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

Comparative experiments were performed on 41 allogenic rat kidney transplants to determine the mitotic behaviour and proliferative metabolism (application of 3H-thymidine) in the first 6 days after recirculation. Three days after transplantation, DNA synthesis in the tubular epithelial cells of the cortex and the medulla reached its peak. After this time the 3H-thymidine labelling index for these cell nuclei dropped. On the 6th day, the value was equal to that of the first day. The following points are signs of rapid transplant rejection. It was predicted that the DNA synthesis in the epithelial cell nuclei would decline, and also that the lymphocytes would proliferate in the interstitial tissue of the transplant's cortex and medulla. From the 4th day on, these changes were observed. The changes in the proliferative metabolism of the tubular epithelial cell nuclei preceded the mitotic changes by a few hr. The transplant changes caused by ischemia followed by tissue rejection can be made comprehensible by the determination of the average cell density of 3H-thymidine-labelled cortical, medullar, and tubular epithelial cells.
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PMID:Mitotic behaviour and proliferative metabolism in allogenic rat kidney transplants in the first 6 days after recirculation. 35 20

A new model for the study of ischemic liver lesion on rats has been worked out. Pretreatment with allopurinol, dibenzyline, methylprednisolone, glucagon, ATP-MgCl2 and aspartic acid reduced the overall mortality of ischemic liver injury. Administered after the anoxic hepatic lesion only glucagon and aspartic acid had beneficial effect on the survival rate. Under the influence of 30 minutes of normothermal ischemia the DNA synthetizing ability of the liver decreased. Aspartic acid, glucagon and ATP-MgCl2 significantly enhanced the regeneration of the ischemically damaged liver. These procedures might be suitable for donor pretreatment in liver transplantation, as well as for the treatment of other pathological states, causing a normothermal ischemia of the liver.
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PMID:Ischemic damage of the liver. Part II: In vivo investigation of the prevention of the ischemic lesion of the liver. 49 25

Epicardial ECG signs have been studied in 26 anesthetized and thoracotomized dogs in an attempt to follow the progress of tissue damage during regional myocardial ischemia. Epicardial ECG's were recorded before and during 15 min, 1 and 5 h of severe left anterior descending coronary artery narrowing. Epicardial ST segment elevation followed a complicated natural history. An analysis of variance showed the significant effects of respiration, heart rate and changes in time during myocardial ischemia. Regional epicardial R waves showed a transient increase in amplitude following coronary narrowing. There was no loss of electrically active myocardium following 15 min of ischemia. Irreversible loss of R waves were noted at between 30 and 45 min and progressed to full development within 5 h following coronary artery narrowing. The loss of electrically active myocardium (R loss plus Q waves) at 5 h was closely related to the myocardial depletion of creatine kinase activity (mu/mg DNA-1) at 24 h in each dog. The early manifestation of myocardial ischemia (ST segment elevation at 17 min) was closely related in the later evidence of cell death (R loss plus Q waves) in each dog. These relationships were less precise when the results were combined and this showed the variability between dogs in heart size and infarct size. The study suggested that the individual complete natural history of these ECG signs must be studied before they can be used to assess the extent and progress of myocardial ischemia and cell death.
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PMID:Electrocardiographic signs in experimental myocardial ischemia and infarction. 69 50

In order to study, autoradiographically, DNA synthesis in tumors, kidneys containing renal carcinomas were for the first time perfused with normothermic oxygenated blood with an addition of radioactively labelled thymidine. Tumor cells preserve the ability of synthesizing DNA in spite of an unavoidable postoperative ischemia. In most cases the incorporation of 3H-TdR was inhibited significantly after preoperative irradiation with a total dose of 1,600 rad applicated 48 h before operation.
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PMID:Autoradiographic studies on DNA synthesis in renal carcinoma after preoperative radiation. 88 Sep 58

A comparative microspectrophotometric study of the nuclear DNA content in the myocardial cells of the periinfarction region of the left ventricle was made in rabbit hearts during different periods of experimental ischemia. A moderate increase of both the polyploid and amitotically divided nuclei were revealed. This results are discussed from the aspect of possible participation of nuclear polyploidia and mitotic division in the mechanisms of intracellular regeneration of the myocardium.
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PMID:[Microspectrophotometric study of DNA concentration in the nuclei of muscle cells in the peri-infarct zone of the rabbit heart]. 95 20

The effects of experimental intrauterine growth retardation on subsequent fetal development, especially with respect to brain development, were studied in a new animal model. The rabbit was chosen since it has a perinatal pattern of brain development similar to that of the human. Experimental ischemia was induced during the last trimester by ligation of spiral arterioles and the differential effects on fetal development at term (30th gestational day) are reported. Specific brain regions were examined for wet weight, total cell number (DNA) and total protein content. Highly significant decreases in all these parameters were found in both the cortex and cerebellum following experimental intrauterine growth retardation; these two organs were differentially affected. The prospects and advantages of using this animal model for the study of the postnatal "catch-up growth" are discussed.
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PMID:Experimental intrauterine growth retardation. 113 84

Acute occlusion of the circumflex branch of the left coronary artery was produced in chronically instrumented conscious dogs. Tracer microspheres were used to measure during an established time period, the distribution of collateral flow within the infarcting myocardium. For up to 2 hours after coronary occlusion the amount and distribution of the collateral flow remained unchanged. Two to 4 hours after coronary occlusion the subendocardial flow fell to almost zero and the subepicardial flow rose. Between 6 and 48 hours subepicardial and total collateral flow rose markedly. A no-reflow phenomenon is responsible for the decline of collateral flow in the subendocardium. Evidence for this hypothesis was provided by releasing the artery 1,2, 4 and 6 hours after occlusion. The amount of subendocardium that could not be reperfused was small after 1 hour and large after 6 hours of occlusion. When the total collateral flow was very low, the subepicardium was not able to be reperfused and a transmural myocardial infarction developed. We conclude that the time delay between onset of ischemia and the appearance of a no-reflow phenomenon depends upon the amount of collateral flow. The occurrence of a no-reflow phenomenon in the subendocardium increases the amount of flow to the subepicardium which increases its chances of survival. Beyond the sixth hour after occlusion the total amount of collateral flow increases which is interpreted as a reduction of collateral resistance by passive caliber changes of the collateral vessels. DNA-synthesis that signal active caliber changes through cellular proliferation were always detected 24 hours after complete occlusion of a coronary artery regardless whether the time between onset of stenosis until complete occlusion was varied between 36 hours and 5 days. When the time to complete occlusion was 4 days, myocardial infarction was prevented due to growth-transformation of pre-existing collaterals. Four phases of collateral reactions in acute coronary occlusion were observed: redistribution of available collateral flow in favor of the subepicardium (t = 1 to 4 hours after occlusion), 2) increase of total collateral flow due to passive "stretch" of collateral vessels (t = 4 to 24 hours after occlusion), 3) radial growth of collateral vessels due to active cellular proliferation, (t = 24 hours to 5 days) 4) cellular proliferation to ensure a normal wall thickness in growth'transformed collaterals (t = 5 days to 20 days after coronary occlusion). In subacute coronary occlusion the first phase does, of course, not apply.
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PMID:Influence of collateral flow on the ischemic tolerance of the heart following acute and subacute coronary occlusion. 125 70

Liver injuries induced by ischemia or physical trauma are characterized by noninflammatory damage frequently observed in a clinical setting. When the liver of rats was injured by ischemic treatment or physical crushing, necrotic tissue degeneration occurred in several sites of lobulus within 24 hr. Hepatocyte growth factor, a potent mitogen for adult rat hepatocytes in primary culture, was markedly induced in the livers of rats injured by ischemia or physical trauma. In both cases, the hepatocyte growth factor messenger RNA level in the injured liver reached about 10 to 20 times that of the normal level during 12 to 24 hr after liver injury. The increase in hepatocyte growth factor messenger RNA correlated well with the degree of liver damage as evaluated by serum ALT activity in the sera of rats. In situ hybridization showed that hepatocyte growth factor messenger RNA expression occurs in nonparenchymal liver cells, primarily in Kupffer cells of the ischemic liver. After the increase of hepatocyte growth factor messenger RNA in the injured liver, a marked compensatory hepatocyte DNA synthesis occurred 48 to 72 hr after these treatments. These results suggest that hepatocyte growth factor acts as a hepatotropic factor for liver regeneration after noninflammatory liver damage caused by ischemia and physical crush, probably through a paracrine mechanism.
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PMID:Rapid and marked induction of hepatocyte growth factor during liver regeneration after ischemic or crush injury. 128 Feb 46

Our previous observations that minimal coronary resistance (MCR) decreases by 60% in a model of chronic ischemia suggest that angiogenesis and vascular remodeling occurred. To test this hypothesis we conducted quantitative morphometry on the arteriolar (ART) and capillary (CAP) beds of 14 pigs subjected to chronic ischemia. We induced chronic ischemia by ameroid occlusion of the left circumflex coronary artery for 2 to 8 weeks. We measured numerical densities (ND) and total cross sectional areas (CSA) of the ART and CAP in the ischemic regions. In the same pigs minimal coronary resistance (MCR) was measured during adenosine infusion, using a constant pressure coronary perfusion pump. In 8 other pigs we gave tritiated thymidine to determine the extent of DNA synthesis in smooth muscle and endothelial cells. At autopsy we injected colored silicone into the vessels of these pigs so we could evaluate the coronary collateral vessels as well as the other arterioles. After 3 weeks of ameroid occlusion, ART ND increased 45% above control, while ART CSA increased 21% above control. After 8 weeks of ameroid occlusion, there were further significant increases in ART CSA, but not in their ND. These changes corresponded to a decrease in MCR to 35% of control after 3 weeks of ameroid occlusion. After 8 weeks of ameroid occlusion, MCR had increased to 49% of control, however there was a further increase in ART CSA to 58% above control. DNA synthesis was occurring since endothelial and smooth muscle cells had total DNA labeling indexes of 1.2% (compared to 0.01% for controls) 2-5 days after ameroid occlusion, but were near control levels by 8 weeks. Many arterioles showed endothelial cell denuding and medial damage. Also capillaries showed degenerative changes and new sprouts. Silicone casts of the left circumflex bed vessels showed increased volumes averaging 55% more than controls. These data imply that angiogenesis is partly responsible for the decreased minimal coronary resistance seen in chronic ischemia. The loss of wall integrity in old arterioles and increased compliance in newly formed arterioles and capillaries also may contribute to the reduced resistance. Newly formed vessels are a significant portion of the total number of vessels. The combined effect of these changes is a reduced minimal coronary resistance that is modulated by 8 weeks. Measurements of coronary collateral growth paralleled the changes in the ischemic bed suggesting that angiogenesis factors controlling growth in both the bed at risk and its periphery are controlled by similar temporal events.
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PMID:Coronary vascular remodeling and coronary resistance during chronic ischemia. 129 95

The functional significance of coronary collaterals in humans has been debated for many years. Correlations have now been made between the anatomic appearance of coronary collateral vessels visualized at the time of intracoronary thrombolytic therapy during the acute phase of myocardial infarction and the creatine kinase time--activity curve, infarct size, and aneurysm formation. These studies demonstrate a protective role of collaterals in hearts with coronary obstructive disease, showing smaller infarcts, less aneurysm formation, and improved ventricular function compared with patients in whom collaterals were not visualized. There is ample evidence that collaterals respond to myocardial ischemia by opening preexistent channels. When the cardiac myocyte is rendered ischemic, collaterals develop actively by growth with DNA replication and mitosis of endothelial and smooth muscle cells. Heparin-binding growth factors are present in the heart, but their biological activity is quiescent under normal physiological conditions. Once ischemia develops, these factors are activated and become available for receptor occupation, which may initiate angiogenesis after exposure to exogenous heparin. This characteristic of heparin to potentiate the mitogenic activity of acidic fibroblast growth factor has recently been used in the clinical setting as a possible therapeutic modality in patients with coronary artery disease. Patients performing 20 rounds of exercise serially after receiving intravenous injection of heparin showed significantly greater increases in exercise capacity and improvement of clinical symptoms compared with the control group who performed the same exercise without heparin. Further study of neovascularization may lead to a new therapeutic strategy for ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recent insights into coronary collateral circulation. 137 32


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