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

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32

Potassium is an important electrolyte in heart cells and has the greatest membrane permeability in the unexcited state. Hence it is responsible for th generation of the resting membrane potential. Clinical disorders of conduction and impulse formation occur within physiological values of serum potassium. Potassium is indirectly involved in excitation-contraction coupling, and its relation to intracellular calcium metabolism is reviewed. While potassium movements within the cell are metabolic-dependent, it is also true that the activity of metabolic pathways is affected by changes in potassium concentration. During anoxia and ischemia, sodium and calcium are gained by the myocyte, and potassium and magnesium are lost by the cell. At the same time, the action potential duration is abbreviated, the slope of the action potential downstroke (phase 2) is increased, and the resting membrane potential may be reduced. A relationship between disturbances in intracellular potassium and ischemic arrhythmias appears likely.
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PMID:Potassium metabolism in the normal and ischemic heart cell. 78 7

Of 431 cadaver kidneys available for transplantation, 75 were discarded after a period of pulsatile perfusion. Kidneys were discarded because of poor flow, multiple arteries with segmental obstruction, prolonged warm ischemia time, perfusion pump malfunction, and lack of donor cells for cross-matching, among other reasons. Certain selected variables common to transplantated kidneys and kidneys discarded have been analyzed. The most significant finding was that 70% of transplanted kidneys came from donors who had recieved pretreatment with either phenoxybenzamine hydrochloride, methylprednisolone sodium succinate, or phentolaminemesylate. Only 33.3% of kidneys discarded were taken from donors who had received such pretreatment (P less than .01). Attention is focused on the need for careful consideration of the technical aspects of donor nephrectomy as well as the need for donor pretreatment, in order to decrease the number of discarded kidneys.
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PMID:Analysis of 75 discarded cadaver kidneys. 78 78

Regional cerebral blood flow (rCBF) measurements with krypton-85 (100 separate determinations) were compared in squirrel monkeys anesthetized with sodium pentobarbital (a cerebral vasoconstrictor) and halothane (a cerebral vasodilator) before, during, and after middle cerebral artery (MCA) occlusion. Prior to MCA occlusion, a normal physiological response to alterations in arterial carbon dioxide tensions (Paco2) was demonstrated in both groups of monkeys; the cerebral vascular resistance was significantly lower in those anesthetized with halothane. During ischemia, there was loss of autoregulation and a failure to respond to alterations in Paco2 in both groups. Flow in the ischemic region remained uniform in the barbiturate group but decreased progressively in the halothane group, suggesting a "paradoxical response" to the dilating agent. Reactive hyperemia (luxury perfusion) was demonstrated in both groups after restoration of flow. The use of a beta-emitting isotope ensured that measurements in regions of ischemia accurately reflected rCBF and were free of the artifacts ("look through" and Compton scatter) related to use of a gamma-emitting indicator.
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PMID:Influence of cerebral vasoconstricting and vasodilating agents on blood flow in regions of focal ischemia. 81 13

The relevance to man of experimental observations on coronary collateral blood flow (CCBF) in dogs has been questioned. The effect of 2 to 3 hour coronary occlusions in the anesthetized dog and a primate, the baboon, were therefore compared, with CCBF measured by injections of 85Kr distal to occlusion with precordial counting. Before killing, additional isotope was infused to compare inner/outer wall flow distribution and myocardial tissue samples were analyzed for electrolyte content. Effects of nitrates on hemodynamics and metabolism were also compared in dog and baboon. Similar values for CCBF and resistance following occlusions were found in dog and baboon (flow approximately 25 per cent control, calculated resistance increase four- to sevenfold). Greater subendocardial ischemia in both species was indicated by isotope distribution less to the inner wall, but electrolyte changes (k+ less and Na+ greater in the ischemic area compared to nonischemic) were similar transmurally in both species. Hemodynamic responses to nitrate infusion (isosorbide dinitrate) were similar, with increase in CCBF and decrease in resistance. In neither group were inner/outer wall isotope distribution or electrolyte changes influenced by nitrate. The coronary collateral response to occlusion is similar in dog and baboon in terms of both hemodynamics and metabolic changes. After 2 to 3 hours of coronary occlusion some hemodynamic benefit may be demonstrated with nitrates but no metabolic advantage, at least in the central area of ischemia.
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PMID:Comparison of the coronary collateral circulation in dogs and baboons after coronary occlusion. 82 26

To examine the origin of digitalis-induced ventricular tachycardia (VT), acetyl strophanthidin (AS) (25 mug/min) was perfused into a limited zone of myocardium in intact anesthetized dogs through a catheter placed fluoroscopically in the left anterior descending artery without ischemia. A second catheter in the great cardiac vein sampled venous effluent from this region. His and left bundle branch depolarizations were recorded and bipolar intramural electrograms from endocardial and epicardial sites within the anterior descending region were obtained. No conduction alterations preceded arrhythmia. Cardiac venous K+ rose from 3.3 +/- to 4.4 +/- 0.2 meq/liter (P less than 0.001), indicating egress from the perfused zone. 10 animals (Group 1) were sacrificed 2 min after onset of VT while 11 (Group 2) continued until fibrillation (4-14 min). All showed normal (endocardial leads to epicardial) transmural depolarization during sinus rhythm, but 10/21 demonstrated reversal, usually late during VT, including 8/11 in Group 2. Epicardial activation preceded fascicular activation and QRS. Recordings from the border and circumflex regions in 10 additional dogs (Group 3) demonstrated activation reversal only in the border zone. Myocardial K+ was reduced (mean 63 +/- 1 mueq/g) and Na+ increased (mean 41 +/- 2 mueq/g) in the perfused zone (nonperfused circumflex area K+ 72 +/- 1, Na+ 33 +/- 1 mueq/g, P less than 0.001 for both); changes were similar in inner and outer ventricular wall. In related experiments, subepicardial injections of AS induced activation reversal within the immediate area, similar to recordings during coronary infusion. Reversed transmural activation with early epicardial depolarization suggest VT arises within myocardium; electrolyte gradients between adjacent regions may be causative.
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PMID:Origin of acetyl strophanthidin-induced ventricular arrhythmias. 83 70

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

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 effects of lidocaine infusion on the ultrastructural damage induced in cardiac muscle by normothermic cardiopulmonary bypass were assessed in 15 dogs. Six dogs received no medication other than sodium pentobarbital (25 mg/kg, intravenously) while 9 dogs were treated with lidocaine after anesthesia. Lidocaine was given as a 2-mg/kg loading dose 10 minutes prior to ischemic arrest and a 2-mg/min continuous infusion during the entire experimental period. Biopsy samples of the left ventricular apex were taken 15 and 45 minutes after the start of ischemic arrest and 5 minutes after resumption of coronary blood flow. Biopsy samples were also obtained from 4 animals after thoracotomy to serve as controls for experimental procedures. Myocardial ultrastructure in the 4 control animals was comparable to that reported by other investigators. Five of 6 of the nontreated dogs and 8 of 9 lidocaine-treated dogs survived the entire period of ischemia and 5 minutes of coronary reperfusion. However, the extent of ultrastructural damage varied considerably between the two groups. In the experimental dogs receiving no lidocaine, mitochondria were swollen, cristae were absent, the mitochondrial matrix was cleared, and sarcomeres were disrupted. Myelin figures and contraction bands were also observed. None of the surviving lidocaine-treated animals had ultrastructural changes comparable to the worst ones in nontreated dogs. Damage was limited to some swelling of mitochondria with focal clearing of matrix. Most cristae remained intact. There were no myelin figures and few contraction bands. The results suggest that lidocaine protects the integrity of ischemic myocardium. It is suggested that this protection resulted from stabilization of plasma and/or mitochondrial membranes. (Am J Pathol 87:399-414, 1977).
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PMID:Reduction of ischemic myocardial damage in the dog by lidocaine infusion. 85 Nov 72

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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