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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the propensity to develop cardiac arrhythmias during an acute period of ischemia between normal and hypertrophied (by means of a swimming training regimen) rat hearts. We used the coronary artery ligation in vivo technique which induced the occurrence of cardiac arrhythmias in rats that was followed by the determination of the occluded zone size. This study was coupled to an in vitro study using a two-compartment tissue bath in which half of the ventricular preparation was exposed to normal conditions and the other to ischemic conditions (low pH, hypoxia, and hyperkalemia). We also measured the collagen content and the DNA/protein ratio of the hearts. Twenty-eight male Wistar rats submitted to an eight-week swimming training (SWT) and twenty-eight cage-confined matched rats were used for the studies. SWT resulted in a 14% decrease in mean body weight and an 8% increase in absolute heart weight. We also observed a resting bradycardia in the trained animals and blood pressure remained unchanged between the two groups. Collagen content was unchanged and DNA/protein ratio was lower in the left ventricle of trained animals. During a 30-min period of coronary artery ligation, SWT rats demonstrated fewer ischemia-induced arrhythmias as compared to controls. The size of the zone affected by the vasal occlusion was lower in trained animals. Electrophysiological data recorded in the two-compartment bath showed a marked prolongation of action potential duration and refractory period in the SWT rat hearts. During the 15-min period of in vitro ischemia there was a global alteration of all electrophysiological parameters which did not differ between the two groups. Our data support the hypothesis that resting bradycardia and decrease in ischemic zone size may be involved in the arrhythmogenic protection observed in hypertrophied hearts of swimming rats after an acute ligation of the left coronary artery. Our results also indicate that cardiac hypertrophy, as defined by quantitative changes in cardiac mass or by the electrophysiological alterations that are related to its development, is not necessarily associated with an increased risk for the occurrence of arrhythmias.
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PMID:Decreased susceptibility to arrhythmias in hypertrophied hearts of physically trained rats. 141 4

Hepatic arterial chemoembolization (CE) with a mixture of particulate collagen and chemotherapeutic agents was evaluated as therapy for hepatic metastases from colorectal carcinoma. This article describes the characteristics sequential pattern of change seen on liver CT scans following CE. Thirty CT scans were performed on seven patients who had undergone a total of 11 CE procedures. All patients had baseline, immediate postprocedural, and follow-up CT exams at 1 to 2 month intervals following CE. Immediate post-procedural CT scans mapped the area of embolization owing to the density of the contrast mixed with the CE agents. Some lesions seen easily on baseline were more difficult to see as they became isodense with normal liver. Reflux of embolic material into the cystic artery and gallbladder wall was also observed on postprocedural scans in three patients. In all patients, early follow-up scans (1 month after CE) demonstrated changes in lesions seen on baseline scans consistent with tumor necrosis. This was corroborated by a decrease in carcinoembryonic antigen (CEA) levels. In three patients, however, low attenuation regions developed in areas in which there had been no lesion before. The significance of these is uncertain, but the low CEA values and the subsequent evolution in appearance of these sites on CT suggest that they were regions of hepatic ischemia/infarction as opposed to heretofore unidentifiable metastases, now "unmasked." Intermediate follow-up scans (2-3 months) revealed maximal effect on tumor volume, with a decrease of > or = 25% in five of seven patients (71%). Late follow-up scans (> or = 3 months after the last CE) confirmed recurrent disease and new lesions in all cases.
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PMID:CT findings after hepatic chemoembolization. 143 Apr 41

Using 12 human fetuses, histological development and changes in connective fiber structure and fine vascular patterns have been investigated in various fetal gestational stages by light and scanning electron microscopy. The main arterial supply of the articular disc was from the bilaminar region and pterygoideus lateralis muscle. The vascular network on the disc surface was related with fluid secretion. When the bilaminar region was compressed, it caused ischemia and fibrosis as the main pathological changes in TMJ derangement. A decrease in fluid from blood vessels might occur in TMJ degeneration. Collagen fibers in the disc passed mainly anteroposteriorly. In the anterior and posterior bands, muscular tendon fibers came from the pterygoideus lateralis muscle and superior stratum of the bilaminar region. In the posterior band three-dimensional structures of collagen fibers suitable for load bearing were observed. The compass network and process on the disc showed the normal structure that is formed gradually and has functions including dispersion, pressure bearing, friction-proofing and storage of the synovial fluid. Attachments of the disc were suitable for disc function. Large elastic fibers in the posterolateral part of the superior stratum of the bilaminar region may be antagonistic to the upper head of the pterygoideus lateralis muscle fibers passing medioanteriorly, indicating that this antagonism is available for disc function.
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PMID:Development of collagen fibers and vasculature of the fetal TMJ. 143 56

VasoSeal is a purified bovine, absorbable collagen plug currently successfully used to close the femoral arterial puncture site after cardiac catheterization under full anticoagulation. Up to now there has been no experience with potential complications. We observed acute ischemia in the right lower leg of 2/100 patients 36 resp. 24 h after successful closure of the puncture site with VasoSeal. Angiography confirmed acute occlusion of the distal A. poplitea dextra. A 25-mm resp. 50-mm long cylindrical foreign body embolus was removed with a Fogarty-catheter by retrograde indirect embolectomy. Histopathology confirmed a fresh collagen clot with appositional thrombosis.
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PMID:[Peripheral embolism of hemostasis collagen (VasoSeal)]. 144 94

The regional mechanics of the beating heart are directly related to factors such as ventricular pumping performance, coronary blood flow, myocardial energetics and oxygen consumption, vulnerability to ischemia and injury, hypertrophy and remodeling, and arrhythmogenesis. Important characteristics include: the complex three-dimensional geometry and fibrous architecture; the nonlinear, nonhomogeneous, anisotropic material properties of the myocardium; the hierarchical collagen connective tissue matrix; the time- and history-dependent active tension development of the cardiac muscle cells; and the three-dimensional anisotropic patterns of cardiac impulse propagation. To model these features realistically requires large-scale computational analysis with sophisticated numerical methods. As described in the chapter by Dr. Hunter and colleagues, an accurate three-dimensional finite element model has been developed to describe the geometry, fiber architecture, and extracellular matrix structure of the heart. The model is based on extensive anatomical measurements in the left and right ventricles (LV and RV) of the canine heart. In this chapter, we illustrate some new approaches to the special problems of large-scale finite element modeling in biomechanics using examples from the analysis of stress and electrical activation in the heart. Prospects for further progress--particularly in coupled problems such as cardiac electromechanics--are examined in light of new developments in high-performance computing.
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PMID:Large-scale finite element analysis of the beating heart. 148 84

Fibrin adhesives have been advocated as a protective sealant in high-risk colonic anastomoses to prevent leakage. To assess the effect of fibrin glue sealing on the healing ischemic anastomosis, we compared the healing of sutured colonic anastomoses in the rat, with and without fibrin adhesive (Groups IA and IB), and ischemic anastomoses with and without fibrin adhesive (Groups IIA and IIB). On days two, four, and seven, 10 animals in each group were sacrificed. Adhesion formation was scored, and the in situ bursting pressure was measured. The collagen concentration and degradation were estimated by measuring hydroxyproline. Adhesion formation was more prominent in Groups IB, IIA, and IIB on day four only; abscesses were noted in the ischemic group in four rats. Anastomotic bursting pressure was significantly lower in sealed (IB) and ischemic anastomoses (IIA) than in normal anastomoses (IA) on day four. Sealing of ischemic anastomoses did not change bursting pressures on days two, four, and seven. The relative decrease of collagen in the sealed anastomoses is significantly higher on day four only. It is concluded that sealing of normal colonic anastomoses in the rat has a negative effect on wound healing. Ischemia at the anastomotic site results in weaker anastomotic strength on day four postoperatively. Also in ischemic anastomoses, fibrin sealant does not improve wound healing during the first seven days. Adhesion formation on ischemic intestinal anastomoses was not prevented by fibrin sealing.
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PMID:Healing of ischemic colonic anastomosis: fibrin sealant does not improve wound healing. 151 51

We administered human growth hormone to a group of rats with experimental myocardial infarctions, in order to observe its action on the connective tissue repair process and the consequent effect on postinfarction ventricular aneurysms. Myocardial connective tissue displays a complex layout around each myocyte and among neighboring ones. It has been shown to be highly vulnerable to acute coronary ischemia which affects its diverse components in accordance with a precise timetable. The ultimate consequence of ischemia on connective tissue is the disappearance of intermyocytic links and the collagen weave that surrounds each cell. Damage to this collagen framework of the heart is responsible for the final disarray of myocytes, with a parallel effect to the myocytolytic actions of ischemia within the very structure of each cell. Hence, the appearance of postinfarction ventricular aneurysms seems to be related to failure in normal repair processes resulting from maturation of new collagen tissue into the area of myocardial necrosis. It has been shown that, besides the well-known actions on chondrocytes, hypothalamic-hypophyseal human growth hormone and somatomedins activate the fibroblasts. Administration of human growth hormone resulted in a significant decrease in the incidence of ventricular aneurysms. Scanning electron microscopy showed a good preservation of connective tissue components of myocardium. A different histological pattern of necrosis resulted in the treated group.
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PMID:Preservation of the myocardial collagen framework by human growth hormone in experimental infarctions and reduction in the incidence of ventricular aneurysms. 156 65

It is stated that fluoride intoxication promotes a sharp intensification of the peroxidation processes in the parodontium tissues. It is caused by a respirator explosion of neutrophils, a decrease in activity of antioxidant system enzymes, thus leading to disturbances of microcirculation and blood coagulation, ischemia development. The last factor can retard the enzymatic oxidation in a cell due to hypoxia, injures lysosomal membranes promoting partial autolysis of parodontium tissues, cell structures, intercellular substance. The interaction of blood with destructive elements of cells and collagen favours the development of trombohemorrhagic reactions in the parodontium tissues. A generalized damage of parodontium arises which intensifies under the effect of any other pathogenetic factors.
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PMID:[The mechanisms of the action of fluorine on periodontal tissues]. 156 4

Prior studies of vascular rejection in transplanted human hearts have stressed the importance of accelerated coronary arteriosclerosis (chronic vascular rejection). We, however, have had four patients with sudden onset of acute heart failure within 90 days of transplantation who have died without significant myocardial interstitial rejection or the concentric intimal thickening with dense collagen that is typical of chronic vascular rejection. In contrast, the coronary arteries in our patients had a prominent lymphocytic infiltrate, a loosely organized intimal thickening composed of smooth muscle cells, and extensive endothelial injury. We believe that these changes define acute vascular rejection of the coronary artery. In 14 transplanted hearts obtained consecutively, at autopsy or at a second transplant procedure, graft failure was caused by acute coronary vascular rejection in six cases and by chronic coronary vascular rejection in one case. The remaining seven patients showed no evidence of vascular rejection and died primarily of sepsis. Cytomegalovirus (CMV) disease was present in 6 of 7 patients with vascular rejection, of which 43% were CMV-negative recipients of hearts from CMV-positive donors. The adoption of a triple-drug protocol, in which azathioprine was added to cyclosporine and prednisone, reduced the incidence of acute vascular rejection from 27% to 8%. We conclude that acute coronary vascular rejection may be initially seen as global cardiac ischemia in the absence of significant interstitial myocardial rejection. Further, acute vascular rejection should be pathologically distinguished from chronic vascular rejection, although both are probably stages in the natural history of immune-mediated vascular injury.
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PMID:Acute vascular rejection of the coronary arteries in human heart transplantation: pathology and correlations with immunosuppression and cytomegalovirus infection. 165 3

The search for the causative factors in Dupuytren's disease has historically progressed form gross anatomical dissection, through microscopical tissue studies, to the biochemistry of the collagen produced. But these elements are merely the end products of cellular activity - not revealing the factors responsible for the changes in cellular activity. Recent biochemical investigations suggest that a number of conditions including localized microvascular ischemia and high alcohol concentrations transform the "benign" xanthine dehydrogenase of endothelial cells to the oxygen-free radical-releasing xanthine oxidase. Oxygen-free radicals are highly reactive species with half-lives in the order of milliseconds capable of both damaging the surrounding peri-microvasculature and stimulating fibroblast proliferation. It is this stimulation of fibroblast proliferation in the palmar fascia that is the key event in the pathogenesis of Dupuytren's contracture.
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PMID:Cell-controlling factors in Dupuytren's contracture. 169 16


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