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Biomedical subjects

W Flameng

Publications and source records attributed to W Flameng.

At least 253 records · Page 14Linked to original sources
PubMed1975

Effects of prindolol on isoproterenol-induced subendocardial ischaemia in dogs with multiple chronic coronary artery occlusion.

Multiple chronic coronary artery occlusions were produced in dogs by implantation of ameroid rings on the circumflex branches of the left and right coronary artery. Sixty-five per cent of the animals survived. Seventy-seven per cent of the remaining animals had no detectable myocardial infarction. Myocardial blood flow distribution was studied 4 weeks after operation using the tracer microsphere technique. During control conditions myocardial blood flow was homogeneously distributed within the left ventricle. In one group of dogs, regional dilatory capacity was tested by intravenous infusion of dipyridamole. Four compartments of myocardial blood flow were found. The collateral dependent subendocardium with 114 ml/min-100 g-1 was the lowest perfusion rate. In another group of dogs myocardial blood flow distribution was examined during isoproterenol infusion and after beta-blockade with prindolol during continuous isoproterenol infusion. During isoproterenol infusion, a nonhomogeneous blood flow pattern was found when the heart rate increased to 200/min together with a slight fall in diastolic perfusion pressure. Under these conditions, the flow to the collateral dependent subendocardium was severely diminished, while the flow to the areas perfused by normal coronary arteries increased, reflecting compensatory vasodilation. After beta-blockade with prindolol 0.1 mg/kg, the myocardial blood flow distribution was also nonhomogeneous but in the opposite direction: the collateral dependent subendocardium was now the best perfused compartment. The flow to the areas perfused by normal coronary arteries decreased due to the reduced oxygen requirements, while the collateral dependent subendocardium remained maximally dilated. This phenomenon was explained as a postischaemic reactive hyperaemic response to the isoproterenol-induced ischaemia in the collateral dependent subendocardium.

Animals↗
PubMedDate not supplied

Ischaemic ATP degradation studied by HPLC and 31P-NMR spectroscopy: do the two techniques observe the same ATP pools?

31P-NMR spectroscopy has become the major tool for studying myocardial high energy phosphates. Conflicting results concerning NMR visibility of ATP in ischaemic myocardium were reported. A detailed study was undertaken to resolve this controversy. After cardioplegic arrest, canine hearts were excised and preserved for 24 h at 1 degree C (group 1) or for 6h at 23 degrees C (group 2). ATP breakdown was followed by 31P-NMR spectroscopy in a transmural piece of the anterior wall introduced in the NMR magnet, and by HPLC analysis using serial transmural biopsies from the rest of the anterior wall. At both temperatures, identical relative ATP decay curves were obtained, whether measured by NMR or by HPLC. Absolute quantification of ATP was carried out after varying periods of ischaemia at 1 degree C. The NMR-measured ATP concentration was 106 +/- 8% of the ATP concentration determined by HPLC. From our experiments, we conclude that ATP visibility for 31P-NMR spectroscopy is complete and constant during prolonged periods of hypothermic ischaemia in canine hearts.

Adenosine Triphosphate↗
PubMedDate not supplied

Improved functional recovery after ischemic preconditioning in the globally ischemic rabbit heart is not mediated by adenosine A1 receptor activation.

Experiments were carried out to test the hypothesis that preconditioning reduces the impairment of recovery of cardiac mechanical function and that this effect is mediated by activation of adenosine A1 receptors. Isolated hearts were Langendorff-perfused at 37 degrees C with oxygenated blood and paced at 3 Hz. They were divided into 5 groups, all subjected to 45 min global ischemia followed by one hour of reperfusion: 1) Control hearts (n = 7) which received no treatment or short ischemia before the long ischemia, 2) preconditioned hearts (n = 7), submitted to 5-min zero-flow global ischemia, followed by 5 min reperfusion before the long ischemia, 3) hearts pretreated with sulfophenyltheophylline (SPT 100 microM) before preconditioning and long ischemia (n = 6), 4) hearts in which preconditioning was substituted by administration of 10 microM phenyl-isopropyl-adenosine (PIA) over 5 min, and 5) hearts in which preconditioning was substituted by the administration of 1.5 mg adenosine over 5 min. Hemodynamic results show significant improvement of the postischemic recovery of left ventricular developed pressure (DP) by preconditioning. SPT pretreatment did not reverse the improvement of recovery, obtained by preconditioning, whereas PIA treatment could not mimic preconditioning. Adenosine treatment caused some improvement of recovery of DP, but which remained lower compared to that caused by preconditioning. The contracture developed during ischemia persisted in control hearts, whereas contracture disappeared in non-treated preconditioned hearts. SPT did not prevent the decrease in contracture by preconditioning although values remained slightly higher than in the non-treated preconditioned hearts. PIA did not substitute for preconditioning in preventing contracture. In the adenosine treated group, some decrease of contracture occurred during reperfusion, but values remained significantly higher than in preconditioning. We conclude that receptor A1 activation is not the main mechanism underlying improved functional recovery conferred by preconditioning since an A1 receptor blocker (SPT) cannot reverse the effect of preconditioning and an A1 receptor agonist (PIA) cannot mimic it. Administration of exogenous adenosine reduces functional impairment to a certain extent, but less than preconditioning.

Adenosine↗
PubMedDate not supplied

Ischemic event characteristics determine the extent of myocardial stunning in conscious dogs.

Both the severity and duration of postischemic myocardial dysfunction ("stunned" myocardium) are unpredictable and may vary considerably between subjects that underwent apparently similar ischemic insults. To explain this heterogeneous response of the heart to ischemia and reperfusion, we investigated the determinants of stunning in conscious dogs. Twenty-five dogs were chronically instrumented for measurement of global and regional myocardial performance (wall thickening) and myocardial perfusion (coloured microspheres). A hydraulic occluder was positioned around the LAD coronary artery. Conscious dogs were subjected to acute coronary artery occlusions of predetermined duration (2, 5 and 10 min), followed by complete reperfusion. Multiple regression analysis identified the following variables as determinants of postischemic contractile recovery: 1) the duration of ischemia (p < 0.01),2) the amount of collateral perfusion (p = 0.01) and 3) left ventricular end-diastolic pressure during ischemia (p < 0.01). Neither the severity of regional dyskinesia during ischemia nor indices of global systolic hemodynamic performance correlated with the rate of recovery. Our data confirm that myocardial stunning relates primarily to the intensity of preceding ischemia. Variations in the preexisting level of collateral perfusion may result in markedly different recovery profiles. Except for LV end-diastolic pressure during ischemia, indices of global and regional cardiac performance fail to predict the severity of postischemic contractile failure.

Animals↗
PubMedDate not supplied

Chronic hibernating myocardium: interstitial changes.

Chronic left ventricular dysfunctional but viable myocardium of patients with chronic hibernation is characterized by structural changes, which consist of depletion of contractile elements, accumulation of glycogen, nuclear chromatin dispersion, depletion of sarcoplasmic reticulum and mitochondrial shape changes. These alterations are not reminiscent of degeneration but are interpreted as de-differentiation of the cardiomyocytes. The above mentioned changes are accompanied by a marked increase in the interstitial space. The present study describes qualitative and quantitative changes in the cellular and non-cellular compartments of the interstitial space. In chronic hibernating myocardial segments the increased extracellular matrix is filled with large amounts of type I collagen, type III collagen and fibronectin. An increase in the number of vimentin-positive cells (endothelial cells and fibroblasts) compared with normal myocardium is seen throughout the extracellular matrix. The increase in interstitial tissue is considered as one of the main determinants responsible for the lack of immediate recovery of contractile function after restoration of the blood flow to the affected myocardial segments of patients with chronic left ventricular dysfunction.

Actins↗
PubMedDate not supplied

Local dilatory reserve in chronic experimental coronary occlusion without infarction. Quantitation of collateral development.

The local dilatory reserve of the canine coronary vasculature was studied with the particle distribution technique. Normal ventricles and hearts with slowly progressive narrowing of both the left circumflex coronary artery and the right coronary artery were studied. In spite of chronic occlusion of 2 coronary arteries myocardial infarction did not occur in the majority of animals because of collateral development. Coronary reserve was determined by producing graded to maximal coronary vasodilation. In normal hearts flow increased homogeneously over the entire left ventricle. In hearts with chronic coronary occlusion coronary vasodilation produced non-homogeneous increases in flow: collateral dependent myocardium received less blood flow than myocardium supplied by normal coronary arteries. Early after coronary occlusion the total coronary reserve was less than normal and the dilatory reserve of collateral dependent vessels was markedly diminished. Late (6 months) after coronary occlusion the total coronary reserve was still below normal but the dilatory reserve of collateral dependent vessels had improved. A new quantitative index of collateral function is defined as the level of coronary flow (delivered through normal coronary arteries) at which collateral flow deviates from homogeneous perfusion. Collateral function, when so defined, increases by a factor of almost 6 times between 4 weeks (early after coronary occlusion) and 6 months (late after occlusion) after the implantation of occluding devices.

Animals↗