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

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

An accurate postmortem method of planimetrically estimating the extent of myocardial infarction was employed in 16 cases. Delineation of necrotic myocardium was enhanced by a macroscopic staining technique, which utilizes a tetrazolium dye. Comparison of infarct size with peak serum creatine phosphokinase levels showed a general correlation between the two that was not statistically significant. Two markedly disparate cases serve to emphasize the need for clinical awareness of the temporal relationship between myocardial infarction and creatinine phosphokinase analysis as well as the possibility of other anatomic sources of elevation of serum enzyme levels. Comparison of infarct sizes in cardiogenic shock and nonshock patients confirms the existence of a significant relationship between a larger myocardial infarct and shock. However, the data from several patients in the group again emphasize the possibility of maintaining a reasonable blood pressure in the face of a massive myocardial infarction or, more importantly, of manifesting "cardiogenic" shock when only a small amount of left ventricular damage has been sustained. The latter possibility may be related to other anatomic events, e.g., bowel infarction, hemorrhage, or possibly right ventricular ischemia, infarction, or dysfunction.
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PMID:Myocardial infarct size: clinicopathologic agreement and discordance. 7 21

To clarify the value of serum enzymes in the detection of intraoperative and postoperative myocardial injury associated with coronary artery bypass grafting, we evaluated 70 consecutive patients (151 grafts). We used electrocardiograms and serial determinations of serum levels: serum glutamic oxaloacetic transaminase (SGOT), creatinine phosphokinase (CPK), lactic dehydrogenase (LDH), and LDH isoenzymes on Days zero, 1, 3, 5, 7, and 10. Patency of all grafts 1 week postoperatively was 92 per cent. Fourteen patients (20 per cent) had ECG evidence of acute myocardial infarction (AMI) or ischemia lasting longer than 48 hours. This incidence of AMI was attendant with no deaths or discernible changes in postoperative ventriculography. LDH-1 (cardiac fraction) was elevated in all patients with myocardial injury. Late elevation of LDH-1 occurred in 2 patients at the time of postoperative catheterization, 1 of whom had negative findings on ECG. Diagnostic correlation was not observed with total LDH, CPK, or SGOT. Predisposing factors to AMI included preinfarction angina (4 of 14 patients), occluded grafts (4 of 14), and a bypass time greater than 120 minutes.
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PMID:Myocardial injury and bypass grafting. Value of serum enzymes in diagnosis. 24 Sep 85

Canine kidneys subjected to 90 min of warm ischemia (37 degrees C) were protected by the administration of methylprednisolone but not by furosemide or mannitol. There was no protective effect observed through the vasodilating or diuretic effect of furosemide in the ischemic canine kidney. Mannitol-induced diuresis before warm ischemia also did not prove to be beneficial for severely ischemic kidneys. Methylprednisolone (30 mg/kg) given 2 h prior to warm ischemia prevented irreversible kidney damage observed in the control and experimental groups. By day 8 the serum creatinine and creatinine clearance returned to normal levels.
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PMID:Study of the protective effect of methylprednisolone, furosemide, and mannitol on ischemically damaged kidneys. 38 34

There are 2 competing methods for cooling the kidney in situ during surgical ischemia: from without by applying ice to the renal surface and from within by perfusing the renal artery. The latter procedure is said to be superior in protecting renal function. Herein the protective effect on renal function of both methods are compared. Pigs of 15--25 kg weight underwent nephrectomy on one side. The remaining kidney was subjected to cold ischemia during 90 minutes while perfusion- or surface cooling was performed. For perfusion cooling the aorta was punctured and the catheter introduced into the renal artery. The perfusing liquid consisted of a physiologic electrolyt solution (Ringer-Lactate) with heparin kept at a temperature of 3--5 degrees C. The initial perfusion lasted 10 minutes and resulted in a median renal core temperature of 23 degrees C. Then the kidney was put on a cooling pad and every 15 minutes again perfused for one minute. For surface cooling sterile melting ice made of glucose solution 5% was applied directly to the kidney. The renal core temperature could be kept at 15--20 degrees C. The two methods of hypothermia were judged by comparing the serum creatinine levels and the I131-hippuran clearances one month after surgery. There was no difference whatever as analysed by the t-test. Hypothermia by applying ice to the renal surface therefore proved to be equivalent to hypothermia by perfusion. Moreover it is much simpler.
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PMID:[Renal hypothermia in situ. Comparison between surface and perfusion cooling concerning renal function in pigs (author's transl)]. 41 41

The effect of chlorpromazine pretreatment of kidneys then damaged by warm ischemia was investigated. The ischemia was inflicted on rabbit kidneys by renal arterial occlusion of 1 1/2 and 3 hours' duration after contralateral nephrectomy. Pretreatment with chlorpromazine, 3.5 mg/kg, was given intravenously before arterial clamping. I-125 Hippuran renography was performed before clamping, immediately after clamp release, and at 2, 4, 6, and 14 days later. Serum creatinine and survival rate were followed. Comparison with untreated control groups was made. The effect on tubular function was investigated by measuring I-125 Hippuran uptake in pretreated slices of renal cortex (compared with untreated contralateral kidney) 48 hr after circulation was restored to the ischemic kidney. Chlorpromazine pretreatment improved recovery from ischemic damage: the renograms showed improved Hippuran uptake after clamp removal, and return to normal was faster. Survival rate after 3 hr of ischemia increased from 1/10 to 6/10 in the pretreated group, and serum creatinine recovered earlier. Hippuran uptake in slices of cortex showed no significant improvement because of pretreatment. It is concluded that the beneficial effect of chlorpromazine pretreatment must be because of decreased vascular resistance, leading to long-lasting increased postischemic renal blood flow.
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PMID:Renographic evaluation of kidney preservation with chlorpromazine. 43 Jan 73

Rats were given 10 or 20 mg of inosine dissolved in 1 ml of 0.9% saline, or a control solution of 1 ml of 0.9% saline, intravenously 10 or 20 min before induction of left renal warm ischemia for 60 min. Further groups of rats were treated with 20 mg inosine or with saline alone 20 min before longer periods of warm ischeamia of 90 and 120 min duration. All animals had immediate contralateral nephrectomy. In all inosine-treated groups the mean plasma creatinine was lower than in their respective control groups and these differences were statistically highly significant.
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PMID:Renal function after warm ischaemia. II. Marked protective effect of intravenous inosine given prior to 60, 90 and 120 min of warm ischaemia. 60 68

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

The pancreas, like the kidney, is highly vulnerable to ischemic necrosis. This form of pancreatic injury may express itself as prolonged hyperamylasemia with only minimal signs or symptoms of inflammation, or may produce severe pancreatitis followed by abscesses and death. Autopsy examination of patients dying after oligemic shock showed a 9% incidence of major pancreatic injury if there was not concomitant acute renal tubular necrosis (ATN), but a 50% incidence in those with ATN. Similarly, among patients dying after non-oligemic shock, 12% of those without ATN had major pancreatic injury but 35% with ATN also had pancreatic ischemic injury. Among 13 selected patients examined prospectively after being in shock, pancreatic injury was indicated by hyperamylasemia, hyperlipasemia, elevated amylase/creatinine clearance ratio, and elevated circulating isoamylases specifically of pancreatic origin. Four of the 13 had clinical manifestations of pancreatitis. Not only must shock be added to this list of causes of pancreatitis, but pancreatic ischemia due to hypoperfusion may also be the critical factor which causes the progression from edema to necrosis in other forms of pancreatitis, including those associated with alcohol and biliary disease.
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PMID:Susceptibility of the pancreas to ischemic injury in shock. 68 87

To determine whether perfusion preservation affected the structure and survival of kidney transplants, we correlated clinical and histologic data in 77 kidneys biopsied one hour after transplantation. Twenty-one of 36 perfusion-preserved kidneys had a glomerular capillary lesion suggestive of intravascular coagulation. None of 41 kidneys preserved by hypothermia alone had this lesion. Presence of the lesion did not correlate with donor or recipient characteristics, warm or cold ischemia time, HLA match, percentage of preformed lymphocytotoxic antibody titers or perfusion characteristics. Of 21 transplants with the lesion, nine required nephrectomy by one month, and one-month serum creatinine was less than 2.0 mg per deciliter in only three of the remaining 12 transplants. We conclude that perfusion preservation may cause pathologic changes that may adversely affect kidney-transplant function. The causes of the pathologic process remain unclear.
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PMID:Perfusion nephropathy in human transplants. 79 Jan 84


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