Subject(s)
Blindness/etiology , Headache Disorders/etiology , Infarction, Posterior Cerebral Artery/diagnosis , Puerperal Disorders/etiology , Seizures/etiology , Adolescent , Diagnosis, Differential , Female , Humans , Infarction, Posterior Cerebral Artery/complications , Magnetic Resonance Imaging , Tomography, X-Ray ComputedSubject(s)
Heart Conduction System/physiopathology , Tachycardia, Atrioventricular Nodal Reentry/physiopathology , Adenosine , Anti-Arrhythmia Agents , Catheter Ablation , Heart Conduction System/drug effects , Humans , Tachycardia, Atrioventricular Nodal Reentry/diagnosis , Tachycardia, Atrioventricular Nodal Reentry/therapyABSTRACT
The passive and active electrical properties of left ventricular myocardium were measured, using conducted action potentials and current clamp of isolated myocytes. The objective was to quantify changes of intracellular resistivity, Ri, during hypertrophic growth and the simultaneous imposition of cellular hypoxia. Ri was estimated from the time course of the rising phase of a conducted action potential using a solution of the two-dimensional cable equation. The thoracic aorta of guinea-pigs was constricted to induce left ventricular hypertrophy (LVH) and myocardium used 50 and 150 days post-operation. Conduction velocity increased in the earlier stage of LVH and declined in the later stage, compared with age-matched controls. Hypoxia reduced conduction velocity in all experimental groups. Ri increased only in the later stage of hypertrophy (253 +/- 39 Omega cm to 544 +/- 130 Omega cm) and was additionally increased by hypoxia in all groups (e.g. control myocardium 252 +/- 39 Omega cm to 506 +/- 170 Omega cm). The magnitude of the increase of Ri in hypertrophied, hypoxic myocardium can create conditions required to generate re-entrant arrhythmias.
Subject(s)
Gap Junctions/physiology , Hypertrophy, Left Ventricular/physiopathology , Neural Conduction/physiology , Action Potentials/physiology , Algorithms , Animals , Aorta, Thoracic/physiopathology , Guinea Pigs , Hypoxia/physiopathology , In Vitro Techniques , Microelectrodes , Muscle Contraction/physiologyABSTRACT
The impedance to current flow in the intracellular compartment of guinea pig left ventricular myocardium was measured at 20 degrees C and 37 degrees C using tissue from hypertrophied hearts subjected to aortic constriction. Alternating current of varying frequency was passed longitudinally along myocardial preparations, which revealed two time constants: one attributed to the surface membrane at the ends of the preparation and a second lying in the intracellular pathway. The longitudinal impedance was quantitatively analyzed in terms of a parallel intracellular and extracellular pathway; the former had two series components, one attributable to the sarcoplasm and the other to the low-resistance junctions between adjacent cells. This interpretation was consistent (1) with control experiments using n-heptanol, which increased the component attributed to intercellular junctions but not sarcoplasmic resistivity, and (2) with suspensions of isolated myocytes, which yielded a similar value for the sarcoplasmic resistivity. Aortic constriction increased the heart weight-to-body weight ratio of experimental animals from a mean value of 3.10 +/- 0.28 to 5.05 +/- 0.83 g/kg after 50 days of constriction and 5.60 +/- 0.95 g/kg after 150 days of constriction. An increase of heart weight-to-body weight ratio at 150 days of constriction was associated with an increased intracellular resistivity, which could be attributed solely to an increase of the junctional resistance between adjacent cells by approximately 44% at 20 degrees C and 140% at 37 degrees C; the sarcoplasmic resistivity was unchanged. The results are discussed in terms of altered conduction in hypertrophied myocardium as a possible basis for arrhythmias in this tissue.
Subject(s)
Cell Communication , Heart/physiopathology , Hypertrophy, Left Ventricular/pathology , Hypertrophy, Left Ventricular/physiopathology , Alcohols/pharmacology , Animals , Electric Impedance , Electrophysiology , Gap Junctions/physiology , Guinea Pigs , Heart/drug effects , Heptanol , Myocardium/pathology , Sarcoplasmic Reticulum/physiologyABSTRACT
Intracellular pH (pHi) was measured in left ventricular myocytes from hearts hypertrophied by constriction of the thoracic aorta. There was a continuous relation between an increase in heart-to-body weight ratio and a decrease in pHi (mean +/- S.D., 7.06 +/- 0.18 pH units in control hearts vs. 6.87 +/- 0.17 pH units in hypertrophied hearts). Intracellular H+ buffering capacity (beta) increased as pHi fell, but the value of beta was independent of hypertrophy per se.
