1-(3-sulfonatopropyl)-4-(beta)(2-(di-n-butylamino)-6-naphthylvinyl)pyridinium-betaine and diacetylmonoxime

In this study, conduction of excitation in the rat left atrial and pulmonary veins myocardium was assessed by the optical mapping technique. Rat atrial myocardium and pulmonary vein myocardium demonstrated weak differences in the activation time and conduction velocity. Maximal conduction velocity in atrial myocardium estimated by the optical mapping was 84 +/- 14 cm/s, the same parameter in pulmonary vein myocardium was 71 +/- 11 cm/s. Period of refractoriness in the atria was significantly shorter (44 +/- 3 ms) than in pulmonary vein myocardium (60 +/- 3 ms). Despite the differences in the period of refractoriness excitation wavelength in the pulmonary veins and atrial myocardium was very similar (43 +/- 7 and 37 +/- 5 mm, respectively). Conduction of excitation in rat atria was characterized by high level of "linearity". Regions with essential decrease of conduction velocity and complete abruption of conduction (conduction blocks) were observed in pulmonary vein myocardium. It was suggested that high histological heterogeneity and intercellular electrical resistance played an important role in conduction abnormalities in rat pulmonary veins.

Topics: Action Potentials; Animals; Diacetyl; Electric Stimulation; Fluorescence; Fluorescent Dyes; Heart Atria; Heart Conduction System; Male; Myocardium; Perfusion; Pulmonary Veins; Pyridinium Compounds; Rats; Tissue Culture Techniques; Voltage-Sensitive Dye Imaging

Fast voltage-sensitive dyes are widely used to image cardiac electrical activity. Typically, the emission spectrum of these fluorochromes is wavelength shifted with altered membrane potential, but the optical signals obtained also decay with time and are affected by contraction. Ratiometry reduces, but may not fully remove, these artifacts. An alternate approach has been developed in which the time decay in simultaneously acquired short- and long-wavelength signals is characterized nonparametrically and removed. Motion artifact is then identified as the time-varying signal component common to both decay-corrected signals and subtracted. Performance of this subtraction technique was compared with ratiometry for intramural optical signals acquired with a fiber-optic probe in an isolated, Langendorff-perfused pig heart preparation (n = 4) stained with di-4-ANEPPS. Perfusate concentration of 2,3-butanedione monoxime was adjusted (7.5-12.5 mM) to alter contractile activity. Short-wavelength (520-600 nm) and long-wavelength (>600 nm) signals were recorded over 8-16 cardiac cycles at 6 sites across the left ventricular free wall in sinus rhythm and during pacing. A total of 451 such data sets were acquired. Appreciable wall motion was observed in 225 cases, with motion artifact classed as moderate (less than modulation due to action potential) in 187 and substantial (more than modulation due to action potential) in 38. In all cases, subtraction performed as well as, or better than, ratiometry in removing motion artifact and decay. Action potential morphology was recovered more faithfully by subtraction than by ratiometry in 58 of 187 and 31 of 38 cases with moderate and substantial motion artifact, respectively. This novel subtraction approach may therefore provide a means of reducing the concentration of uncoupling agents used in cardiac optical mapping studies.

Topics: Action Potentials; Animals; Artifacts; Chromogenic Compounds; Diacetyl; Electrophysiology; Fiber Optic Technology; Fluorescent Dyes; Heart; In Vitro Techniques; Models, Cardiovascular; Motion; Myocardial Contraction; Optical Fibers; Osmolar Concentration; Pyridinium Compounds; Subtraction Technique; Swine; Ventricular Function, Left

We tested whether the interventions typically required for optical mapping affect activation patterns during ventricular fibrillation (VF). A 21 x 24 unipolar electrode array (1.5 mm spacing) was sutured to the left ventricular epicardium of 16 anesthetized pigs, and four episodes of electrically induced VF (30-s duration) were recorded. The hearts were then rapidly excised and connected to a Langendorff perfusion apparatus. Four of the hearts were controls, in which 24 additional VF episodes were then mapped. In the remaining 12 hearts, four VF episodes were mapped after isolation, four more episodes were mapped after exposure to the voltage-sensitive dye di-4-ANEPPS, and six more episodes were mapped after exposure to the electromechanical uncoupling agents diacetyl monoxime (DAM; 20 mmol/l, n = 6) or cytochalasin D (CytoD; 10 micromol/l, n = 6). VF episodes were separated by 4 min. VF activation patterns were quantified using custom pattern analysis algorithms. From comparisons with time-corrected control data, all interventions significantly changed VF patterns. Most changes were broadly consistent with slowing and regularization due to loss of excitability. Heart isolation had the largest effect on VF patterns, followed by CytoD, DAM, and dye.

Topics: Animals; Cytochalasin D; Denture Liners; Diacetyl; Electric Stimulation; Enzyme Inhibitors; Female; Fluorescent Dyes; Heart; Male; Models, Biological; Nucleic Acid Synthesis Inhibitors; Pyridinium Compounds; Swine; Ventricular Fibrillation

Transmembrane, voltage sensitive fluorescent dye (TMF) recording techniques have shown that high voltage shocks (HVS), typically used in defibrillation, produce either hyper- or depolarization of the transmembrane potential (TMP) when delivered in the refractory period of an action potential (AP) in normal cardiac tissue (NT). Further, HVS produce an extension of the AP, which has been hypothesized as a potential mechanism for electrical defibrillation. We examined whether HVS modify TMP of ischemic tissue (IT) in a similar manner. In seven Langendorff rabbit hearts, recordings of APs were obtained in both NT and IT with TMF using di-4-ANEPPS, and diacetylmonoxime (23 microM) to avoid motion artifacts. Local ischemia was produced by occlusion of the LAD, HVS of either biphasic (5 + 5 ms) or (3 + 2 ms) or monophasic shapes (5 ms) were delivered at varying times (20%-90%) of the paced AP. Intracardiac ECG and TMF recordings of the TMP were each amplified, recorded, and digitized at a frequency of 1 kHz. The paced AP in IT was triangular in shape with no obvious phase 3 plateau, typically seen in NT. There was normally a reduced AP amplitude (expressed as fractional fluorescence) in IT (2.6% +/- 1.79%) compared to 3.8% +/- 0.66% in NT, and shortened AP duration (137 +/- 42 vs 171 +/- 11 ms). One hundred-Volt HVS delivered during the refractory period of paced AP in IT in five rabbits, elicited a depolarization response of the TMP with an amplitude up to three times greater than the paced AP. This is in contrast to NT where the 100-V HVS produced hyperpolarization in four hearts, and only a slight depolarization response in one heart. These results suggest that HVS, typically delivered by a defibrillation shock, modify TMPs in a significantly different manner for ischemic cells, which may influence success in defibrillation.

Topics: Action Potentials; Analysis of Variance; Animals; Cardiac Pacing, Artificial; Chromogenic Compounds; Diacetyl; Electric Countershock; Electrocardiography; Female; Fluorescent Dyes; Heart; Male; Membrane Potentials; Myocardial Ischemia; Oscillometry; Pyridinium Compounds; Rabbits; Refractory Period, Electrophysiological; Regression Analysis; Signal Processing, Computer-Assisted