Calciumkanaldichte in humanem ischämischen und reperfundierten, rechtsatrialen Myokardgewebe
type: CreativeWork
description: Intracellular calcium overload is one of the major pathophysiological mechanisms contributing to myocardial ischemic injury. Two important calcium handling proteins responsible for the maintenance of an intracellular calcium homeostasis are the sarcolemmal voltage-gated L-type calcium channel (DHPR) and the sarcoplasmic reticulum calcium release channel (CRC). This study evaluated the density of both channels in human myocardium subjected to ischemia and reperfusion during cardia surgery. Biopsies of human right atria were collected during cardiac surgery: 1) before aortic cross-clamping (serving as controls, 2) during ischemia and 3) after reperfusion. DHPR and CRC densities were studied using radioligand binding. A 25% reduction in CRC density was found during ischemia and reperfusion. The calcium sensitivity of ryanodine binding to CRC was unchanged. DHPR density was unaltered during ischemia and reperfusion. A downregulation of CRC may lead to a defective release of Ca2+ from the sarcoplasmic reticulum which may lead to excitation-contraction uncoupling ultimately contributing to postischemic contractile dysfunction.
abstract: Intracellular calcium overload is one of the major pathophysiological mechanisms contributing to myocardial ischemic injury. Two important calcium handling proteins responsible for the maintenance of an intracellular calcium homeostasis are the sarcolemmal voltage-gated L-type calcium channel (DHPR) and the sarcoplasmic reticulum calcium release channel (CRC). This study evaluated the density of both channels in human myocardium subjected to ischemia and reperfusion during cardia surgery. Biopsies of human right atria were collected during cardiac surgery: 1) before aortic cross-clamping (serving as controls, 2) during ischemia and 3) after reperfusion. DHPR and CRC densities were studied using radioligand binding. A 25% reduction in CRC density was found during ischemia and reperfusion. The calcium sensitivity of ryanodine binding to CRC was unchanged. DHPR density was unaltered during ischemia and reperfusion. A downregulation of CRC may lead to a defective release of Ca2+ from the sarcoplasmic reticulum which may lead to excitation-contraction uncoupling ultimately contributing to postischemic contractile dysfunction.
author: Greiser, Birte Maura
language: ger
keywords: info:eu-repo/classification/ddc/610, Medizin
date published: 2001
date modified: 2026-07-30T19:42:48Z
provider: RWTH Aachen University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Publikationsserver der RWTH Aachen University