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

Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.
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PMID:Catecholamines in experimental brain ischemia. 23 32

The effect of ischemia on renal blood flow (RBF) in the rat has been an unsettled question. This study used a totally extractable indicator, radioactive microspheres, with a reference arterial sample, to study RBF quantitatively 10 and 60 min after 1 h of unilateral renal artery clamping in anesthetized, heparinized rats. The results indicate that after release of the arterial clamp, the kidney is enlarged and exhibits an increase in renal vascular resistance. RBF to the contralateral non-ischemic kidney is not different from that of a time-control series.
Nephron 1978
PMID:Effect of ischemia on renal blood flow in the rat. 67 90

As soon as there is evidence of left ventricular dysfunction, even before clinical signs of chronic cardiac failure (CCF) have developed, intrinsic and extrinsic compensatory mechanisms are brought into play by the body. The majority of these mechanisms are under the influence of neurohumoral systems. When neurohormonal responses persist, as in CCF, they take on a beneficial nature since they participate in adaptation of the cardiovascular system as a whole, but they are also harmful since they worsen the working conditions of the myocardium by their cardiac and peripheral effects. Hyperactivity of the noradrenergic sympathetic nervous system is seen in CCF with levels 2 to 3 times higher as compared with subjects with normal left ventricular function. The circadian rhythm of catecholamines is modified. The increase in circulatory catecholamines is all the greater when cardiac failure is advanced. This release of noradrenaline (NA) is under the control of arterial baroreceptors which normally send to the central nervous system inhibitory inflow from the sympathetic nervous system. Inhibitory tone is released in case of a fall in blood pressure. Noradrenaline acts on beta-predominant myocardial receptors (inotropic and tachycardic) and alpha-predominant vascular receptors, resulting in arteriolar vasoconstriction. There is rapid onset of down regulation of myocardial beta-receptors. This fall essentially concerns beta 1, but beta 2 also, since they may be affected according to the etiology of CCF (ischemia). The Renin Angiotensin System (RAS) is also activated by the fall in systemic blood pressure. This consists of a cascade of reactions leading to the synthesis of angiotensin II responsible for powerful vasoconstriction of all arterial areas, including the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes in cardiac failure]. 130 Sep 20

Phospholipase A2 (PLA2) activity results in the formation of lysophospholipids and free fatty acids which may contribute to ischemic myocardial dysfunction. We evaluated the cardioprotective activity of two putative PLA2 inhibitors, quinacrine and 7,7-dimethyleicosadienoic acid (DEDA), in isolated globally ischemic rat hearts. Pretreatment with 1, 5 and 50 microM quinacrine before ischemia did not alter coronary flow but did cause significant cardiodepression. Twenty five minutes of global ischemia and 30 min of reperfusion caused severe myocardial dysfunction and lactate dehydrogenase release. Quinacrine significantly improved reperfusion contractile function and reduced lactate dehydrogenase release, indicative of cardioprotection. In contrast, 30 to 100 microM DEDA produced neither preischemic cardiodepression nor cardioprotective activity. PLA2 inhibition was inferred from measurements of the prostacyclin metabolite, 6-keto-prostaglandin F1 alpha in the coronary effluent and myocardial palmitoyl-lysophosphatidylcholine. Quinacrine and DEDA reduced both 6-keto-prostaglandin F1 alpha and palmitoyl-lysophosphatidylcholine by similar degrees. These results suggest that the cardioprotective activity of quinacrine is independent of PLA2 inhibition. A possible role of calcium inhibition was investigated in rat aortic smooth muscle strips. Norepinephrine-, KCl- and BAY K8644-induced contractions were antagonized in the presence of 5 and 50 microM quinacrine, but were unaffected by 30 to 60 microM DEDA. The ability of quinacrine to inhibit calcium was investigated further in cardiac ventricular myocytes. Measurement of mean whole cell calcium currents showed that quinacrine (5 microM) could inhibit this current up to 70%. Thus, these results suggest that quinacrine-induced cardioprotection may not be due to PLA2 inhibition, but may be related to calcium entry blocking activity.
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PMID:Effect of the phospholipase A2 inhibitors quinacrine and 7,7-dimethyleicosadienoic acid in isolated globally ischemic rat hearts. 138 29

We investigated the incidence of painless (silent) myocardial ischemia, manifested as S-T segment deviation, by Holter ECG monitoring in patients with chronic renal failure undergoing regular hemodialysis. Forty-five patients underwent Holter ECG monitoring for a continuous 48-hour period covering dialysis and the intermediate period of everyday activity at home. ECG criteria for ischemia were found in 15.5% of patients mainly during and immediately after dialysis with a simultaneous increase of R,S,R + S amplitude. There was no correlation of S-T segment deviation with the existence of cardiac dysfunction and coronary artery disease proved by hemodynamic and angiographic studies. It is concluded that hemodialysis itself seems to play an important role in the genesis of the above ECG findings, possibly by means of serum K and Mg changes.
Nephron 1992
PMID:Painless myocardial ischemia in chronic hemodialysed patients: a real event? 155

Local anesthetic agents in high concentrations may cause local irritation by ischemia especially after the use of adrenaline whereas felypressin has no tissue-irritating properties. Adrenaline but not felypressin increases the intravenous systemic toxicity. Noradrenaline has to be avoided as a vasoconstrictor. An aspiration test before injection will decrease the risk of inadvertent intravenous injection.
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PMID:[Can choice of medications and adjuvants reduce risks of local anesthetic complications?]. 187 40

The effects of the calcium antagonists verapamil, gallopamil, nifedipine, felodipine and diltiazem on noradrenaline release during ischemia were studied in isolated perfused rat hearts. Endogenous levels of noradrenaline and its intraneuronal metabolite dihydroxyphenylethyleneglycol (DOPEG) were determined by high pressure liquid chromatography. Global isothermic ischemia of 20 min caused a release of endogenous noradrenaline amounting to 180 +/- 15 pmol/g. The calcium antagonists tested significantly suppressed ischemia-induced noradrenaline release (IC50 in mumols/l: verapamil 1, gallopamil 0.3, nifedipine 1, felodipine 3). Noradrenaline release during ischemia and the inhibitory effect of the calcium antagonists, were independent of extracellular calcium, indicating a nonexocytotic release mechanism. Interaction of the calcium antagonists with the major components of nonexocytotic release, intraneuronal storage and carrier-mediated transport, was tested in normoxic rat hearts. Vesicular storage was not stabilized by the calcium antagonists. In fact, verapamil, gallopamil, diltiazem and felodipine disturbed storage function, as indicated by an increased DOPEG release. Direct interaction with the noradrenaline carrier (uptake1) was demonstrated for verapamil, gallopamil, and diltiazem in a model of 3H-noradrenaline uptake. In conclusion, the calcium antagonists investigated inhibit noradrenaline release in ischemia by a mechanism which is different from blockade of neuronal calcium influx, and is rather due to an interaction with carrier-mediated transport of noradrenaline across the plasma membrane.
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PMID:Calcium antagonists and cardiac noradrenaline release in ischemia. 188 Aug 12

In this study, 16 patients matched with 16 controls were hypnotized prior to angioplasty. The hypnotized patients had a 25% increase in the time the cardiologist was able to keep the balloon inflated compared to the controls. Of the hypnotized patients, 13% required additional narcotic pain medication during the procedure as compared to 44% for the controls. Although we found no differences in rhythm, ischemia, blood pressure, or pulse between the two groups, the results of arterial catecholamine levels drawn at the start and at the end of the procedure were unexpected and seemed paradoxical. Norepinephrine levels were significantly higher in the hypnotized group (432 pg/ml, SE 51) than in the control group (281 pg/ml, SE 23) at the start of the procedure and fell more during the procedure than in control patients. Because catecholamines reportedly act as a barometer of neuroanxiety, further studies defining their role are needed.
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PMID:Use of hypnosis before and during angioplasty. 195 Nov 41

Larger NMR magnets with relatively high field strengths have become available recently, allowing the application of magnetic resonance spectroscopy (MRS) in larger mammalian organs. The aim of this study was to develop and test a new and simple kidney perfusion model from slaughterhouse swine using a new 4.7-tesla/40-cm diameter system, with the intention behind to provide a human-like mammalian experimental kidney perfusion model, and to avoid sensitive in vivo animal experiments on higher-developed mammalians, 35 pig kidneys obtained 10-15 min post mortem were studied to evaluate and define conditions for optimum metabolic preservation with the following perfusion protocols: (1) immediate plegia with cold Collins solution, 1-3 h cold storage, P-31 MRS; (2) immediate plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (3) immediate blood reperfusion, plegia, 1-3 h cold storage, blood reperfusion, P-31 MRS; (4) immediate blood reperfusion, plegia, 24 h cold storage, blood reperfusion, P-31 MRS, P-31 MRS at 81 MHz with a double-tuned surface coil yielded the following results: [table: see text] Blood flow showed a weak correlation with beta-ATP/inorganic phosphate in protocols 3 and 4 of r = 0.64. Repeated reperfusion and ischemia experiments of this model allowed the on-line observation of the metabolic response of the energy phosphate pattern for several hours. In conclusion, slaughterhouse-harvested swine kidneys lend themselves to a simple, low-cost in vitro perfusion model, provided they are reperfused with arterial blood immediately after harvesting.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1991
PMID:Application of P-31 nuclear magnetic resonance spectroscopy to a new experimental kidney perfusion model using cadaveric porcine kidneys from slaughterhouse. 201 76

Recently we reported that maintaining rats on restricted dietary protein regimens prior to renal ischemia will significantly improve postischemic survival rates. This effect required a week or more of maintenance on a restricted protein diet prior to the renal insult and appeared to be independent of the postischemic dietary protein regimen. The present study was designed to evaluate the role of systemic toxicity in this protection. Adult male Sprague-Dawley rats were pair-fed by weight on restricted or high isocaloric protein diets for 8-10 days prior to 45 min of renal ischemia induced by renal pedicle clamping. When placed on a normal dietary protein regimen immediately following ischemia, the rats preconditioned to restricted dietary protein exhibited significantly less acidosis, less hyperkalemia, lower blood urea nitrogen values, and improved survival rates compared with rats preconditioned on a high dietary protein regimen. In order to separate the possible effects of prior dietary protein regimen on acute tubular necrosis suffered during renal ischemia from its effects on the uremic response, bilateral nephrectomies were performed on rats preconditioned for 14 days to low, normal, and high dietary protein regimens. Although all of the rats were placed on the same dietary protein regimen immediately following bilateral nephrectomy, those that had previously been on a lower dietary protein regimen exhibited a significantly reduced uremic response and lived longer. These findings indicate that dietary protein regimen prior to renal ischemia is a risk factor which can have a significant lingering effect on the severity of postischemic systemic toxicity.
Nephron 1990
PMID:Dietary protein regimen prior to renal ischemia significantly affects the postischemic uremic response. 237 Sep 27


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