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W Schaper

Publications and source records attributed to W Schaper.

At least 235 records · Page 13Linked to original sources
PubMed1967

Heart.

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Coronary Vessels↗
PubMedDate not supplied

Salvage of jeopardized myocardium by ischemic preconditioning: is the quest over?

Helmholtz is quoted to have said that if he'd had any influence in creation he would have returned the human eye to its maker for revisions. The same could be said of the heart with its only very rudimentary ability to defend itself against ischemia. Ischemia was obviously not a problem during evolution: Early man did not live much longer than prime time for reproduction and no selection bias existed to prevent vascular diseases, an affliction of later life. In spite of this natural disadvantage of aged males the number of existing although not very efficient defense mechanisms is surprisingly large. It is the general belief that the knowledge of these mechanisms may lead to the development of new therapies that hopefully improve the imperfect product of natural selection.

Adenosine↗
PubMedDate not supplied

Intramyocardial infusion of tool drugs for the study of molecular mechanisms in ischemic preconditioning.

Many of the new tool drugs useful for the study of molecular mechanisms of ischemic preconditioning (IP) are very valuable in in vitro systems but produce undesired side-effects after systemic injection in intact animals that limit their applicability. Our aim was to develop an experimental in vivo model that allows the use of said drugs in sufficiently high local concentrations, but avoiding at the same time the systemic side-effects. Several techniques were combined to study regional damage or protection as a result of local drug infusion such as nuclear staining, NADH fluorescence, fluorescent microspheres and tetrazolium salts. In open-chest pigs, the intramyocardial infusion (20 microliters/min) of the adenosine A1-receptor agonist N6-cyclohexyladenosine (0.3 mmol) for 10 min prior to a 60-min LAD-occlusion and 120-min reperfusion mimicked IP by exerting a local protection (n = 9, p < 0.001). Krebs-Henseleit buffer (negative control) was without protective effect. IP's cardioprotection was locally prevented by the intramyocardial application of the adenosine A1-receptor antagonist cyclopentyltheophylline (1 mmol, infused during IP; n = 6, p < 0.001) but not by KHB. The protein kinase C (PKC)-inhibitors staurosporine (100 nmol, n = 6) or bisindolylmaleimide (BIS, 25 mumol, n = 9) did not prevent IP locally. The PKC activator phorbol myristate acetate (PMA, 1 mumol, n = 6) was ineffective in preventing ischemic injury and increased the amount of necrosis in IP, whereas BIS exerted a local myocardial protection (n = 9, p < 0.001). In conclusion, the new model of intramyocardial infusion appears to be useful for the investigation of IP's signal transduction. Our data support the role of the adenosine A1-receptor in IP, but suggest that inhibition instead of activation of PKC may protect ischemic myocardium from infarction.

Adenosine↗
PubMedDate not supplied

Stunned myocardium, an opinionated review.

Brief coronary occlusions cause stunning and ischemic preconditioning, the molecular mechanisms of which are insufficiently known. A marked reprogramming of sarcolemmal functions (including those of the sarcoplasmic reticulum) seems to occur and may be the basis for many of the observed phenomena. A bewilderingly complex pattern of gene expression emerges from mRNA-studies with reperfused tissue which at present does not permit a focussed or coherent view of mechanisms.

Animals↗
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↗