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

In cats air embolism of the brain was produced by injecting 0.6 ml blood foam into the innominate artery proximal to the origin of both common carotid arteries. Air embolism caused transient ischemia of the brain, reaching a maximum within 1 min after injection. Resolution of the air embolism began a few minutes later and was completed within 15 min in the center and within 30 min in the border zone of the main supplying arteries. During this phase tissue perfusion was inhomogenous with reduced flow rates in some areas and reactive hyperemia up to 300% in others. This resulted in venous hyperoxia and a decrease of arteriovenous oxygen difference to as low as 2 ml/100 ml blood. Reactive hyperemia was accompanied by brain swelling and an increase in intracranial pressure from 3.6 +/- 1.2 to 12.3 +/- 2.0 mm Hg. The reason for hyperemia was a decrease of cortical pH which fell from 7.33 +/- 0.03 to 7.03 +/- 0.05, and which caused a dilation of pial arteries up to 260%. Immediately after embolism, the EEG flattened and oxygen consumption decreased. After normalization of flow, oxygen consumption returned to normal, but EEG only partially recovered. Air embolism had little effect on the water and electrolyte content of the brain, and produced very little damage to the blood-brain barrier.
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PMID:Arterial air embolism in the cat brain. 4 47

This review will begin by giving the highlights of the history and explain development of the basic science knowledge of hemoglobin chemistry, function, and physiology. The necessary involvement of red cell metabolism, as it pertains to the maintenance of 2,3-diphosphoglycerate (2,3-DPG) levels, both normally and under the perturbed and experimental conditions of blood storage, will be given as part of the basic science data. The clinical science and transfusion data will comprise the main critical aspects of the paper. Analysis and comment of over 20 studies will be given on the effects of animal and human transfusions with altered 2,3-DPG levels. Decreased survival and organ function have been demonstrated with transfusion of low 2,3-DPG red cells, with or without anemia, in the conditions of exercise, shock, hypotension, ischemia, cardiac surgery, hypoxia, sepsis, and acidosis. By critical analysis of these studies, recommendations on general and specific patient needs for red cell transfusions with normal or high 2,3-DPG levels are given.
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PMID:The significance of 2,3-DPG in red blood cell transfusions. 4 84

Phosphorylation rates of canine heart mitochondria isolated after various periods of myocardial ischemia after cardioplegic arrest were correlated with the myocardial ATP-, lactate- and undissociated lactic acid content as well as with interstitial H+-concentration. The following correlation coefficients were found: ATP: 0.87, lactate: 0.93, interstitial H+: 0.73. The calculated undissociated lactic acid content and the mitochondrial phosphorylation rate during ischemia showed a correlation coefficient of r = 0.95. Swelling measurements of mitochondria, isolated immediately after cardioplegic arrest, demonstrated that an undissociated lactic acid- and an ATP-concentration of 70 microM and 28 microM respectively are necessary for a half maximal swelling reaction under anaerobic conditions. The results suggest that the accumulation of undissociated lactic acid during myocardial ischemia could play an important role for mitochondrial damage in vivo.
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PMID:The role of ATP and lactic acid for mitochondrial function during myocardial ischemia. 4 43

Subendocardial hemorrhagic necrosis in an important cause of death following cardiopulmonary bypass. The transmural distribution of flow across the left ventricle (LV), septum (SP), and right ventricle (RV) is a complex interaction of vascular resistance and myocardial compressive resistance. We studied the change in transmural blood flow in LV, SP, and RV, and left ventricular volume, following administration of cardiotonic and vasoactive drugs in the fibrillating heart. The drugs studied included calcium with and without ATP-induced vasodilation, isoproterenol, epinephrine, angiotensin, and ouabain. Calcium produced underperfusion of LV subendocardium with or without previous ATP vasodilation. Isoproterenol also caused underperfusion of LV subendocardium. Both calcium and isoproterenol decreased ventricular volume. Angiotensin increased resistance in the subepicardium and increased flow in the subendocardium, with no change in ventricular volume. Epinephrine and ouabain caused no consistent changes in transmural flow. The decreased ventricular volume produced by calcium and isoproterenol restricts flow in the subendocardium because of increased compressive resistance. Increased subendocardial flow with angiotensin indicates that subepicardial vasodilation in the fibrillating heart causes epicardial "steal," which contributes to subendocardial ischemia.
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PMID:Effect of cardiotonic and vasoactive drugs on transmural flow distribution and ventricular volume in the fibrillating heart on cardiopulmonary bypass. 4 21

Retinal ganglion cell protein synthesis and slow axonal protein flow have been measured in eight optic nerves from four macacus rhesus monkeys after producing ganglion cell ischemia. Comparison of the slow axonal protein flowing into the two optic nerves of the same control animal reveals a variability of up to 27 per cent. Following central retinal artery ligation, infarction of the retinal ganglion cells was reflected by a 97 per cent reduction in the radioactively labeled protein within the optic nerve. This profound reduction in labeled protein within the nerve confirmed that only ganglion cell dependent intra-axonal protein flow was being measured. Ischemia to the ganglion cell axons, with preservation of blood flow to the cell soma, was obtained in two optic nerves from different animals by severing all the posterior ciliary vessels entering about the optic nerve. Six weeks later, only a modest histologic loss of axons was present in these optic nerves. However, a profound reduction (up to 97 per cent) in labeled optic nerve protein was found at four days following intravitreal leucine injection. This is the time when the optic nerve slow axonal protein flow is dominated by the foveomacular ganglion cells. The reduction in slow axonal protein flow corresponds histologically to a preferential retrograde degeneration of the foveomacular ganglion cells, suggesting increased sensitivity of the smaller foveal axons to the induced ischemia. Electrophysiologic measurements support this conduction.
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PMID:Slow axonal protein transport and visual function following retinal and optic nerve ischemia. 4 18

In poorly perfused myocardium with resultant ischemic dysfunction, augmentation of contractility can, under certain conditions, be used to detect viable but ordinarily noncontracting muscle. Two methods of inotropic augmentation, pharmacologic inotropic stimulation and postextrasystolic potentiation (PESP), were studied in acutely ischemic canine myocardium with controlled coronary blood flow. A caliper length gauge to record segmental shortening and left ventricle pressure was used to construct pressure-length loops. Acute regional ischemia depressed segmental function: early segmental shortening decreased (-20 plus or minus 0.02% [SE]) and frequent dyskinesia occurred. Restoring coronary blood flow corrected segmental shortening to control levels. During acute regional ischemia, PESP consistently augmented segmental function (+49 plus or minus 0.03%) and abolished dyskinesia. Pharmacologic inotropic stimulation with isoproterenol or calcium administered into the coronary arteries did not produce a comparable improvement in segmental function (+9 plus or minus 0.05%). Although early shortening markedly increased with pharmacologic stimulation, there was no consistent change in total shortening, and the area of the pressure-length loop decreased. Due to late dyskinesia, there was a decrease in injection shortening. Systemically administered pharmacologic agents accentuated early dyskinesia but caused no consistent change in total shortening. Unlike PESP, pharmacologic agents either worsened segmental function or caused responses that were minimum and inconsistent; such responses clearly cannot be used to identify viable ischemic myocardium.
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PMID:Detection of latent function in acutely ischemic myocardium in the dog: comparison of pharmacologic inotropic stimulation and postextrasystolic potentiation. 4 92

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.
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PMID:Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis. 4 31

In order to study the occurrence and frequency of ischemia-induced ventricular arrhythmias, we analyzed 105 episodes of spontaneous angina pectoris occurring at rest in 28 hospitalized patients with unstable angina pectoris and proved coronary artery disease. Of 24 patients with serious ventricular arrhythmias during pain, 17 (57%) were arrhythmia-free during monitoring. In the other four patients, 17 of 29 (59%) pain episodes were associated with serious ventricular arrhythmias, and three of these four had serious ventricular arrhythmias during pain-free periods. Each patient tended to manifest the same type of arrhythmia during repeat episodes of pain. It appears that continuous electrocardiogram (ECG) monitoring is important during the initial hospitalization of the patient with unstable angina. The presence of ventricular arrhythmias during pain-free periods indicates a high risk for serious ventricular arrhythmias during episodes of spontaneous pain. These patients should be considered for continued ECG monitoring and antiarrhythmic therapy.
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PMID:Ventricular arrhythmias during unstable angina pectoris. 5 51

Embolism of the right middle cerebral artery regularly failed to induce clinical or electrical seizure activity during acute ischemia in primates. This negative correlation casts some doubt on the popular interpretation of seizures at the outset of clinical stroke as evidence of cerebral embolism.
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PMID:Laboratory note. EEG changes after acute cerebral embolism. 5 70

A microscopic histopathological study was done on 500 full-eyelid-thickness surgical specimens: 25 with the diagnosis of senile ectropion and 25 with that of senile entropion. Five different staining techniques were used. There appears to be significantly more orbicularis and Riolan's muscle ischemia, atrophy, and collagen fragmentation with ectropion than with entropion. Entropion shows more septal and tarsal atrophy. In both conditions, the skin and conjunctiva show chronic inflammation and scarring as a constant feature. Statistical significance at the 1% level was present for all six characteristics studied. These histopathological changes, if not etiological, are at least concomitant features differentiating senile ectropion from entropion at the microscopic tissue level.
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PMID:Senile ectropion and entropion: a comparative histopathological study. 5 35


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