Acetylcholine Suppresses Ventricular Arrhythmias and Improves Conduction and Connexin-43 Properties During Myocardial Ischemia in Isolated Rabbit Hearts.

Introduction: Acetylcholine (ACh), a vagal efferent neurotransmitter, markedly improves survival in rats with myocardial ischemia (MI) by preventing ischemic loss of gap junction (Gj) and by inducing anti-apoptotic cascades. However, electrophysiological mechanisms of the antiarrhythmic effect of ACh after acute MI are still unclear.

Methods: Acute MI was induced by ligation of the left anterior descending (LAD) coronary artery in Langendorff-perfused rabbit hearts with (ACh(+):n = 11) or without (ACh(-):n = 12) 10 μmol/L ACh delivered continuously starting at 5 minutes before LAD ligation.

Relevance of cardiomyocyte mechano-electric coupling to stretch-induced arrhythmias: optical voltage/calcium measurement in mechanically stimulated cells, tissues and organs.

Stretch-induced arrhythmias are multi-scale phenomena in which alterations in channel activities and/or calcium handling lead to the organ level derangement of the heart rhythm. To understand how cellular mechano-electric coupling (MEC) leads to stretch-induced arrhythmias at the organ level, we developed stretching devices and optical voltage/calcium measurement techniques optimized to each cardiac level. This review introduces these experimental techniques of (1) optical voltage measurement coupled with a carbon-fiber technique for single isolated cardiomyocytes, (2) optical voltage mapping combined with motion tracking technique for myocardial tissue/whole heart preparations and (3) real-time calcium imaging coupled with a laser optical trap technique for cardiomyocytes.

Structural heterogeneity in the ventricular wall plays a significant role in the initiation of stretch-induced arrhythmias in perfused rabbit right ventricular tissues and whole heart preparations.

Rationale: Mechanical stress is known to alter the electrophysiological properties of the myocardium and may trigger fatal arrhythmias when an abnormal load is applied to the heart.

Objective: We tested the hypothesis that the structural heterogeneity of the ventricular wall modulates globally applied stretches to create heterogeneous strain distributions that lead to the initiation of arrhythmias.

Methods And Results: We applied global stretches to arterially perfused rabbit right ventricular tissue preparations.

Cellular basis for trigger and maintenance of ventricular fibrillation in the Brugada syndrome model: high-resolution optical mapping study.

Objectives: We examined how repolarization and depolarization abnormalities contribute to the development of extrasystoles and subsequent ventricular fibrillation (VF) in a model of the Brugada syndrome.

Background: Repolarization and depolarization abnormalities have been considered to be mechanisms of the coved-type ST-segment elevation (Brugada-electrocardiogram [ECG]) and development of VF in the Brugada syndrome.

Methods: We used high-resolution (256 x 256) optical mapping techniques to study arterially perfused canine right ventricular wedges (n = 20) in baseline and in the Brugada-ECG produced by administration of terfenadine (5 micromol/l), pinacidil (2 micromol/l), and pilsicainide (5 micromol/l).

Automated drug delivery system to control systemic arterial pressure, cardiac output, and left heart filling pressure in acute decompensated heart failure.

Pharmacological support with inotropes and vasodilators to control decompensated hemodynamics requires strict monitoring of patient condition and frequent adjustments of drug infusion rates, which is difficult and time-consuming, especially in hemodynamically unstable patients. To overcome this difficulty, we have developed a novel automated drug delivery system for simultaneous control of systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (Pla). Previous systems attempted to directly control AP and CO by estimating their responses to drug infusions.

Prediction of circulatory equilibrium in response to changes in stressed blood volume.

Accurate prediction of cardiac output (CO), left atrial pressure (PLA), and right atrial pressure (PRA) is a prerequisite for management of patients with compromised hemodynamics. In our previous study (Uemura et al. Am J Physiol Heart Circ Physiol 286: H2376-H2385, 2004), we demonstrated a circulatory equilibrium framework, which permits the prediction of CO, PLA, and PRA once the venous return surface and integrated CO curve are known.

Effects of nicardipine and diltiazem on fractal features of short-term heart rate variability--application of coarse graining spectral analysis.

Purpose: This study was designed to investigate the effects of nicardipine and diltiazem on the fractal features of short-term heart rate variability (HRV), using coarse graining spectral analysis (CGSA).

Methods: Eighteen healthy volunteers participated in this study; they were divided into two groups according to the drug administered. Five-minute electrocardiogram and arterial pressure recordings were made during stepwise infusions of either nicardipine (0.

Effects of phytosterol ester-enriched vegetable oil on plasma lipoproteins in healthy men.

It has been reported that phytosterol esters reduce cholesterol absorption and lower serum cholesterol concentration. There have been very few studies published on the effect of dose of phytosterol esters less than 1.0 g/day on plasma cholesterol levels in healthy subjects using commonly consumed foods.

Transmural heterogeneity of the action potential configuration in the feline left ventricle.

There are M cells in the canine, rabbit, guinea pig, and human left ventricle (LV), but it is not known if they are present in the feline LV. Arterially perfused feline LV preparations were used for the recording of transmembrane action potentials from the epicardium (Epi), midmyocardium (M) and endomyocardium (Endo) under control conditions (n=12) and in the presence of I(Ks) blocker (chromanol 293B: 10 micromol/L, n=6) or I(Kr) blocker (E-4031: 2 micromol/L, n=6). The steady-state action potential duration at 90% repolarization and cycle length (APD90/CL) relation was obtained and fitted by the hyperbolic function APD(90) = CL/[(a x CL) + b].

Noise-induced compensation for postural hypotension in primary autonomic failure.

Noise can have a beneficial effect on sensory neurological systems, enhancing detection of small afferent signals and thereby improve efferent neural responses. We hypothesized whether a similar mechanism would facilitate impaired neural transmission associated with neurological disease, and tested whether addition of external noise to baroreceptor signaling could improve blunted autonomic efferent responses to a postural challenge in patients with primary autonomic failure (PAF). Five PAF patients were tested, one in duplicate and another triplicate, for their transient responses of heart rate (measured from electrocardiographic RR intervals; RRIs) and systolic (SBP) and diastolic (DBP) blood pressures to either 30 degrees or 60 degrees head-up tilt, with and without continuous application of beat-to-beat Gaussian white noise to the carotid sinus baroreceptors.