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

This article presents an analysis of acute gastroduodenal mucosal lesions (AGML) based on a review of current literature and the personal experience of the authors. The pathology of AGML involes two distinct types of lesions, namely, superficial erosions confined to the acid-secreting gastric mucosa and presenting as erosive hemorrhagic gastritis, and acute ulcers that occur in the alkaline gastric mucosa and duodenum. The etiology of these two lesions is very likely different. Acut gastroduodenal ulcers, best known as stress ulcers, are probably "peptic" lesions, whereas erosive hemorrhagic gastritis appears to be due to pathologic back diffusion of hydrogen ions caused by a breakdown of the gastric mucosal barrier as a result of endogenous factors, such as gastric mucosal ischemia, and sometimes exogenous factors, such as alcohol, urea, and acetylsalicylic acid. Catecholamine hypersecretion resulting from severe stress, such as occurs in hypovolemia, sepsis, and hypercapnea, contributes to ischemia of the gastric mucosa by producing splanchnic vasoconstriction. The key to the diagnosis of AGML is early endoscopy in all cases of upper gastrointestinal bleeding. Therapy for AGML should begin with a trial of medical measures directed at restoring effective perfusion of tissues and removing hydrogen ions from the stomach by gastric washing. Medical therapy is effective in 80% of patients with erosive hemorrhagic gastritis, but surgical treatment is usually required in acute gastroduodenal ulcer. When surgery is necessary for either type of lesion, vagotomy with hemigastrectomy appears to be the most effective operation. The personal experience of the authors has involved 36 patients with AGML who were treated in three periods between 1968 and 1976. The mortality rate of patients with AGML has been reduced from 50% in the first 2 years to zero in the last 2 years by the use of emergency endoscopy for diagnosis, appropriate medical therapy, properly timed and executed surgery, and, most recently, selective angiography.
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PMID:Progress in the treatment of acute gastroduodenal mucosal lesions (AGML). 1 30

Antianginal drugs were evaluated on the basis of their ability to protect against subepicardial electrogram changes induced by local ventricular ischemia in anesthetized dogs. Sch 11973 [N-(2-phenylisopropyl)-N-p-toluene sulfonyl urea], a potential new antianginal agent, was also effective against local ventricular ischemia with its maximum effect appearing at 1mg/kg, i.v. or i.d. and with a duration of at least 2 hours. Nitroglycerin, at a dose of 0.04 mg/kg given bucally, exerted less protection, lasting on the average less than 15 minutes. Protection by propranolol at 1 mg/kg, i.v., was not better than nitroglycerin, but lasted up to one hour, while dipyridamole was ineffective when given in a dose range of 0.1-10 mg/kg, i.v. Sch 11973 differed from standard antianginal agents which may act via beta-adrenergic blocking activity or alteration of cardiac or circulatory dynamics since no acute pharmacological changes were observed after Sch 11973 was administered.
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PMID:Pharmacology of Sch 11973, N-(2-phenylisopropyl)-N-p-toluene sulfonyl urea, a potential new antianginal agent. 2 76

70 rats were subjected to tourniquet ischemia of a hind limb for a period of two and three hours. 12 rats served as controls. After release of the 3 hours tourniquets 20 rats were treated either with Ringer's solution or with hydroxyethyl starch. Kidney function and morphology, systolic blood pressure, hematocrit, serum electrolytes, creatinine and urea were studied as different times of recirculation. 1. Reduction in renal function was only observed after releasing the tourniquets. 2. The extent of reduction in renal function depended on the time of ischemia and time of recirculation. 3 hours of tourniquet with two hours of recirculation led to the largest extent of reduction in renal function and renal parenchymal lesions. 3. If the infusion of HES was applied at the beginning of recirculation, reduction in renal function was prevented, as well as parenchymal lesions. Ringer's infusion, however, did not improve kidney function to a normal range.
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PMID:[Animal experimental studies on partial kidney function after temporary tourniquet ischemia with and without blood substitute therapy]. 3 60

Nephroblastomas are induced in rats with N-Methyl-N-Nitroso-Urea, and selective renal artery occlusion is performed. This procedure has the same effect like occlusion by embolization. The effect of renal artery occlusion on the growth rate of nephroblastmas is controlled by angiography and gross and microscopic examinations up to 70 days following ischemia, the results are compared with a group of untreated nephroblastoma rats. There is a marked reduction of tumor size and a decrease in tumor proliferation. There is an immediate tumor cell death induced by acute and complete ischemia. Collateral blood vessels cause residual arterial blood supply of tumor parenchyma. There seems to be a correlation between collateral blood delivery and tumor size. Even 70 days after permanent ischemia there are areas of obviously absolute normal tumor cells. The conclusion of this experimental study demonstrated that growth rate of tumors can be reduced by ischemia although potentially malignancy still remains. Clinical embolization therapy is justified only in nonoperable patients with hypernephroma and with massive hematuria.
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PMID:[The influence of renal artery occlusion on tumor growth of experimental nephroblastomas (author's transl)]. 20 93

The LD50 of tobramycin sulphate administered intravenously, intraperitoneally, subcutaneously and orally to albino mice was 77 (73--82), 262 (234--294), 560 (500--627) and greater than 10500 mg/kg respectively. With an increase in the rate of intravenous administration tobramycin toxicity increased. When tobramycin sulphate was administered subcutaneously daily in multiple doses equivalent to the daily therapeutic doses from humans (calculated for the body surface) and in the doses 2--3 times higher than the above therapeutic ones, the function of the kidneys, liver and the Preier's reflex did not significantly change. When the doses were 8--10 times higher than the therapeutic ones, an increase in the urea level in the blood serum, disappearance and a decrease in the Preier's reflex were observed. The impairment of the kidney function was accompanied by degenerative changes in the convoluted tubules of the kidneys, ischemia of the renal glomeruli and appearance of protein secretion in their capsule cavities. The picture of the peripheral blood did not suffer significant changes. The studies on the acute and chronic toxicity of tobramycin sulphate prepared at the Institute of New Antibiotics showed that the drug did not differ from the import tobramycin samples.
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PMID:[Toxicity of tobramycin in single and multiple administrations to laboratory animals]. 42 96

Electron transport in tissue cubes, isolated mitochondria and submitochondria particles were examined as a function of ischemic time. It was found that electron transport remains active in all systems beyond the 2 hour ischemic time interval. The NADH stimulated respiration, however, declined after 2 hours of ischemia in ASU (Ammonia-Sephadex-Urea) particles followed by respiration with matrix-located dehydrogenases tested by substrates such as glutamate, alpha-ketoglutarate and pyruvate plus malate. Succinate dependent respiration remains active at control levels. In contrast proton gradient reveals changes in two phases: Phase A is characterized by gradually increasing gradient without valinomycin and by a rapidly declining gradient with valinomycin in the medium. Phase B is characterized by a declining proton gradient with or without valinomycin. It is suggested that the alteration of the proton gradient between 1 and 2 hours ischemia is an important factor contributing to irreversible cell injury.
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PMID:Studies on the pathogenesis of ischemic cell injury. VII. Proton gradient and respiration of renal tissue cubes, renal mitochondrial and submitochondrial particles following ischemic cell injury. 60 84

The present study has defined conditions whereby a reversible form of ischemia-induced ARF can be produced in the dog. Unlike previous studies [9-11] which examined the acute phase of NE-induced ARF, this study demonstrates the feasibility of using the model for the longitudinal study of ARF. Such a model may be useful in studying the pathologic and physiologic changes which occur during different phases of ARF. Perhaps most important, this model should also provide a setting in which treatment measures, either prophylactic or therapeutic for ARF, can be examined.
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PMID:Norepinephrine-induced acute renal failure: a reversible ischemic model of acute renal failure. 69 76

Differential survival times of various organ allografts in the rat across the same histocompatiblity barrier were studied by transplanting the kidney, heart, intestine, pancreas, and skin from (BN X Le)F1 hybrid donors to Lewis recipients. Some (one-third) of the kidney grafted rats survived for a prolonged period of time (32-72 days, plus one rat surviving over 9 months), whereas all other organs and skin were promptly rejected between 7 and 21 days. Possible factors responsible for the prolonged kidney survival are discussed; the reason for this was not clear but was not related to the period of operative ischemia or postoperative blood-urea-nitrogen, nor were animals tolerant to donor antigen as evidenced by the popliteal lymph node weight assay and signs of mild rejection on histology of grafted kidneys. A hypothesis of autoenhancing mechanism is presented.
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PMID:Differential survivals of F1 hybrid allografts in parental recipients. 77 4

It is commonly assumed that the decrease in the effective circulatory volume (ECV) is the major event in acute renal failure (ARF) and the preferential ischemia of the cortex another major modification. Frusemide has been given to try to prevent this change in glycerol-induced ARF because of its effect in redistributing renal blood flow from medulla to cortex. Isontonic saline was also tried to avoid the ECV depletion. The pretreatment with frusemide not only fails to protect against the ARF but increases its severity. Isotonic saline adminstration and replacement of urinary losses almost prevent glycerol-induced ARF but when both isotonic saline frusemide are administered together their effect is only a slight increase in the excretion rate of urea and creatinine during the first days of the experiment. The importance of the changes in the ECV or a possible direct action of frusemide on the renin-angiotensin axis are discussed. There is a good correlation between plasma creatinine levels and interstitial oedema. The importance of the oedema in the maintenance of ARF is discussed.
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PMID:Negative effect of frusemide pretreatment in glycerol induced acute renal failure. 87 19

We studied the effect of different chronic (3-4 weeks) dietary salt intakes on intrarenal hemodynamics of normal and mercury-intoxicated rats. Cardiac output (CO), total renal blood flow (RBF), and the zonal perfusion rate in the outer cortex (OC) and inner cortex (IC) were measured by the radioactive microsphere method. The distribution of cortical blood flow was calculated as the distribution index (DI), which reflects the ratio OC/IC. Rats were placed on a high salt diet (group I), intermediate salt diet (group II), or low salt diet (group III). For each group control rats (subgroup A) and mercury-intoxicated rats (subgroup B) were studied. No effect of the different salt intakes on the DI could be detected. The DI in group IA was 2.35 +/- 0.14; in IIA, 2.40 +/- 0.16; and in IIIA, 2.38 +/- 0.09 (P greater than 0.05). After mercury injection RBF changed from 5.32 +/- 0.36 ml/g.min(-1) (IIA) to 3.31 +/- 0.20 ml/g.min(-1), IIB and from 4.32 +/- 0.11ml/g.min(-1) (IIIA) to 1.98 +/- 0.10 ml/g.min(-1) (IIIB) P less than 0.01). The DI was lowered to 1.53 +/- 0.06 (IIB) (P less than 0.05) and to 1.16 +/- 0.10 (IIIB) (P less than 0.01). In both IIB and IIIB a marked elevation of the blood urea was noted (IIB = 97 +/- 9 MG/100 ML AND IIIB = 182 +/- 25 mg/100 ml). In group IB no effect on RBF, OC, IC, or DI could be observed (for all values, P greater than 0.05) despite similar histological renal lesions. Group IB rats also had normal blood urea levels (31 +/- 6 mg/100 ml;P greater than 0.05). We conclude (1) that variations in dietary salt intake appear to have no detectable effect on the intracortical blood flow distribution; and furthermore (2) that the mercury-induced acute renal failure (ARF) is characterized hemodynamically by a total renal and preferential outer cortical ischemia and that chronic salt loading prevents the ARF while preserving normal renal perfusion.
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PMID:Effect of variation in dietary NaCl intake on total and fractional renal blood flow in the normal and mercury-intoxicated rat. 96 34


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