery (IA) may affect flow conditions in the carotid arteries. However, alternating flow in ipsilateral anterior cerebral artery (ACA) due to IA stenosis is extremely rare. A 49-year-old woman who was evaluated for symptomatic cerebrovascular disease presented with right latent subclavian and right carotid system steal. Transcranial Doppler examination displayed systolic deceleration wave-forms in the right terminal internal carotid artery and alternating flow in the right ACA. Magnetic resonance angiography demonstrated tight stenosis of the right IA. For a thorough study of the hemodynamic effects of IA stenosis, a combination of duplex and transcranial Doppler examination is required. [source]

ORIGINAL RESEARCH,PHARMACOTHERAPY: Hemodynamic Effects of Sildenafil Citrate and Isosorbide Mononitrate in Men with Coronary Artery Disease and Erectile Dysfunction

THE JOURNAL OF SEXUAL MEDICINE, Issue 3 2005
Graham Jackson
ABSTRACT Introduction., Mild hemodynamic effects have been reported with sildenafil citrate therapy. Aim., To compare the hemodynamic effects of sildenafil and isosorbide mononitrate (ISMN) in men with coronary artery disease and erectile dysfunction. Methods., A total of 31 men aged 35 years or older with coronary artery disease (at least 50% narrowing of the left main stem or at least 70% narrowing of any other coronary artery) and erectile dysfunction (receiving medication for erectile dysfunction or scoring less than 26 out of a maximum score of 30 on the erectile function domain questions of International Index of Erectile Function) were randomized to sildenafil 100 mg (n = 10), ISMN 40 mg (n = 11), or placebo (n = 10) in this single-dose multicenter study. Main Outcome Measures., Hemodynamic parameters were measured at baseline, 1, 2, 4, and 6 hours post dose. Results., Compared with baseline, cardiac index increased slightly with sildenafil (0.29 L/min/m2 at 1 hour) and decreased slightly with placebo (,0.12 L/min/m2 at 4 hours) and ISMN (,0.14 L/min/m2 at 1 hour). The stroke volume index increased from baseline at each time point post dose with sildenafil (4.4 mL/m2 at 2 hours), but decreased with ISMN (,5.8 mL/m2 at 1 hour) and placebo (,2.8 mL/m2 at 4 hours). ISMN reduced mean arterial pressure more than sildenafil did (,22 vs. ,10 mm Hg at 2 hours, respectively). Both sildenafil and ISMN increased heart rate (4 vs. 7 beats/minute at 1 hour, respectively) and decreased systemic vascular resistance, but sildenafil produced greater reductions in pulmonary vascular resistance. There were no serious adverse events in the sildenafil group. Conclusions., Sildenafil 100 mg was well tolerated and induced smaller changes in central and peripheral hemodynamic pressures compared with ISMN 40 mg. Moreover, sildenafil selectively reduced pulmonary resistance, which may have clinical importance in pulmonary hypertension. [source]

Hemodynamic Effects of Intralipid after Verapamil Intoxication May Be Due to a Direct Effect of Fatty Acids on Myocardial Calcium Channels

ACADEMIC EMERGENCY MEDICINE, Issue 8 2007
Gildas Gueret MD
No abstract is available for this article. [source]

Hemodynamic Effects of Intravenous Fat Emulsion in an Animal Model of Severe Verapamil Toxicity Resuscitated with Atropine, Calcium, and Saline

ACADEMIC EMERGENCY MEDICINE, Issue 2 2007
Theodore C. Bania MD
Background Intravenous fat emulsion (IFE) decreases cardiotoxicity from several lipid-soluble drugs, including verapamil. Objectives To verify if the addition of IFE to the standard treatment of severe verapamil toxicity would improve hemodynamics and survival. Methods Fourteen dogs were instrumented to measure systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), heart rate, cardiac output, central venous pressures, left ventricular pressure changes over time, mixed venous oxygen saturation, pH, and base excess. Verapamil toxicity, defined as a 50% decrease in MAP, was induced with verapamil at 6 mg/kg/hr and maintained for 30 minutes by titrating the verapamil infusion rate. Following verapamil toxicity, the verapamil infusion rate was changed to 2 mg/kg/hr and continued for 90 minutes. All dogs were resuscitated with atropine (0.04 mg/kg intravenously) and calcium chloride (15 mg/kg intravenously every 5 minutes for three doses) and then randomized to receive either IFE (7 mg/kg of 20%) intravenously or equivalent volumes of 0.9% normal saline over 30 minutes. Measurements were recorded for 120 minutes by investigators blinded to the treatment. Data were analyzed using analysis of variance, survival analysis, and log-rank test. Results Before the 30-minute IFE or normal saline infusion, there were no differences in hemodynamic parameters. After IFE or normal saline infusion, the IFE-treated group had higher MAP at 30 minutes (95% confidence interval [CI] = 5.6 to 44.7 mm Hg), 45 minutes (95% CI = 10.8 to 50.0 mm Hg), and 60 minutes (95% CI = 10.2 to 53.1 mm Hg). Kaplan,Meier 120-minute survival rate was 14% (95% CI = 0.5% to 53%) for the saline group as compared with 100% (95% CI = 59% to 100%) for the IFE group (p = 0.01). Conclusions Standard resuscitation and IFE increase MAP and survival in an animal model of severe verapamil toxicity compared with standard resuscitation alone. [source]

Hemodynamic effects of PEEP in a porcine model of HCl-induced mild acute lung injury

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2009
C. K. MARUMO
Background: Positive end-expiratory pressure (PEEP) and sustained inspiratory insufflations (SI) during acute lung injury (ALI) are suggested to improve oxygenation and respiratory mechanics. We aimed to investigate the hemodynamic effects of PEEP with and without alveolar recruiting maneuver in a mild ALI model induced by inhalation of hydrochloric acid. Methods: Thirty-two pigs were randomly allocated into four groups (Control,PEEP, Control,SI, ALI,PEEP and ALI,SI). ALI was induced by intratracheal instillation of hydrochloric acid. PEEP values were progressively increased and decreased from 5, 10, 15 and 20 cmH2O in all groups. Three SIs maneuvers of 30 cmH2O for 20 s were applied to the assignable groups between each PEEP level. Transesophageal echocardiography (TEE), global hemodynamics, oxygenation indexes and gastric tonometry were measured 5 min after the maneuvers had been concluded and at each established value of PEEP (5, 10, 15 and 20 cmH2O). Results: The cardiac index, ejection fraction and end-diastolic volume of right ventricle were significantly (P<0.001) decreased with PEEP in both Control and ALI groups. Left ventricle echocardiography showed a significant decrease in end-diastolic volume at 20 cmH2O of PEEP (P<0.001). SIs did not exert any significant hemodynamic effects either early (after 5 min) or late (after 3 h). Conclusions: In a mild ALI model induced by inhalation of hydrochloric acid, significant hemodynamic impairment characterized by cardiac function deterioration occurred during PEEP increment, but SI, probably due to low applied values (30 cmH2O), did not exert further negative hemodynamic effects. PEEP should be used cautiously in ALI caused by acid gastric content inhalation. [source]

BNP Consensus Panel 2004: A Clinical Approach for the Diagnostic, Prognostic, Screening, Treatment Monitoring, and Therapeutic Roles of Natriuretic Peptides in Cardiovascular Diseases

CONGESTIVE HEART FAILURE, Issue 2004
Marc A. Silver MD
Among the most exciting developments in the field of heart failure in recent times has been the rediscovery of the natriuretic peptide system and its pleuripotent effects on cardiac structure and function. This is particularly true of its natriuretic and hemodynamic effects. There has been an explosion of the knowledge base seeking to understand the wide range of homeostatic, regulatory, and counter-regulatory functions in which the natriuretic peptide system participates. Additional interest has been stimulated by advances in technology such as point-of-care and core laboratory BNP assays and the use of the recombinant B-type natriuretic peptide nesiritide as a treatment option. Despite this recent interest, the available literature lacks a comprehensive expert review of the current science and roles of natriuretic peptides for diagnostic, prognostic, screening, treatment monitoring, and therapeutic purposes. More importantly, a summary updating and guiding the clinician on most of these advances was lacking. An expert Consensus Panel with basic, methodological, and clinical expertise was convened to summarize current knowledge in these areas and the findings and consensus statements are contained herein. [source]

Etiology of strokes in children with sickle cell anemia

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 3 2006
Michael R. DeBaun
Abstract The most devastating complication of sickle cell anemia is cerebral infarction, affecting ,30% of all individuals with sickle cell anemia. Despite being one of the most common causes of stroke in infants and children, the mechanism of cerebral infarction in this population has not been extensively studied and is poorly understood. Multiple, synergistic factors are important in the pathogenesis of stroke including the hemodynamic effects of cerebral arterial occlusive disease, viscosity, chronic and acute anemia and acute medical events. This review focuses on the relationship between these factors in order to provide a foundation for further study of the etiology of strokes in this high-risk population. MRDD Research Reviews 2006;12:192,199. © 2006 Wiley-Liss, Inc. [source]

Reversal of portal hypertension and hyperdynamic splanchnic circulation by combined vascular endothelial growth factor and platelet-derived growth factor blockade in rats,

HEPATOLOGY, Issue 4 2007
Mercedes Fernandez
Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) pathways are crucial to angiogenesis, a process that contributes significantly to the pathogenesis of portal hypertension. This study determined the effects of inhibition of VEGF and/or PDGF signaling on hyperdynamic splanchnic circulation and portosystemic collateralization in rats with completely established portal hypertension, thus mimicking the situation in patients. Portal vein,ligated rats were treated with rapamycin (VEGF signaling inhibitor), Gleevec (PDGF signaling inhibitor), or both simultaneously when portal hypertension was already fully developed. Hemodynamic studies were performed by transit-time flowmetry. The extent of portosystemic collaterals was measured by radioactive microspheres. The expression of angiogenesis mediators was determined by Western blotting and immunohistochemistry. Combined inhibition of VEGF and PDGF signaling significantly reduced splanchnic neovascularization (i.e., CD31 and VEGFR-2 expression) and pericyte coverage of neovessels (that is, ,-smooth muscle actin and PDGFR-, expression) and translated into hemodynamic effects as marked as a 40% decrease in portal pressure, a 30% decrease in superior mesenteric artery blood flow, and a 63% increase in superior mesenteric artery resistance, yielding a significant reversal of the hemodynamic changes provoked by portal hypertension in rats. Portosystemic collateralization was reduced as well. Conclusions: Our results provide new insights into how angiogenesis regulates portal hypertension by demonstrating that the maintenance of increased portal pressure, hyperkinetic circulation, splanchnic neovascularization, and portosystemic collateralization is regulated by VEGF and PDGF in portal hypertensive rats. Importantly, these findings also suggest that an extended antiangiogenic strategy (that is, targeting VEGF/endothelium and PDGF/pericytes) may be a novel approach to the treatment of portal hypertension. (HEPATOLOGY 2007.) [source]

Effects of clonidine on diuretic response in ascitic patients with cirrhosis and activation of sympathetic nervous system,,

HEPATOLOGY, Issue 4 2006
Anne Lenaerts
The effects of the addition of clonidine to diuretics on the mobilization of ascites in the short term (diuretic response and requirement of diuretics) and the long term (readmissions for tense ascites and requirement of diuretics) were examined in patients with cirrhosis and with increased sympathetic nervous system (SNS) activity. We also studied neurohormonal, hemodynamic effects and side effects of clonidine and diuretics. Patients were randomized to receive placebo (group1, n = 32) or clonidine (0.075 mg) twice daily (group 2, n = 32) for 3 months. After 8 days and for 10 days duration, spironolactone (200 mg/day) was added in both groups. After this period, the dosages of diuretics were individually increased until diuretic response. Responding patients were discharged and followed at the outpatient clinic. During the first hospitalization, the time needed for diuretic response was shorter in group 2 than in group 1. The mean requirement for diuretics was significantly higher in group 1 than in group 2, and the diuretic complications (hyperkalemia and renal impairment) were significantly lower in group 2. Clonidine induced a permanent decrease in SNS activity and delayed decrease in renin/aldosterone levels. During the follow-up, the time to the first readmission for tense ascites was shorter in group 1 than in group 2. Readmissions related to tense ascites or diuretic complications were significantly lower in group 2. The mean requirement for diuretics was significantly higher in group 1 than in group 2. In conclusion, the additional administration of clonidine to diuretics induced an earlier diuretic response associated with fewer diuretic requirements and complications. (HEPATOLOGY 2006;44:844,849.) [source]

Humoral and cardiac effects of TIPS in cirrhotic patients with different "effective" blood volume

HEPATOLOGY, Issue 6 2003
Francesco Salerno M.D.
The aim of this study was to evaluate the cardiac effects of transjugular intrahepatic portosystemic shunts (TIPS) in cirrhotic patients with different effective blood volume. Two-dimensional echocardiography was performed before and 7 and 28 days after TIPS insertion in 7 cirrhotic patients with PRA <4 ng/mL/h (group A, normal effective blood volume) and 15 with PRA >4 ng/mL/h (group B, reduced effective blood volume). Before TIPS, most cirrhotic patients showed diastolic dysfunction as indicated by reduced early maximal ventricular filling velocity (E)/late filling velocity (A) ratio. Patients of group B differed from patients of group A because of smaller left ventricular volumes and stroke volume, indicating central underfilling. After TIPS insertion, portal decompression was associated with a significant increase of cardiac output (CO) and a decrease of peripheral resistances. The most important changes were recorded in patients of group B, who showed a significant increase of both the end-diastolic left ventricular volumes and the E/A ratio and a significant decrease of PRA. In conclusion, these results show that the hemodynamic effects of TIPS differ according to the pre-TIPS effective blood volume. Furthermore, TIPS improves the diastolic cardiac function of cirrhotic patients with effective hypovolemia. This result is likely due to a TIPS-related improvement of the fullness of central blood volume. [source]

Hemodynamic effects of PEEP in a porcine model of HCl-induced mild acute lung injury

Hemodynamic Effects of Innominate Artery Occlusive Disease on Anterior Cerebral Artery

Facilitation of Myocardial PI3K/Akt/nNOS Signaling Contributes to Ethanol-Evoked Hypotension in Female Rats

ALCOHOLISM, Issue 7 2009
Mahmoud M. El-Mas
Background:, The mechanism by which ethanol reduces cardiac output (CO) and blood pressure (BP) in female rats remains unclear. We tested the hypothesis that enhancement of myocardial phosphatidylinositol 3-kinase (PI3K)/Akt signaling and related neuronal nitric oxide synthase (nNOS) and/or endothelial nitric oxide synthase (eNOS) activity constitutes a cellular mechanism for the hemodynamic effects of ethanol. Methods:, We measured the level of phosphorylated eNOS (p-eNOS) and p-nNOS in the myocardium of ethanol (1 g/kg intragastric, i.g.) treated female rats along with hemodynamic responses [BP, CO, stroke volume, (SV), total peripheral resistance, (TPR)], and myocardial nitrate/nitrite levels (NOx) levels. Further, we investigated the effect of selective pharmacological inhibition of nNOS with N, -propyl- l -arginine (NPLA) or eNOS with N5 -(1-iminoethyl)- l -ornithine (l -NIO) on cellular, hemodynamic, and biochemical effects of ethanol. The effects of PI3K inhibition by wortmannin on the cardiovascular actions of ethanol and myocardial Akt phosphorylation were also investigated. Results:, The hemodynamic effects of ethanol (reductions in BP, CO, and SV) were associated with significant increases in myocardial NOx and myocardial p-nNOS and p-Akt expressions while myocardial p-eNOS remained unchanged. Prior nNOS inhibition by NPLA (2.5 or 12.5 ,g/kg) attenuated hemodynamic effects of ethanol and abrogated associated increases in myocardial NOx and cardiac p-nNOS contents. The hemodynamic effects of ethanol and increases in myocardial p-Akt phosphorylation were reduced by wortmannin (15 ,g/kg). On the other hand, although eNOS inhibition by l -NIO (4 or 20 mg/kg) in a dose-dependent manner attenuated ethanol-evoked hypotension, the concomitant reductions in CO and SV remained unaltered. Also, selective eNOS inhibition uncovered dramatic increases in TPR in response to ethanol, which appeared to have offset the reduction in CO. Neither NPLA nor l -NIO altered plasma ethanol levels. Conclusions:, These findings implicate the myocardial PI3K/Akt/nNOS signaling in the reductions in BP and CO produced by ethanol in female rats. [source]

The Effect of Angiotensin-Converting Enzyme Inhibitors of Left Atrial Pressure in Dogs with Mitral Valve Regurgitation

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2010
T. Ishikawa
Background: Despite many epidemiological reports concerning the efficacy of angiotensin-converting enzyme (ACE) inhibitors in dogs with mitral regurgitation (MR), the hemodynamic effects of ACE inhibitor administration have not been fully evaluated. Objectives: To document left atrial pressure (LAP) in dogs with MR administered ACE inhibitors, in order to obtain interesting information about daily LAP changes with administration of ACE inhibitors. Animals: Five healthy Beagle dogs weighing 9.8 to 14.2 kg (2 males and 3 females; aged 2 years). Methods: Experimental, crossover, and interventional study. Chordae tendineae rupture was induced, and a radiotelemetry transmitter catheter was inserted into the left atrium. LAP was recorded for 72 consecutive hours during which each of 3 ACE inhibitors,enalapril (0.5 mg/kg/d), temocapril (0.1 mg/kg/d), and alacepril (3.0 mg/kg/d),were administered in a crossover study. Results: Averaged diurnal LAP was significantly, but slightly reduced by alacepril (P= .03, 19.03 ± 3.01,18.24 ± 3.07 mmHg). The nightly drops in LAP caused by alacepril and enalapril were significantly higher than the daily drops (P= .03, ,0.98 ± 0.19 to ,0.07 ± 0.25 mmHg, and P= .03, ,0.54 ± 0.21,0.02 ± 0.17 mmHg, respectively), despite the fact that the oral administrations were given in the morning. Systolic blood pressure (122.7 ± 14.4,117.4 ± 13.1 mmHg, P= .04) and systemic vascular resistance (5800 ± 2685,5144 ± 2077 dyne × s/cm5, P= .03) were decreased by ACE inhibitors. Conclusions and Clinical Importance: ACE inhibitors decrease LAP minimally, despite reductions in left ventricular afterload. ACE inhibitors should not be used to decrease LAP. [source]

The electrocardiographic and hemodynamic effect of metohexital and propofol with and without esmolol

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2006
R. Korpinen
Background:, Metohexital and propofol are short-acting induction agents, which have a tendency to prolong the QTc interval of the ECG. We studied whether this increase could be prevented by combining a beta-blocking agent, esmolol, with these drugs. Simultaneously, we studied the hemodynamic effects of these combinations. Methods:, In a randomized, double-blind study, 80 ASA I,II young adults were premedicated with oxycodone and atropin and allocated to one of four groups: propofol (P), propofol + esmolol (P + E), metohexital (E) or metohexital + esmolol (M + E). The doses were 2 mg/kg propofol/metohexital and 1 mg/kg esmolol. Alfentanil 15 µg/kg was used in all groups. The hemodynamic parameters were measured non-invasively and the electrocardiographic parameters using the signal processing method. Result:, The highest QTc values, which often exceeded the normal upper limit of 440 ms, were recorded at the baseline or immediately after the administration of the induction drugs. The intervals were significantly shorter if esmolol was co-administered with either propofol or metohexital. The heart rate increased in the group M and decreased in the group P + E but remained unchanged in the groups P and M + E. Systolic and diastolic arterial pressures decreased during the study in all groups, most prominently in group P + E. Conclusions:, During the anesthesia induction, the QTc interval was significantly shorter when esmolol was co-administered with either propofol or metohexital. The hemodynamic responses were properly controlled with the combination of metohexital and esmolol as well as with propofol alone, but the combination of propofol and esmolol tended to cause hemodynamic depression. [source]

Electrophysiologic Effects of Carvedilol: Is Carvedilol an Antiarrhythmic Agent?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2005
NABIL EL-SHERIF
The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks ,1 -, ,2 -, and ,1 - adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its ,-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance. [source]

Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgery

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2000
N. Kieler-Jensen
Background: The aim was to evaluate the use of clevidipine, a new vascular selective, ultra-short-acting calcium antagonist for blood pressure control after coronary artery bypass grafting (CABG). Methods: The effects of clevidipine on central hemodynamics, myocardial blood flow and metabolism were studied at two different phases after CABG. In phase 1 (n=13), the hypertensive phase, the effects of clevidipine were compared to those of sodium nitroprusside (SNP) when used to control postoperative hypertension. In phase 2 (n=9), the normotensive phase, a clevidipine dose-response relationship was established. Results: At a target mean arterial pressure (MAP) of 75 mmHg, systemic vascular resistance (SVR) and heart rate (HR) were lower, preload, stroke volume (SV) and pulmonary vascular resistance (PVR) were higher, while there were no differences in myocardial lactate metabolism or oxygen extraction with clevidipine compared to SNP. In the normotensive phase, clevidipine induced a dose-dependent decrease in MAP (,19%), SVR (,27%) and PVR (,15%), accompanied by an increase in SV (10%), but no reflex increase in HR or changes in cardiac preload. Clevidipine caused a direct coronary vasodilation, as indicated by a decrease in myocardial oxygen extraction from 54% to 45%. Myocardial lactate metabolism was unaffected by clevidipine. The blood clearance of clevidipine was 0.05 l ,· ,min,1 ,· ,kg,1, the volume of distribution at steady state was 0.08 l ,· ,kg,1 and the initial and terminal half-lives were <1 min and 4 min, respectively. Conclusions: Clevidipine rapidly reduced MAP and induced a systemic, pulmonary and coronary vasodilation with no effect on venous capacitance vessels or HR. Clevidipine caused no adverse effects on myocardial lactate metabolism. Clevidipine thus appears suitable to control blood pressure after CABG. [source]

Hypercapnic acidosis and compensated hypercapnia in control and pulmonary hypertensive piglets,

PEDIATRIC PULMONOLOGY, Issue 2 2003
K. Jane Lee MD
Abstract Low tidal volume/inspiratory pressure ventilator strategies result in hypercapnia, which has been shown to increase pulmonary vasomotor tone. This may be particularly detrimental in infants and children with preexistent pulmonary hypertension. In this study, a piglet model of chronic hypoxia-induced pulmonary hypertension was used to test the hypotheses that: 1) the effects of hypercapnic acidosis are exaggerated by preexistent pulmonary hypertension; and 2) the pulmonary hemodynamic effects of hypercapnic acidosis are attenuated by normalizing pH. Pulmonary hypertension was induced by 2 weeks of hypoxia. Hemodynamic responses were measured in control and pulmonary hypertensive piglets during both normoxia and hypoxia under normocapnic, hypercapnic acidotic, and compensated hypercapnic conditions. We found that: 1) hypercapnic acidosis increased both normoxic and hypoxic pulmonary vascular resistance index (PVRI) in control piglets; 2) the pressor effects of hypercapnia were not attenuated by infusing bicarbonate to normalize the pH; and 3) piglets with chronic hypoxia-induced pulmonary hypertension had elevated baseline normoxic and hypoxic PVRI, but responded to hypercapnic acidosis and compensated hypercapnia in a similar way to control piglets. These data suggest that acute hypercapnic acidosis may have deleterious effects on the pulmonary hemodynamics of normal and pulmonary hypertensive subjects which may not be acutely reversed by buffering the pH. Pediatr Pulmonol. 2003; 36:94,101. © 2003 Wiley-Liss, Inc. [source]

Anatomy and ultrasonography of the normal kidney in brown lemurs: Eulemur fulvus

AMERICAN JOURNAL OF PRIMATOLOGY, Issue 8 2009
Fidiniaina Raharison
Abstract The purpose of this study is to describe the anatomy and obtain echographic measurements of normal kidneys in brown lemurs (Eulemur fulvus). The anatomical findings show that brown lemur kidneys are comparable to those of rats except for an elongated papilla. The kidneys of 16 (7 females and 9 males) lemurs were examined with two-dimensional and power Doppler ultrasonography under general anesthesia. Morphometrically, the left and right kidney surface areas are comparable (3.29 and 3.51,cm2). Kidney area has a significant linear correlation with body weight. Echo-Doppler findings show that the mean renal arterial blood flow speeds for the left and right kidneys are comparable (0.70 and 0.73,m/s). However, flow speed is higher in the male (0.79,m/s) than in the female (0.60,m/s). The renal arterial diameters are between 1.0 and 1.8,mm. The fact that anesthesia can have hemodynamic effects on renal vasculature should be taken into consideration when assessing these echographic results. Am. J. Primatol. 71:647,653, 2009. © 2009 Wiley-Liss, Inc. [source]

ORIGINAL RESEARCH,PHARMACOTHERAPY: Hemodynamic Effects of Sildenafil Citrate and Isosorbide Mononitrate in Men with Coronary Artery Disease and Erectile Dysfunction

Cardioprotective Effects of Angiotensin II Type 1 Receptor Blockade with Olmesartan on Reperfusion Injury in a Rat Myocardial Ischemia-Reperfusion Model

CARDIOVASCULAR THERAPEUTICS, Issue 1 2010
Wangde Dai
We determined the effects of olmesartan on infarct size and cardiac function in a rat ischemia/reperfusion model. Rats underwent 30 min of left coronary artery (CA) occlusion followed by 2 h of reperfusion. In protocol 1, the rats received (by i.v.) 1 mL of vehicle at 10 min after CA occlusion (Group 1, n = 15); olmesartan (0.3 mg/kg) at 10 min after CA occlusion (Group 2, n = 15); 1 mL of vehicle at 5 min before CA reperfusion (Group 3, n = 15); or olmesartan (0.3 mg/kg) 5 min before CA reperfusion (Group 4, n = 15). In protocol 2, the rats received (by i.v.) 1 mL of vehicle at 5 min before CA reperfusion (Group 5, n = 21); or olmesartan (3 mg/kg) at 5 min before CA reperfusion (Group 6, n = 21). Systemic hemodynamics, left ventricular (LV) function, LV ischemic risk zone, no-reflow zone, and infarct size were determined. In protocol 1, olmesartan (0.3 mg/kg) did not affect blood pressure (BP), heart rate, LV ± dp/dt or LV fractional shortening during the experimental procedure, and did not alter no-reflow or infarct size. In protocol 2, olmesartan (3 mg/kg) significantly reduced infarct size to 21.7 ± 4.1% from 34.3 ± 4.1% of risk zone in the vehicle group (P= 0.035), but did not alter the no-reflow size. Prior to CA reperfusion, olmesartan (3 mg/kg) significantly reduced mean BP by 22% and LV ±dp/dt, but did not affect heart rate. At 2 h after reperfusion, olmesartan significantly decreased heart rate by 21%, mean BP by 14%, and significantly increased LV fractional shortening from 54.1 ± 1.4% to 61.3 ± 1.6% (P= 0.0018). Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects. [source]

KC 12291: An Atypical Sodium Channel Blocker with Myocardial Antiischemic Properties

CARDIOVASCULAR THERAPEUTICS, Issue 1 2004
Gareth W. John
ABSTRACT KC 12291 was designed as a voltage-gated sodium channel (VGSC) blocker with cardioprotective properties. KC 12291 has moderate inhibitory effects on peak (or rapid) Na+ current, and markedly reduces sustained (or slowly or non-inactivating) Na+ current. This distinguishes KC 12291 from conventional VGSC blockers such as local anesthetics or antiarrhythmics, which have little or no cardioprotective properties. Since VGSCs represent the main pathway for ischemic Na+ loading by failing to inactivate fully, KC 12291 exerts pronounced antiischemic activity principally by reducing the amplitude of sustained Na+ current. In isolated atria and Langendorff-perfused hearts, KC 12291 inhibits diastolic contracture, renowned for its resistance to pharmacological inhibition, reduces ischemic Na+ loading and preserves cardiac energy status. KC 12291 exerts oral antiischemic activity in vivo in the absence of major hemodynamic effects. Cardiac VGSC blockers such as KC 12291, which block cardiac VGSCs in atypical fashion by effectively inhibiting the sustained component of Na+ current, represent, therefore, promising potential antiischemic and cardioprotective drugs. [source]

Impact of medication on ocular blood flow

ACTA OPHTHALMOLOGICA, Issue 2009
L SCHMETTERER
Purpose Reduced ocular blood flow appears to play a role in the pathophysiology of glaucoma. Hence, there is considerable interest in drugs that are capable of improving ocular perfusion. Methods A large numer of clinical trials have been performed investigating the ocular hemodynamic effects of topical and systemic medications. Such trials used a variety of different methods to assess ocular blood flow parameters. Results When adminsitered systemically most vasodilators decrease systemic blood pressure thereby reducing ocular perfusion pressure (OPP). Only few classes of drugs have been reported to increase ocular blood flow with no or minimal effect on OPP. Among these carbonic anhydrase inhibitors and endothelin receptor anatgonists show the most prononced ocular vasodilator effects. The ocular hemodynamoic effects of topical medications is generally considered small. Conclusion When drugs are given systemically the effects on OPP have to be considered. In addition, the potentially positive effects on ocular perfusion need to be carefully weighed against the side effects. With topically administered drugs the ocular hemodynamic effects will be generally small, because the drugs reach the posterior pole of the eye in small concentrations only. [source]

Inotropes in the beta-blocker era

CLINICAL CARDIOLOGY, Issue S3 2000
B. D. Lowes M.D.
Abstract Beta-adrenergic blocking agents are now standard treatment for mild to moderate chronic heart failure (CHF). However, although many subjects improve on beta blockade, others do not, and some may even deteriorate. Even when subjects improve on beta blockade, they may subsequently decompensate and need acute treatment with a positive inotropic agent. In the presence of full beta blockade, a beta agonist such as dobutamine may have to be administered at very high (> 10 ,g/kg/min) doses to increase cardiac output, and these doses may increase afterload. In contrast, phosphodiesterase inhibitors (PDEIs) such as milrinone or enoximone retain their full hemodynamic effects in the face of beta blockade. This is because the site of PDEI action is beyond the beta-adrenergic receptor, and because beta blockade reverses receptor pathway desensitization changes, which are detrimental to PDEI response. Moreover, when the combination of a PDEI and a beta-blocking agent is administered long term in CHF, their respective efficacies are additive and their adverse effects subtractive. The PDEI is administered first to increase the tolerability of beta-blocker initiation by counteracting the myocardial depressant effect of adrenergic withdrawal. With this combination, the signature effects of beta blockade (a substantial decrease in heart rate and an increase in left ventricular ejection fraction) are observed, the hemodynamic support conferred by the PDEI appears to be sustained, and clinical results are promising. However, large-scale placebo-controlled studies with PDEIs and beta blockers are needed to confirm these results. [source]