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

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.
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PMID:Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity. 62 53

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The effect of long-term tourniquet ischemia on electrolyte levels in muscle tissue and plasma during and after occlusion was investigated in man. Muscle tissue electrolytes were studied in nine patients using a percutaneous muscle biopsy technique. The estimation of the intra- and extracellular electrolyte content was based on the determination of the chloride space. In another similar group of patients (n=11) plasma electrolytes were investigated by taking blood samples from fine plastic catheters inserted into both femoral veins and one radial artery. Capillary blood flow was measured using the 133Xenon-clearance technique. During occlusion there were no significant changes in muscle tissue or plasma electrolytes. After release of the tourniquet an increase in plasma potassium of the operated leg and arterial plasma were observed. Maximal muscle blood flow and maximal potassium values occurred at the same time giving a pronounced potassium release from the operated leg. The osmol release from the occluded leg showed a maximum 1 min after tourniquet release. The total and intracellular content of potassium and sodium in the muscle tissue did not significantly alter after release of the occlusion. A moderate increase in extracellular water was found after tourniquet release.
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PMID:Electrolyte changes in muscle tissue and plasma in tourniquet-ischemia. 66 4

Although the PGs operate mainly in the renal medulla the demonstration of PG biosynthesis in the renal cortex has provided a biochemical basis for a direct relationship between the PGs and the renin-angiotensin system. The formation of PGs is influenced by circulating levels of A I probably by indirect mechanisms. That the release of renin at least under certain experimental conditions is dependent on the PG system is suggested by the following findings: 1. C20:4 increases PRA in the rabbit and rat. 2. Indomethacin decreases PRA in the rabbit. 3. C20:4 stimulates renin release from slices of rabbit kidney cortex. 4. Reduced renal perfusion pressure and ischemia are accompanied by release of both PGs and renin. 5. The release of PG and renin following renal ischemia is blocked by treatment with indomethacin. The actions of the renin-angiotensin system and the renal PGs are, as far as we know them, antagonistic to each other. PGEs are vasodilator, increase renal blood flow, inhibit adrenergic neurotransmission, and cause excretion of electrolytes and water. Conversely, A II is vasoconstrictor, decreases renal blood flow, stimulates adrenergic neurotransmission, and conserves water and electrolytes. Thus, the interaction between the renal PGs and renin seems to be one in which the two hormonal systems stimulate each other's formation or release, but opposes each other's actions. Further studies are necessary to reconcile this apparent contradiction.
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PMID:Interactions between the renal prostaglandins and the renin--angiotensin system. 79 Sep 16

The authors present the results of a study of the amount of water and potassium in small samples of skeletal muscle and of the intestinal wall of albino rats. Five groups of 10 animals were separated according to the following conditions: peritonitis, pyloric obstruction, intestinal obstruction, mesenteric ischemia and a control group. The results suggest that skeletal muscle is capable of buffering the increased amount of potassium liberated by the tissues which undergo acute trauma, until a critical concentration is reached. Further studies are needed to clarify some of the conflicting results obtained.
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PMID:[Metabolic response and aggression: potassium and water content of skeletal muscles]. 82 84

In normothermic anesthetized cats cerebral blood flow was interrupted completely for one hour by arterial clamping and induced hypotension. The effect of ischemia on the ionic gradients of the cerebral cortex was assayed by determining total cortical electrolytes and by recording the activities of extracellular potassium ([K+i1e) and subarachnoid sodium ions ([Na+])s) with ion-sensitive electrodes. During ischemia [K+]e increased from 3.3+/-0.3 to 56+/-5.4 mEq per liter (means+/-SE) and [Na+]s decreased from 133+/-3.8 to 53+/-5.8 mEq per liter. When the brains were recirculated with blood after one hour's ischemia, [K+]e and [Na+]a gradually returned to normal within 45 minutes. The calculated intracellular uptake of sodium during ischemia amounted to 139 mEq per kilogram dry weight, whereas the intracellular release of potassium was only 64 mEq per kilogram. The increase in intracellular cation was accompanied by a movement of water from the extracellular into the intracellular compartment, causing a reversible shrinkage of the extracellular space from 18.9 to 8.5 vol %. The changes in ionic gradients were related to the development and resolution of ischemic brain swelling, and to the elctrophysiological events during and after ischemia.
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PMID:Cation activities in reversible ischemia of the cat brain. 83 60

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

Dog kidneys were subjected to one, two, or three hours' normothermic ischemia in situ and were then excised for biochemical and histological evaluation. The uptake of para-aminohippurate (PAH) by cortical slices progressively decreased with prolongation of the ischemia, but active transport was never abolished. Glycine uptake and oxygen consumption were only reduced to a modest extent by the ischemia. The intracellular ion levels were drastically altered, with loss of potassium and gain of sodium and chloride, and considerable increases in tissue water were observed. Acid phosphatase was liberated by the whole organ into the venous blood and by the incubated slices into the incubation medium, but both biochemical and histochemical techniques showed that the total quantity of the enzyme in the cells was hardly changed. The histochemical reaction product was localized exclusively in the lysosomes. Morphological damage was slight after one or two hours' ischemia, but more pronounced after three hours, when some cells were seen to be detached from the basement membrane. These relatively minor changes seem insufficient to predict the ultimate fate of the organ after ischemia.
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PMID:Alterations in the dog renal tubular epithelium during normothermic ischemia. 84 66

The effect of nearly total renal ischemia during a two hour period on glomerular filtration and urine composition was studied in relation to tubular permeability and tubular obstruction, two mechanisms that could explain renal insuficiency after iscehmia. Studies on creatinine clearance, micropuncture and microinjection of 14C-inulin into the proximal tubules by means of a hydraulic system were performed before and after the period of ischemia. Thirty minutes after the withdrawal of arterial obstruction, the animals exhibited a maintained diuresis, 50 per cent reduction in glomerular filtration in the superficial nephrons and in the total kidney, a reduction in the proximal fractional absorption of water, and also an increase in the urinary elimination of sodium. The glomerular filtrate of cortical nephorns obtained by micropuncture in anterior areas of the proximal tubules did not differ significantly from the one obtained by micropuncture in more distal areas. The inulin injected into the proximal tubules of a kidney was entirely eliminated by it.
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PMID:[Tubular permeability maintained in post-ischemic acute renal failure (author's transl)]. 85 78


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