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

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

Reduce nicotinamide adenine dinucleotide (NADH) fluorescence was recorded from an avascular area on the squirrel monkey cortex prior to, during, and after focal incomplete ischemia. By using the instrumentation described, stable recordings were obtained free from hemoglobin artifact and with only minimal photodecomposition. Pentobarital was compared to urethane and halothane as the anesthetic agent and was found acceptable for these types of studies in the dosages used. NADH levels were constant prior to ischemia, increased during ischemia, returned to pre-ischemic levels after restoration of blood flow, and then increased greatly at death produced by anoxia. The use of the infrared microscope for semiquantitative measurements of cortical blood flow throughout the duration of these acute studies was investigated and found to the reliable.
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PMID:Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 1. animal preparation, instrumentation, and validity of model. 16 72

Experiments were conducted in anesthetized open-chest dogs subjected to occlusion of the left anterior descending coronary artery for three hours. The oxygenation of myocardial tissue was monitored by a polarographic technique capable of recording simultaneously the oxygen tension (Po2) of myocardial tissue and electrograms. Ischemic injury was monitored by means of ST-segment elevations on myocardial and epicardial electrograms. The volume of the myocardial infarct was measured at the end of each experiment by incubation of transverse slices of left ventricle in a solution of nitroblue tetrazolium and by separation of the unstained (ischemic) from the stained (normal) portions. In one group of dogs, hemodilution was performed after 15 minutes of ischemia by exchanging blood with a stroma-free hemoglobin solution (from a hematocrit reading of 45 +/- 3 percent to 23 +/- 2 percent). Changes occurring in this group were compared with those occurring in dogs that did not undergo hemodilution, underwent hemodilution with dextran 75, or were transfused with whole blood. Hemodilution with hemoglobin reduced aortic and left ventricular filling pressures while increasing coronary blood flow, increased myocardial Po2 from 2 +/- 2 mm Hg to 8 +/- 2 mm Hg (P less than 0.005), lowered the ST-segment elevation of both myocardial and epicardial electrograms, and reduced the volume of the myocardial infarct. These effects were unmatched by hemodilution with dextran or infusion of whole blood.
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PMID:Improved oxygenation of ischemic myocardium by hemodilution with stroma-free hemoglobin solution. 42 81

Although microvascular occlusion has been considered a basis for pathophysiology of the myocardium during the crisis of sickle cell anemia, the status of the left ventricle in uncertain. To determine if left ventricular performance is affected by crisis, 11 patients were evaluated noninvasively by the systolic time interval method on the first day of crisis and serially until recovery. There were no significant differences in the time intervals over this period. In addition, since the serum CPK-MB isoenzyme was not elevated during crisis and evidence of acute injury was not present on ECG, myocardial necrosis appeared unlikely. Four patients on subsequent admission exhibited systolic time interval values similar to the earlier crisis. To determine if there were chronic changes in cardiac function, subjects with sickle cell hemoglobin were studied between crises. Those under 23 years of age were not dissimilar from a group of normals and a group of patients with chronic blood loss anemia A significant abnormality of the PEP/LVET ratio was observed in subjects over 23 years of age. Similar observations were made on echocardiography, with subjects over the age of 23 demonstrating an abnormal ejection fraction compared to the younger group, despite enhanced end-diastolic diameter. Thus, it is suggested that the chronic hemolytic process in subjects with sickle cell anemia may effect cumulative myocardial alterations, resulting in chronic cardiac malfunction in the apparent absence of acute ischemia during crises.
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PMID:Left ventricular performance during and after sickle cell crisis. 43 33

To avoid the compensatory hemodynamic responses, which have limited interpretation of hemoglobin-oxygen affinity modifications in animal experimentation, an isolated blood-perfused rabbit heart model providing metabolic, functional, and vectorcardiographic measurements has been developed. Fixed-flow perfusions of unchanged or affinity-modified red blood cell suspensions were carried out to assess the benefits of high affinity during hypoxic hypoxia and of low affinity during posthypoxic recovery. Using fully saturated suspensions, the influence of affinity level during restricted flow and reperfusion was also studied. Higher myocardial oxygen consumption (MVO2) was associated with high-affinity blood during mild hypoxia and low-affinity blood during posthypoxic recovery. At low flows, heart rate and MVO2 tended to be lower in high-affinity perfusions, and to recover more completely during low-affinity reperfusions. Ventricular function, vectorcardiographic patterns, and lactate levels were affected by hypoxia and ischemia, but not by level of affinity. The relevance of these observations to the therapeutic potential of hemoglobin-oxygen affinity modification is discussed.
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PMID:Application of an isolated heart model to investigate blood-oxygen delivery. 47 72

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.
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PMID:Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs. 47 72

A method is described to determine local oxygen consumption quantitatively in the brain cortex under in vivo conditions. Local oxygen consumption is calculated from the slope of local tissue PO2 decrease during a few seconds of total ischemia of the brain for each second after the stop of circulation. The decrease of tissue PO2 is recorded simultaneously at several measuring sites. To be independent of oxygen chemically bound to hemoglobin, tissue PO2 values are raised above 100 Torr. The calculation of local oxygen consumption for each second during the short period of ischemia showed that the O2 consumption remains constant only for a few seconds ranging from 5 to maximally 15 s at different locations. The O2 consumption decreases continuously although the tissue PO2 values are still above the full saturation of hemoglobin. The rate of local oxygen consumption varies considerably at different measuring sites of the superficial layers of the brain cortex (cat). The mean value amounts to 3 +/- 1.5 ml O2/100 g tissue and minute.
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PMID:Direct determination of local oxygen consumption of the brain cortex in vivo. 56 39

Male Wistar rats were used to investigate the effects of stromafree hemoglobin (200 mg Hb/100 g body weights, i.v. as a 16.4% solution) on kidney function and morphology. Ischemia of the kidney was induced by bilateral clamping of the renal pedicle. The most severe disturbances of kidney function occurred in kidneys damaged by ischemia during the peak of Hb excretion; endogenous creatinine clearance decreased to 5% of control values, serum creatinine concentration rose 6 times as high as control values, and Hb excretion in the urine was reduced. Kidney damage after Hb loading and ischemia was more severe than damage caused by ischemia alone. These results demonstrate that the vulnerability of kidneys to damage by ischemia is increased by Hb loading.
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PMID:Effect of hemoglobin loads on the function and morphology of ischemic kidneys in the rat. 61 Jul 8

Hepatic morphology was studied in rats that were exchange transfused with either a stroma-free hemoglobin solution (SFHS) or with various asanguineous resuscitative fluids. The animals under-went 75 per cent blood volume replacement and tissues were collected and fixed at timed intervals after the exchange transfusion. In addition, blood volumes were determined, using chromium labeled red blood cells, in both albumin and SFHS-treated rats at varying time periods after exchange transfusion. One hour following exchange transfusion, livers of animals infused with asanguineous fluids demonstrated marked centrolobular hepatocellular vacuolization and mitochondrial shape alterations consistent with the effects of hypoxia. SFHS appeared to protect the liver from these early abnormalities. However, at later time intervals livers of albumin-treated animals appeared normal, whereas those of SFHS-transfused rats exhibited centrolobular necrosis. Blood volume was reduced approximately 10 per cent during the first 18 hours after exchange transfusion with albumin, while SFHS-treated rats experienced a 42 per cent blood volume decrement in only 6 hours. Blood volumes were near normal in all animals by 48 hours. These findings suggest that SFHS protects the liver from hypoxia immediately after exchange transfusion, presumably by its ability to transport and release oxygen. However, the eventual disappearance of hemoglobin from the intravascular space is associated with a marked reduction in blood volume which is accompanied by hepatic ischemia and centrolobular necrosis.
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PMID:Morphologic effects following massive exchange transfusions with a stroma-free hemoglobin solution. I. Liver. 68 1

Regional lung ischemia was imaged with a rapidly diffusible radioaerosol of pertechnetate. The method is compared with similar techniques using 11C and 15O. The principles involved include (A) the rapid alveolar-capillary diffusion of inhaled radioactive gases (11CO, C15O, and C15O2) and the radioaerosol of 99mTcO4-; (B) the patency of the airways to the ischemic regions; and, most importantly; (C) the much slower tracer removal from lung tissue with a stagnant circulation as opposed to the surrounding normal lung. The 11CO and C15O label the hemoglobin in red blood cells, and the C15O2 labels water in the circulation and in the stagnant ischemic region. The TcO4- probably labels the albumin of the plasma in the embolized regions and in the circulating blood. Experiments involving pulmonary embolism in dogs, proved by pre- and post-mortem angiography and gross post-mortem examination, show that positive ischemic lesions (hot spots) are observed, after TcO4- aerosol and C15O2 gas inhalation, in the embolized region on the same day. Clinical trials with aerosol-inhalation method in suspected pulmonary embolism and now under way.
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PMID:Imaging experimental pulmonary ischemic lesions after inhalation of a diffusible radioaerosol: concise communication. 83 71


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