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Biomedical subjects

J Schaper

Publications and source records attributed to J Schaper.

At least 163 records · Page 9Linked to original sources
PubMed1980

Ultrastructural evaluation of the effects of global ischemia and reperfusion on human myocardium.

During open-heart surgery, myocardial biopsies were taken from 31 patients undergoing aortic valve replacement on total cardiopulmonary bypass. The first needle biopsy was taken before the induction of cardiac arrest (Kirsch cardioplegia), the second at the end of global ischemia, and the third during the reperfusion period. The tissue was investigated by electron microscopy using a semiquantitative scoring system for changes in both myocytes and blood vessels. Mitochondrial volume and surface density were determined by morphometry. Reversible ischemic injury of moderate to severe degree occurred in cardiac cells and in small blood vessels. On reperfusion, signs of damage regressed earlier in myocardial than in vascular tissue. Morphometry revealed significant mitochondrial swelling during the reperfusion phase, but this was not present after ischemia alone. It is concluded that Kirsch cardioplegia as applied here, is unable to protect the heart from ischemic cellular damage.

Biopsy↗
PubMed1980

Structural characteristics in regional versus global ischemia.

In regional ischemia the tissue is damaged by the lack of oxygen, by mechanical stress, and by the consequences of a low-flow condition caused by collateral flow. In global ischemia the lack of oxygen is the only cause of cellular injury. Although mitochondrial and nuclear changes are similar, it is evident that regional and global ischemia are distinctly different situations from a pathophysiological and structural point of view. Results from either model of ischemia should be considered separately and should not be transferred from one situation to the other.

Animals↗
PubMed1979

Recovery of the heart after normothermic ischemia. Part I: Ultrastructural findings during postischemic reperfusion.

The influence of controlled ischemia on myocardial ultrastructure was investigated in isolated, metabolically supported canine hearts. Recovery of functionally normal tissue as indicated by the reversibility of morphological alterations was observed up to 60 minutes of anoxia. It was shown that prolonged reperfusion of the empty beating heart supports the recovery of normal cellular ultrastructure. Severe ischemic damage of mitochondria due to ischemia of 60 minutes was almost completely reversible after a reperfusion period of 50 minutes.

Animals↗
PubMed1979

Recovery of the heart after normothermic ischemia. Part II: Myocardial function during postischemic reperfusion.

Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was also a disturbance in the autoregulative mechanisms of coronary perfusion and an uncoupling of O2-consumption and mechanical efficiency. A prolonged reperfusion period of the heart beating empty allowed ultrastructural recovery of the damaged myocardium. In contrast, functional recovery of the myocardium, as determined by several parameters of contraction and relaxation, did not correlate with ultrastructural recovery and was not improved by prolonged reperfusion.

Animals↗
PubMed1976

The endothelial surface of growing coronary collateral arteries. Intimal margination and diapedesis of monocytes. A combined SEM and TEM study.

Slowly progressing coronary artery stenosis leading to complete occlusion within about 3 weeks was produced in dogs. Within this time collateral vessels had enlarged sufficiently to prevent myocardial infarction. Early, intermediate, and late (1 year after occlusion) stages of collateral development were studied with the scanning and transmission electron microscope. Early after coronary occlusion the number of endothelial cells per unit inner vascular surface had markedly increased and longitudinal bulges appeared in growing collaterals as opposed to the completely flat inner surface of small normal coronary arteries. The surface of many endothelial cells appeared rough and large numbers of monocytes adhered to the inner vascular surface. The endothelial cells formed three types of patterns: streams, whorls, and nonoriented mosaics suggesting different types of flow-jets, eddies, and lowshear flow, respectively. The existence of nonlaminar flow patterns could well be explained by the extremely tortuous course of collaterals and by segmental caliber changes (microstenoses) resulting from irregularities of the internal elastic lamina. Later stages showed a tendency toward normal endothelial cell density, flattening of bulges, and absence of microstenoses. A completely normal inner surface was, however, never observed in midzone segments although the observation period extended up to 1 year after coronary occlusion.

Animals↗
PubMed1976

Cholesteatoma of the middle ear in human patients. An ultrastructural study.

The structure of middle ear cholesteatoma obtained at surgical interventions in 12 patients was investigated by light and electron microscopy. Keratinizing squamous epithelium with underlying granulomatous, partly necrotic tissue showing signs of an acute or chronic inflammatory reaction was observed. Cholesterol clefts were only observed in two specimens in which a chronic hemorrhage was present. It is proposed that a cholesteatoma starts by immigration of epidermal tissue from the tympanic membrane. Destruction of the middle ear components and of the neighboring osseous walls results from invasion of squamous epithelium, underlying necrotizing connective tissue, and keratin.

Cholesteatoma↗