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Coronary Blood Flow (coronary + blood_flow)
Selected AbstractsThe Effect of Progesterone on Coronary Blood Flow in Anaesthetized PigsEXPERIMENTAL PHYSIOLOGY, Issue 1 2001C. Molinari The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h,1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h,1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of N, -nitro-L-arginine methyl ester (L-NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide. [source] Coronary Blood Flow Produced by Muscle Contractions Induced by Intracardiac Electrical CPR during Ventricular FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009HAO WANG M.D. It has been reported that transthoracic electrical cardiopulmonary resuscitation (ECPR) generates coronary perfusion pressures (CPP) similar to manual chest compressions (MCC). We hypothesized that intracardiac ECPR produces similar CPP. Methods: ECPR pulse train protocols were applied for 20 seconds in a porcine model following 10 seconds of ventricular fibrillation (VF), using a defibrillator housing electrode and a right ventricular coil (IC-ECPR). Each protocol consisted of 200-ms electrical pulse trains applied at a rate of 100 pulse trains/min. The protocols were grouped in skeletal-based versus cardiac-based stimulation measurements. CPP was recorded and compared to historical MCC values generated by a similar experimental design. CPP > 15 mm Hg at 30 seconds of VF following the application of an IC-ECPR protocol was defined as successful. Results: Mean CPP for all intracardiac ECPR pulse train protocols at 30 seconds of VF was 14.8 ± 3.8 mm Hg (n = 39). Mean CPP in seven successful skeletal-based IC-ECPR protocols was 19.4 ± 3.2 mm Hg, and mean CPP in 10 successful cardiac-based IC-ECPR protocols was 17.4 ± 2.1 mm Hg. Reported CPP for 15 MCC experiments at 30 seconds of VF was 22.9 ± 9.4 mm Hg (P = 0.35 compared to skeletal-based IC-ECPR, P = 0.08 compared to cardiac-based IC-ECPR). Conclusions: Intracardiac applied electrical CPR produced observable skeletal muscle contractions, measurable pressure pulses, and coronary perfusion pressures similar to MCC during a brief episode of untreated VF. [source] Intracoronary enalaprilat during angioplasty for acute myocardial infarction: alleviation of postischaemic neurohumoral and inflammatory stress?JOURNAL OF INTERNAL MEDICINE, Issue 2 2007U. Schaefer Abstract. Aims., Reperfusion after myocardial ischaemia is associated with a distinct ischaemia/reperfusion injury. Since ACE-inhibition, beyond its influence on cardiac angiotensin II formation and kinin metabolism, has been shown to be cardioprotective by decreasing leucocyte adhesion and endothelin-1 (ET-1) release, we investigated the effects of intracoronary (i.c.) enalaprilat during primary angioplasty in acute myocardial infarction. Methods and Results., Twenty-two patients were randomized to receive i.c. enalaprilat (50 ,g) or placebo immediately after reopening of the infarct-related artery (IRA). Plasma concentrations of soluble L-selectin, P-selectin, intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), ET-1 and nitric oxide metabolite concentrations (NO(x)) were measured in pulmonary arterial blood. Coronary blood flow was assessed using corrected thrombolysis in myocardial infarction (TIMI) frame counts (CTFC). During reperfusion, there was a significant increase in sL-selectin, sP-selectin and ET-1 in the placebo group, which was greatly diminished by enalaprilat. Levels of sVCAM-1 and sICAM-1 were not affected in either group. CTFC in the placebo group remained higher than normal in both the IRA and nonculprit vessels, whereas myocardial blood flow improved with enalaprilat. Conclusion., Enalaprilat as adjunct to primary angioplasty might be a protective approach to prevent leucocyte adhesion and the release of ET-1, thereby improving coronary blood flow. [source] Noninvasive Assessment of Coronary Flow Reserve in the Left Anterior Descending Artery by Transthoracic Echocardiography before and after StentingECHOCARDIOGRAPHY, Issue 8 2007Elie Chammas M.D., F.E.S.C. Background: Noninvasive assessment of coronary flow reserve in the left anterior descending artery (LAD) by transthoracic Doppler echocardiography (TTDE) has been already validated as a new method for determining the degree of stenosis over the proximal flow. Objectives: The aim of the study is to determine, by TTDE, the feasibility and the value of the coronary flow reserve (CFR) (defined as the maximal increase in coronary blood flow above its basal pressure for a given perfusion pressure when coronary circulation is maximally dilated) in the mid-to-distal LAD before and after percutaneous angioplasty and to demonstrate the early recovery of microvascular tone immediately after stenting. Methods: The study population consisted of 36 patients with significant isolated LAD stenosis (70,90%) identified by coronary angiography. CFR was recorded in the mid-to-distal LAD at rest and during hyperemia obtained after adenosine intravenous infusion before and after stenting. Results: Adequate visualization of the LAD was obtained in 25 out of 36 patients (70%). At rest the mean CFR was 1.5132 ± 0.33 (1.1,2.58). However, after stenting the mean CFR was significantly higher: 2.18 ± 0.55 (1.3,3.8), with P <0.01. Conclusions: CFR can be easily determined by TTE in approximately 70% of patients. Noninvasive Doppler echocardiography shows impaired CFR in patients with LAD disease. After stenting CFR is restored, demonstrating early recovery of microvascular tone. These results are comparable to those published in the same conditions. Larger series with a long-term follow-up may allow identifying patients at high risk for restenosis after stenting. [source] Effects of percutaneous transluminal coronary angioplasty on coronary adenosine concentrations in humansEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2000Paganelli Background Even minimal amounts of adenosine is released during myocardial ischemia. Its role in coronary blood flow has been extensively studied, but little is known about its behaviour during percutaneous transluminal angioplasty (PTCA) in man. Material and methods Using in situ samples the aim of this study was to evaluate adenosine plasma concentration before and after PTCA. Ten patients (8 men and 2 women, mean age 65 ± 9 years) with a single stenosis of the left anterior descending coronary artery (LAD) of at least 70% and 10 healthy volunteers (4 men and 6 women, mean age 55 ± 9 years) were included in the study. Results and discussion We found that there is a close relationship between the degree of the stenosis and the adenosine concentrations in the great cardiac vein and in the LAD, and that after PTCA there is a drop in adenosine concentration downstream from the stenosis. This study confirms the crucial role of adenosine in coronary blood flow control. [source] The Effect of Progesterone on Coronary Blood Flow in Anaesthetized PigsEXPERIMENTAL PHYSIOLOGY, Issue 1 2001C. Molinari The present study was designed to investigate the effect of progesterone on the coronary circulation and to determine the mechanisms involved. In pigs anaesthetized with sodium pentobarbitone, changes in left circumflex or anterior descending coronary blood flow caused by intravenous infusion of progesterone at constant heart rate and arterial blood pressure were assessed using an electromagnetic flowmeter. In 14 pigs, infusion of 1 mg h,1 of progesterone caused an increase in coronary blood flow without affecting left ventricular dP/dtmax (rate of change of left ventricular systolic pressure) and filling pressures of the heart. In a further four pigs, this vasodilatory coronary effect was enhanced by graded increases in the dose of the hormone of between 1, 2 and 3 mg h,1. The mechanisms of the above response were studied in the 14 pigs by repeating the experiment after haemodynamic variables had returned to the control values observed before infusion. In six pigs, blockade of muscarinic cholinoceptors and adrenoceptors with atropine, propranolol and phentolamine did not affect the coronary vasodilatation caused by progesterone. In the remaining eight pigs, this response was abolished by intracoronary injection of N, -nitro-L-arginine methyl ester (L-NAME) even when performed after reversing the increase in arterial blood pressure and coronary vascular resistance caused by L-NAME with continuous intravenous infusion of papaverine. The present study showed that intravenous infusion of progesterone primarily caused coronary vasodilatation. The mechanism of this response was shown to involve the endothelial release of nitric oxide. [source] Pharmacology of the Selective 5-HT1B/1D Agonist FrovatriptanHEADACHE, Issue 2002M.B. Comer BSc Objective.,To determine the pharmacological profile of frovatriptan. Background.,Frovatriptan is a new 5-HT1B/1D agonist developed for the treatment of migraine. Methods.,Pharmacological studies were performed using in vitro and in vivo techniques. Results.,Radioligand-binding studies showed that frovatriptan has a high affinity for 5-HT1B and 5-HT1D receptors, and moderate affinity for 5-HT1A, 5-HT1F, and 5-HT7 receptors. In vitro, frovatriptan acts as a potent full agonist at human cloned 5-HT1B and 5-HT1D receptors, and as a moderately potent full agonist at 5-HT7 receptors. Studies of frovatriptan in isolated human arteries demonstrated a lower threshold for constriction of cerebral than coronary vasculature and a bell-shaped dose-response curve was apparent in the coronary arteries. In anesthetized dogs, frovatriptan administration produced no measurable effect on cardiac function or on blood pressure. Frovatriptan had no effects on coronary blood flow following transient coronary artery occlusion, whereas sumatriptan produced a prolonged and significant decrease in coronary blood flow. Conclusion.,The pharmacology of frovatriptan suggests that it should be an effective agent for the acute treatment of migraine, with a low potential for undesirable peripheral effects. [source] Intracoronary enalaprilat during angioplasty for acute myocardial infarction: alleviation of postischaemic neurohumoral and inflammatory stress?JOURNAL OF INTERNAL MEDICINE, Issue 2 2007U. Schaefer Abstract. Aims., Reperfusion after myocardial ischaemia is associated with a distinct ischaemia/reperfusion injury. Since ACE-inhibition, beyond its influence on cardiac angiotensin II formation and kinin metabolism, has been shown to be cardioprotective by decreasing leucocyte adhesion and endothelin-1 (ET-1) release, we investigated the effects of intracoronary (i.c.) enalaprilat during primary angioplasty in acute myocardial infarction. Methods and Results., Twenty-two patients were randomized to receive i.c. enalaprilat (50 ,g) or placebo immediately after reopening of the infarct-related artery (IRA). Plasma concentrations of soluble L-selectin, P-selectin, intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), ET-1 and nitric oxide metabolite concentrations (NO(x)) were measured in pulmonary arterial blood. Coronary blood flow was assessed using corrected thrombolysis in myocardial infarction (TIMI) frame counts (CTFC). During reperfusion, there was a significant increase in sL-selectin, sP-selectin and ET-1 in the placebo group, which was greatly diminished by enalaprilat. Levels of sVCAM-1 and sICAM-1 were not affected in either group. CTFC in the placebo group remained higher than normal in both the IRA and nonculprit vessels, whereas myocardial blood flow improved with enalaprilat. Conclusion., Enalaprilat as adjunct to primary angioplasty might be a protective approach to prevent leucocyte adhesion and the release of ET-1, thereby improving coronary blood flow. [source] Restored Atrial Excitability After Late Recanalization in a Patient with Atrial Standstill and Acute Myocardial InfarctionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002TAKA-AKI KOSHIMIZU KOSHIMIZU, T-A., et al.: Restored Atrial Excitability After Late Recanalization in a Patient with Atrial Standstill and Acute Myocardial Infarction. Atrial standstill is electrophysiologically characterized by the loss of spontaneous excitation in atrial muscle and the inability to cause action potential firing upon electrical stimulation. Clinical diagnosis of transient standstill of the right atrium was made in a patient with acute occlusion of the right coronary artery and acute renal failure. Percutaneous coronary intervention, performed 5 days after the onset, restored the coronary blood flow and resulted in full recovery of electrical activity and regular sinus rhythm. [source] Ginkgo biloba extract improves coronary artery circulation in patients with coronary artery disease: contribution of plasma nitric oxide and endothelin-1PHYTOTHERAPY RESEARCH, Issue 6 2008Yu-Zhou Wu Abstract In patients with coronary artery disease (CAD), coronary blood flow is usually impaired due to imbalanced vasoactive substances such as nitric oxide (NO) and endothelin-1 (ET-1). The study was designed to test the effects of Ginkgo biloba extract (GBE) on the distal left anterior descending coronary artery (LAD) blood flow and plasma NO and ET-1 levels. Eighty CAD patients were randomly assigned to GBE (n = 42) and control (n = 38) groups. The LAD blood flow was assessed non-invasively using Doppler echocardiography at baseline and after 2 weeks. GBE treatment demonstrated a significant improvement in maximal diastolic peak velocity (MDPV), maximal systolic peak velocity (MSPV) and diastolic time velocity integral (DTVI) compared with controls (14.61 ± 4.51% vs 0.67 ± 2.66%, 9.03 ± 4.81% vs 0.34 ± 2.67% and 14.69 ± 5.08% vs 0.68 ± 3.00%, respectively, p < 0.01). NO was increased by 12.42% (p < 0.01), whereas ET-1 was decreased by 5.82% (p < 0.01). The NO/ET-1 ratio was increased by 19.47% (p < 0.01). A linear correlation was confirmed between the percentage change in LAD blood flow and in NO, ET-1 or NO/ET-1 ratio following GBE treatment. The results suggest that GBE treatment in CAD patients led to an increase of LAD blood flow, which might at least be related partly to the restoration of the delicate equilibrium between NO and ET-1. Copyright © 2008 John Wiley & Sons, Ltd. [source] Rudimentary Coronary Artery in Syrian Hamsters (Mesocricetus auratus)ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 4 2009A. C. Durán Summary Congenital underdevelopment of one or more main branches of the coronary arteries has been reported in man, but not in non-human mammals. In man, this defective coronary artery arrangement may cause myocardial ischaemia and even sudden death. The main goal of this study was to describe the coronary artery distribution patterns associated with the presence of a markedly underdeveloped (rudimentary) coronary artery in Syrian hamsters. Moreover, an attempt was made to explain the morphogenesis of these patterns, according to current knowledge on coronary artery development. Eleven affected hamsters belonging to a laboratory inbred family were examined by means of internal casts of the heart, great arterial trunks and coronary arteries. The aortic valve was tricuspid (normal) in seven hamsters and bicuspid in the other four. A rudimentary coronary artery arose from the right side of the aortic valve in four specimens, from the left side of the aortic valve in a further three, and from the dorsal aortic sinus in the remaining four. In all cases, a second, well-developed coronary artery provided for all the coronary blood flow. Except for the existence of a rudimentary coronary artery, the present anomalous coronary artery distribution patterns are similar to coronary artery patterns reported in Syrian hamsters, dogs and humans in association with a solitary coronary ostium in aorta. We suggest that an unusual prolonged time interval in the development of the embryonic coronary stems might be a key factor in the formation of coronary arteries displaying significantly dissimilar developmental degrees. [source] Cocaine and Ethanol: Combined Effects on Coronary Artery Blood Flow and Myocardial Function in DogsACADEMIC EMERGENCY MEDICINE, Issue 7 2009Lance D. Wilson MD Abstract Objectives:, In combination, cocaine and ethanol are more cardiotoxic than is either substance alone. These substances together constitute a drug abuse combination that commonly results in fatality. Previously the authors have demonstrated that cardiotoxicity of cocaine and ethanol is in part due to synergistic myocardial-depressant effects. However, it remains unclear whether this myocardial depression is associated with concomitant adverse effects on coronary blood flow in relation to these substances. The aim of this study was to investigate combined effects of cocaine and ethanol on myocardial blood flow, in relation to indices of myocardial function. Methods:, Anesthetized dogs were instrumented for hemodynamic monitoring with Doppler flow probes placed on the circumflex and left anterior descending (LAD) coronary arteries. Dogs were randomized to three groups (each n = 6): ethanol (E, 1.5 g/kg followed by placebo), cocaine (C, placebo followed by cocaine, 7.5 mg/kg IV), or cocaine plus ethanol (C + E). All measurements were made at control, after placebo or ethanol, and then at fixed time intervals after cocaine or placebo bolus over 3 hours. Results:, In both the C + E and the C groups, circumflex blood flow (CBF) decreased by 71% (95% confidence interval [CI] = 56% to 85%) and 57% (95% CI = 43% to 72%, both p < 0.04 vs. baseline) immediately after cocaine bolus. This was associated with transient depression of cardiac output, myocardial contractile function, and rate-pressure product (RPP), all indices of myocardial oxygen demand. A subsequent rebound increase of coronary sinus blood flow (CSBF) of 56% (95% CI = 26% to 137%, p < 0.03) compared to baseline occurred only in the C group and was associated with increases of myocardial contractile function and RPP. In the C + E group, 2 hours after drug administration, there was a decrease in CSBF of 49% (95% CI = 32% to 67%; p < 0.01) compared to baseline, which was associated with concomitant numerical decreases of the indices of myocardial oxygen demand and accumulation of cocaethylene. Conclusions:, Acute decreases in myocardial flow secondary to cocaine, and cocaine and ethanol in combination, were similar and temporally associated with cocaine's direct myocardial-depressant effects. Rebound increases in myocardial function and blood flow due to cocaine were attenuated by ethanol. Delayed myocardial depression and decreases in myocardial blood flow were observed only with coadministration of cocaine and ethanol. [source] Numerical Simulation of Hemodynamic Changes During Beating-heart Surgery: Analysis of the Effects of Cardiac Position Alteration in an Animal ModelARTIFICIAL ORGANS, Issue 1 2007Gianfranco Ferrari Abstract:, Hemodynamic instability, mostly due to vertical lifting of the heart, is usually observed during beating-heart surgical procedures. However, some hemodynamic parameters, such as coronary blood flow, are not routinely measured. A digital computer model of the circulation able to simulate and analyze the effects of heart lifting and the Trendelenburg maneuver, and thus supply detailed hemodynamic information to the clinicians would provide a useful analytical tool. A lumped parameters model of the circulation was applied to both ,-blocked and not ,-blocked pigs. The results confirmed a drop of cardiac output and coronary flow during heart lifting and a rise of both variables after the Trendelenburg maneuver for ,-blocked animals. In not ,-blocked pigs, the analysis was more complex but the model reproduced experimental data and permitted coronary flow to be estimated. These results showed the feasibility of numerical simulation for specific circulatory conditions encountered during beating-heart surgery. [source] The Role of Myocardial KATP -Channel Blockade in the Protective Effects of Glibenclamide against Ischaemia in the Rat HeartBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2002Roger J. Legtenberg This study addresses the possible involvement of KATP channels in this beneficial action of glibenclamide. We hypothesized that if glibenclamide improved postischaemic cardiac function by blocking of KATP channels, opening of these KATP channels should result in the opposite, namely detrimental effects on postischaemic heart function. Postischaemic functional loss and coronary blood flow were recorded during treatment with glibenclamide (4 ,mol.l,1; n=5), the KATP channel openers pinacidil (1 ,mol.l,1; n=5) and diazoxide (30 ,mol.l,1; n=5), the combination of glibenclamide with pinacidil (n=5) and glibenclamide with diazoxide (n=5), and vehicle (n=8). Both pinacidil and diazoxide significantly increased coronary blood flow 2,3 times, which was abolished by glibenclamide pre- and postischaemically. This confirms that under both flow conditions glibenclamide significantly blocks KATP channels in the coronary vasculature. The 12 min. global ischaemic incident resulted in a cardiac functional loss of 22.2±2.9% during vehicle. Glibenclamide reduced the cardiac functional loss to 4.3±1.2% (P<0.01). Interestingly, both pinacidil and diazoxide reduced the cardiac functional loss to 4.0±1.5% (P<0.01) and 2.9±1.4% (P<0.001), respectively. The combination pinacidil+glibenclamide resulted in additional protection compared with the individual components (0.6±0.1 versus 4.0±1.5%, P<0.05). Thus, in contrast to its effect on coronary vascular tone, the glibenclamide-induced improvement of postischaemic cardiac function may not be mediated through blockade of the KATP channel. Alternative mechanisms may be operative, such as uncoupling of the mitochondrial respiratory chain, thereby preconditioning the hearts against stunning. [source] Protein kinase G regulates the basal tension and plays a major role in nitrovasodilator-induced relaxation of porcine coronary veinsBRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2007H Qi Background and purpose: Coronary venous activity is modulated by endogenous and exogenous nitrovasodilators. The present study was to determine the role of protein kinase G (PKG) in the regulation of the basal tension and nitrovasodilator-induced relaxation of coronary veins. Experimental approach: Effects of a PKG inhibitor on the basal tension and responses induced by nitroglycerin, DETA NONOate, and 8-Br-cGMP in isolated porcine coronary veins were determined. Cyclic cGMP was measured with radioimmunoassay. PKG activity was determined by measuring the incorporation of 32P from ,- 32P-ATP into the specific substrate BPDEtide. Key results: Rp-8-Br-PET-cGMPS, a specific PKG inhibitor, increased the basal tension of porcine coronary veins and decreased PKG activity. The increase in tension was 38% of that caused by nitro- L -arginine. Relaxation of the veins induced by nitroglycerin and DETA NONOate was accompanied with increases in cGMP content and PKG activity. These effects were largely eliminated by inhibiting soluble guanylyl cyclase with ODQ. The increase in PKG activity induced by the nitrovasodilators was abolished by Rp-8-Br-PET-cGMPS. The relaxation caused by these dilators and by 8-Br-cGMP at their EC50 was attenuated by the PKG inhibitor by 51,66%. Conclusions and implications: These results suggest that PKG is critically involved in nitric oxide-mediated regulation of the basal tension in porcine coronary veins and that it plays a primary role in relaxation induced by nitrovasodilators. Since nitric oxide plays a key role in modulating coronary venous activity, augmentation of PKG may be a therapeutic target for improving coronary blood flow. British Journal of Pharmacology (2007) 152, 1060,1069; doi:10.1038/sj.bjp.0707479; published online 24 September 2007 [source] A Review of HNS-32: A Novel Azulene-l-Carboxamidine Derivative with Multiple Cardiovascular Protective ActionsCARDIOVASCULAR THERAPEUTICS, Issue 4 2001Yoshio Tanaka ABSTRACT HNS-32 [N1,N1 -dimethyl- N2 -(2-pyridylmethyl)-5-isopropyl-3,8-dimethylazulene-1-carboxamidine] (CAS Registry Number: 186086-10-2) is a newly synthesized azulene derivative. Computer simulation showed that its three dimensional structure is similar to that of the class Ib antiarrhythmic drugs, e.g., lidocaine or mexiletine. HNS-32 potently suppressed ventricular arrhythmias induced by ischemia due to coronary ligation and/or ischemia-reperfusion in dogs and rats. In the isolated dog and guinea pig cardiac tissues, HNS-32 had negative inotropic and chronotropic actions, prolonged atrial-His and His-ventricular conduction time and increased coronary blood flow. In the isolated guinea pig ventricular papillary muscle, HNS-32 decreased maximal rate of action potential upstroke (V,max) and shortened action potential duration (APD). These findings suggest that HNS-32 inhibits inward Na+ and Ca2+ channel currents. In the isolated pig coronary and rabbit conduit arteries, HNS-32 inhibited both Ca2+ channel-dependent and -independent contractions induced by a wide variety of chemical stimuli. HNS-32 is a potent inhibitor of protein kinase C (PKC)-mediated constriction of cerebral arteries. It is likely to block both, Na+ and Ca2+ channels expressed in cardiac and vascular smooth muscles. These multiple ion channel blocking effects are largely responsible for the antiarrhythmic and vasorelaxant actions of HNS-32. This drug may represent a novel approach to the treatment of arrhythmias. [source] Assessment of coronary blood flow and the reactivity of the microcirculation non-invasively with transthoracic echocardiographyCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 3 2008Tuomas Kiviniemi Summary Background:, The development in ultrasound technology has allowed the use of non-invasive transthoracic echocardiography (TTE) for the study of coronary artery physiology and pathophysiology. TTE can be used to detect atherosclerotic changes in epicardial coronary arteries and to study the effects of specific interventions on coronary microcirculation. Aim:, The purpose of this review was to summarize the development of TTE, and outweigh the strenghts and weaknesses of the method for the evaluation of coronary artery blood flow. Moreover, findings from clinical trials studying microcirculatory reactivity using TTE are presented. Conclusions:, TTE is a feasible and reproducible method for the evaluation of coronary artery blood flow. It can also be used in assessing the vasodilation of the epicardial coronary artery simultaneously with flow velocity measurement during the cold pressor test and coronary flow velocity reserve assessment. It is specifically suitable for repeated measurements in interventional trials. [source] | |||||||||||||||||||||||||