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

Heparin sodium-induced thrombosis is insidious and difficult to diagnose. If untreated, it results in death or major amputation. We have treated seven patients with thromboses resulting from platelet aggregation induced by heparin. Four patients had acute arterial ischemia of the lower extremity, venous gangrene developed in two, and one patient had an occluded autogenous vein femoral popliteal bypass in the immediate postoperative period. The platelet count was noticeably reduced in affected patients. White platelet thrombi were noted in four patients, three of whom had acute arterial occlusion. A white thrombus was the cause of immediate failure of a femoral popliteal graft. Electron microscopic examination of these thrombi demonstrated predominantly fibrin platelet aggregates with an occasional entrapped WBC and a rare RBC. All patients receiving heparin therapy must have platelet counts performed regularly. If thrombocytopenia is detected, platelet aggregation studies are indicated. When abnormal platelet aggregation is noted, heparin therapy should be reversed with protamine sulfate and the patient treated with low-molecular-weight dextran and warfarin sodium.
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PMID:White clot syndrome. Peripheral vascular complications of heparin therapy. 43 52

The effect of preliminary administration of alpha-tocopherol acetate (1 mg/kg) and sodium selenite (1 mg/kg) on RNA synthesis rate and changes in the macroergic content in ischemic myocardium was studied. It was shown to be conducive to ATP level maintenance after 30- and 60-minute heart ischemia. A statistically significant accumulation of RNA by the myocardium following I-hour ischemia as well as this polynucleotide synthesis activation were recorded. Preservation of the energetic resources by the cell along with RNA metabolism returning to normal contributes to inhibiting the emergence of irreversible cell damage and increases regenerative potentialities of the myocardium.
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PMID:[Effect of alpha-tocopherol acetate and sodium selenite on the change in ATP content and the RNA synthesis rate in the ischemic myocardium]. 44 4

Intravenous infusion of acetylstrophanthidin to 6 dogs, after a 60 min left anterior descending coronary artery occlusion, was associated with a 43.0 +/- 10.5% decrease in the dose of digitalis needed to produce ventricular arrhythmias as compared to the pre-ischemic dose (97.5 +/- 8.0 microgram/kg). Reperfusion of the ischemic region for 2 h after a 90 min occlusion resulted in a 54.4 +/- 6.7% decrease in the arrhythmogenic dose. Direct intracoronary infusions of digitalis into the ischemic region, after a 90 min coronary occlusion followed by 2 h of reperfusion, was associated with a 47.7 +/- 6.4% decrease in the dose of digitalis needed to produce arrhythmias. The pre-ischemic (control) arrhythmogenic dose of digitalis via the intracoronary infusion method was 1.5 +/- 0.3 microgram/kg (mean +/- S.E.M. of 7 dogs). Sodium pump activity, estimated from the ouabain-sensitive 86Rb uptake in sodium-loaded ventricular slices, was significantly higher in slices obtained from the ischemic regions (6.84 +/- 0.30 nmoles 86Rb/mg dry wt. (mean +/- S.E.M.), than from the non-ischemic regions (3.43 +/- 0.64 nmoles 86Rb/mg dry wt.). Sensitivity of the sodium pump activity to the inhibitory effect of ouabain also was increased in the ischemic regions as indicated by a shift in the log dose--response curve to the left. Thus, it appears that there is an increase in myocardial sensitivity to the toxic effect of digitalis after temporary ischemia and it appears to be related to an increase in the sensitivity of the Na+,K+-ATPase or sodium pump to the inhibitory effect of digitalis.
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PMID:Ischemic-induced alterations in cardiac sensitivity to digitalis. 48 58

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
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PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

The present paper reviews studies which utilize x-ray microanalysis to determine intracellular ion shifts following several types of cell injury. New data from our own laboratory on several cell injury systems are discussed. Concentration estimates are made by comparison of data from tissues with a series of standards prepared in 20% albumin followed by cryosectioning. Hemorrhagic shock in rats is followed by rapid changes of ions in both muscle and liver. These include increased levels of sodium and chlorine and decreased levels of potassium which can be correlated with deficits in the energy charge. Measurements made over hepatocellular carcinomas in the mouse, induced by safrole show marked changes in comparison with non-transformed cells. These include striking increases in sodium and chloride and decreases in potassium and phosphorus which may be related to growth control. Studies on ischemia produced by arterial clamping in the rat kidney and the dog heart show somewhat similar changes. Moreover, in these models much interest is directed at early increases of cytoplasmic calcium with decreased mitochondrial calcium levels at later intervals. Following reflow, there is a prominent increase of calcium in the cytosol. These changes in calcium may be related to activation of phospholipases producing permeability changes which may contribute to further ion shifts as well as ultimately to cell death. The paper also comments on the use of cryostat sections for some types of routine pathological analysis.
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PMID:The role of ion shifts in cell injury. 52 92

Eight patients with transient ischemic attacks, and three with partial nonprogressive strokes associated with mitral valve prolapse, are reported. No other etiology for their ischemic events was found. Only one episode of ischemia recurred on aspirin treatment, whereas none recurred on sodium warfarin therapy.
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PMID:TIA, stroke, and mitral valve prolapse. 57 14

Arterial thromboembolism is a recognized complication of systemic heparin therapy. Characteristic of the entity is arterial occlusion by platelet-fibrin thrombi with distal ischemia occurring four to twenty days after the initiation of heparin therapy, preceded by profound thrombocytopenia with platelet counts in the range of 30,000 to 40,000 per cubic millimeter. The clinically apparent occlusion may be preceded by gastrointestinal and musculoskeletal symptoms that appear to be ischemic in origin, and might serve to warn the clinician of these complications. Previous reports of these phenomena as well as recent studies of the effect of heparin are reviewed. The common factor relating thromboembolism and thrombocytopenia is heparin-induced platelet aggregation. Appropriate treatment consists of discontinuation of heparin, and anticoagulation with sodium warfarin if necessary. Vascular procedures are performed as indicated.
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PMID:Arterial thromboembolism in patients receiving systemic heparin therapy: a complication associated with heparin-induced thrombocytopenia. 59 36

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

Guinea-pig and dog heart mitochondria were isolated in a KEA-medium. Ca2+-transport across mitochondrial membranes was measured continuously with an Aminco Dual-Wavelength-Spectrophotometer and murexide as a Ca2+-sensitive indicator. Ischemia was produced by cardioplegia at 15 degrees C according to Bretschneider. Guinea-pig heart mitochondria as well as mitochondria from dog heart show a spontaneous Ca2+-release without nonphysiological influence. Addition of 3.5 M Na+ can induce a very quick release of Ca2+ taken up by heart mitochondria. This release is different from that occurring spontaneously. Progressive ischemia results in a marked depression of Ca2+-uptake and spontaneous Ca2+-release.
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PMID:Ca2+-uptake and -release phenomena from cardiac mitochondria under normal and ischemic conditions. 65 15


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