Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reperfusion injury following prolonged ischemia is thought to be caused primarily by microvascular failure. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution with Dextran 60 (hct 30%) could improve microvascular perfusion after 4 h of pressure-induced ischemia in skeletal muscle. In 28 Syrian golden hamsters (6-8 weeks/60-80 g b. wt.) a dorsal skinfold chamber and permanent arterial and venous catheters were implanted under Nembutal anesthesia (50 mg/kg b. wt.). Following a recovery period of 48 h pressure-induced ischemia was applied to the skeletal muscle within the skinfold chamber by means of a transparent stamp. Quantitative analyses of microhemodynamics were performed in the awake animal prior to and 15 min, 1, 2, 4 and 24 h after ischemia using vital fluorescence microscopy. In non-treated animals, functional capillary density decreased after 4 h of ischemia to 30% of the initial values (P less than 0.001); after 24-h reperfusion only 50% of the initially perfused capillaries were reperfused (P less than 0.001). The heterogeneity of functional capillary density increased after ischemia to a maximum of 2.19 +/- 0.94 as compared to 0.48 +/- 0.11 prior to ischemia. Capillary RBC-velocity suffered a marked reduction in the early reperfusion phase and did not recover up to the 24-h observation time. In contrast, prophylactic isovolemic hemodilution was associated with only a small and reversible reduction of functional capillary density after 4-h ischemia. At 24-h reperfusion 90% of the initially perfused capillaries were reperfused. Capillary RBC-velocity was reduced in the early reperfusion phase, but returned to normal values within 24 h. Thus, prophylactic isovolemic hemodilution resulted in a marked reduction of microvascular reperfusion failure in skeletal muscle. A hematocrit lower than normal prior to ischemia provides better conditions for capillary reperfusion after prolonged ischemia.
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PMID:Quantitative analysis of microcirculatory disorders after prolonged ischemia in skeletal muscle. Therapeutic effects of prophylactic isovolemic hemodilution. 342 Feb 98

Though the delivery of elemental oxygen to tissues ravaged by anaerobic infection may be useful, little data exists that suggests that such therapy may benefit ischemic tissue. We report the development of a model to test the question that peritoneal lavage with an oxygen containing solution may favorably influence occlusive intestinal ischemia. Adult Sprague-Dawley rats with Nembutal (sodium pentobarbital) anesthesia underwent midline laparotomy; a microvascular clamp was applied to the superior mesenteric artery (SMA); and an inflow and outflow lavage catheter was placed. Treatment groups included control rats undergoing SMA occlusion only without lavage, rats lavaged with albumin during SMA occlusion (medium control), and rats lavaged during SMA occlusion with oxygenated perfluorochemical FC-47 emulsified in albumin (O2-FC-47). The increase in serum L-lactate following occlusion was used as an index of intestinal injury whether the perfusate was maintained at room temperature (28 degrees C) or body temperature (37 degrees C). Beginning with time O, which corresponded to the time of unclamping, subsequent samples were collected at 15, 30, and 60 minutes after a 30-minute SMA occlusion. Sequential lactates in 13 control rats were 4.18, 4.10, 3.88, and 4.52 mmol/L. Albumin lavaged animals had values at 28 degrees C of 2.23, 1.35, 1.8, and 2.44 mmol/L and values at 37 degrees C of 2.22, 1.40, 2.07, and 3.21 mmol/L, respectively. With O2-FC-47 lavage the respective lactates were 1.89, 1.09, 1.32, and 1.44 mmol/L at 28 degrees C and 2.14, 2.19, 2.50, and 2.1 mmol/L at 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal ischemia: treatment by peritoneal lavage with oxygenated perfluorochemical. 344 Sep 10

It is known that pentobarbital, which has been used for severe brain infarct or head injury as a brain protective drug, inhibits the increase of free fatty acids (FFAs) liberated from membrane phospholipids during ischemia. However, the mechanisms of FFA liberation from phospholipids and the mode of action of pentobarbital are still unclear. Therefore we have investigated the effects of induction of global ischemia and pentobarbital pretreatment upon lipid metabolism in rat brain. Brain ischemia was evoked by rat decapitation and pentobarbital (60 mg/kg) was administered i.p. for 15 min prior to decapitation. Removed brains were incubated for 1, 5, 15 or 30 min at 37 degrees C and then quickly frozen in liquid nitrogen. After extraction of lipids from the brains, neutral lipid and phospholipid compositions were analyzed by thin-layer and gas-liquid chromatography. The results demonstrated that FFAs, either unsaturated or saturated, were rapidly accumulated in the brain during early period of ischemia, but attenuated significantly by pentobarbital pretreatment. Pentobarbital attenuated the accumulations of stearic and arachidonic acids, with little effect on palmitic and oleic acids. Diacylglycerol (DG), which is considered to be as a plausible candidate for the source of FFA, was also produced in the ischemic brain, and its acyl chain composition was similar to that of liberated FFAs. Furthermore, the increase of DG was inhibited significantly by pentobarbital anesthesia. In particular, pentobarbital attenuated the accumulation of DG enriched in arachidonic and stearic acids. This fatty acyl composition resembled the principal composition of phosphatidylinositol (PI) in rat brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of pentobarbital on brain lipid metabolism during global ischemia]. 373 Feb

The time course of the reduction in brain protein synthesis following transient bilateral ischemia in the gerbil was characterized and compared with changes in a number of metabolites related to brain energy metabolism. The recovery of brain protein synthesis was similar following ischemic periods of 5, 10, or 20 min; in vitro incorporation activity of brain supernatants was reduced to approximately 10% of control at 10 or 30 min recirculation, showed slight recovery at 60 min, and returned to 60% of control activity by 4 h. Protein synthesis activity was indistinguishable from control at 24 h. One minute of ischemia produced no detectable effect on protein synthesis measured after 30 min reperfusion; longer periods of ischemia resulted in progressive inhibition, with 5 min producing the maximal effect. Pentobarbital (50 mg/kg) increased by 1-2 min the threshold ischemic duration required to produce a given effect. Whereas most metabolites recovered quickly following 5 min ischemia, glycogen showed a delayed recovery comparable to that seen for protein synthesis. These results are discussed in relation to possible mechanisms for the coordinate regulation of brain energy metabolism and protein synthesis. An improved method for the fluorimetric measurement of guanine nucleotides is described.
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PMID:Changes in brain energy metabolism and protein synthesis following transient bilateral ischemia in the gerbil. 396 20

The effect of indomethacin on rCBF was studied in cats anesthetized with Nembutal either under resting conditions or with temporary middle cerebral artery (MCA) occlusion. RCBF was measured by the microsphere method. In control animals (n = 3), indomethacin (4 mg/kg, i.v.) significantly reduced rCBF by about 25% in both cortex (from 44 +/- 6 to 32 +/- 3 ml/100 g/min, p less than 0.001) and white matter (from 36 +/- 4 to 26 +/- 2 ml/100 g/min, p less than 0.001). After MCA occlusion rCBF was markedly decreased in the sylvian region ipsilateral to occlusion (ischemic core) (from 38 +/- 4 to 14 +/- 2 ml/100 g/min in cortex, 4 animals). Although pretreatment with indomethacin (4 mg/kg) (4 animals) 30 min prior to occlusion did not alter rCBF during ischemia, a marked enhancement of reactive hyperemia was observed in the ischemic core immediately upon reperfusion following 2 h occlusion (54 +/- 11 untreated vs 95 +/- 13 treated, p less than 0.05). In the delayed postischemic period, namely 2 h after recirculation, rCBF still remained to be higher in the animals treated with indomethacin (40 +/- 6 untreated vs 96 +/- 9 treated, p less than 0.001). Such an effect of indomethacin for ameliorating postischemic blood flow in both the immediate and delayed period was less prominent in the adjacent area (penumbra) ipsilateral to occlusion. In the contralateral hemisphere, indomethacin caused slight reduction in rCBF during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of indomethacin on rCBF during and after focal cerebral ischemia in the cat. 397 61

The influence of a new eburnamenine derivative RU 24722 [(3 beta, 14 alpha, 16 alpha)-(+/-)-14,15-dihydro-20,21-dinoreburnamenin -14-ol] on post-ischemic EEG recovery was studied in N2O anesthetized rats subjected to 1 min of global-compression cerebral ischemia. RU 24722 was compared with vincamine, dihydroergotoxine mesylate and nicergoline. Treatment with RU 24722 (2 mg/kg i.v.) significantly decreased the EEG recovery time and increased the electrocortical activity during the first phase of the post-ischemic recovery. Vincamine (2 mg/kg i.v.), dihydroergotoxine mesylate (0.5 mg/kg i.v.) and nicergoline (0.5 mg/kg i.v.) were devoid of activity. In an attempt to elucidate its mechanism of action, the influence of RU 24722 on changes in the cerebral metabolic energy reserves was studied in mouse brain after different periods of decapitation ischemia. The changes occurring during the first 10 s of ischemia were used to calculate the baseline cerebral metabolic rate (CMR). The activity of RU 24722 was compared with that of vincamine and pentobarbital. RU 24722 (10 mg/kg i.p.) significantly retarded glucose, phosphocreatine and adenosine triphosphate utilisation and lactate production. Vincamine (10 mg/kg i.p.) had no effect on cerebral energy substrates. Pentobarbital (100 mg/kg i.p.) markedly increased the tissue concentration of glucose and phosphocreatine and decreased lactate levels before and after ischemia. The improvement of EEG recovery suggests that RU 24722 may be therapeutically effective in cerebral insufficiency, and the decreased brain energy demand may be one of the mechanisms by which RU 24722 has a protective effect against cerebral ischemic damage.
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PMID:Effects of the new eburnamenine derivative RU 24722 on EEG recovery and cerebral energy metabolism after complete ischemia. 403 69

Glucose consumption and regional blood flow were determined using the [14C]-2-deoxyglucose (2-DG) method and microspheres in the optic nerve, the retina and different parts of the brain in monkeys. The relationship between the 2-DG accumulation and blood flow in the optic nerve head region was similar to that in grey matter of the brain under pentobarbital anaesthesia as well as under urethan anaesthesia. Pentobarbital anaesthesia resulted in lower values for blood flow and glucose metabolism in most regions. In the optic nerve the highest values were observed in the distal part; there was a fall in blood flow and metabolism along the nerve. There was a corresponding increase in myelin content. Artificial increments in intraocular pressure resulting in a perfusion pressure (mean arterial pressure minus intraocular pressure) of 40 cm H2O had no appreciable effect on the 2-DG accumulation. At a perfusion pressure of 20 cm H2O 2-DG accumulation in the retina and prelaminar part of the optic nerve was markedly increased indicating partial ischemia resulting in anaerobic glycolysis. At intraocular pressures higher than the systolic arterial blood pressure there was still some accumulation of 2-DG in the intraocular tissues, but no blood flow, which indicates that glucose could diffuse into the eye through the sclera. Behind the lamina cribrosa there was no indication of a reduction in blood flow or a metabolic disturbance. The results indicate that the blood flow and metabolism of the retina and prelaminar part of the optic nerve is disturbed only at very high intraocular pressures, and that even at extreme pressures there is no disturbance behind the lamina cribrosa in acute experiments. The 2-DG method will be useful in further studies on the nutritional status of the optic nerve head since it can detect abnormal glycolysis even in very discrete regions due to its high spatial resolution.
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PMID:Blood flow and glucose consumption in the optic nerve, retina and brain: effects of high intraocular pressure. 409 55

Effect of nizofenone on pyramidal response (PR), electrocorticogram (ECoG) and regional cerebral blood flow (rCBF) following recirculation after complete global brain ischemia was compared with that of pentobarbital in gallamine-immobilized cats. The basilar artery and the branches of both carotid arteries (superior thyroid artery, dorsal muscular branch, internal carotid artery, occipital artery and ascending pharyngeal artery) were all ligated. The cats were subjected to complete brain ischemia by occluding both common carotid arteries for 45 min, followed by 180 min recirculation. rCBF of the cortex (suprasylvian gyrus) and the internal capsule was monitored by the hydrogen clearance method. Blood gases were regulated within a range determined previously in freely-moving cats throughout the experiment. Nizofenone (1 mg/kg, i.v.) facilitated the recovery of PR and ECoG, and it inhibited the phenomenon of secondary suppression evidenced by interruption and reversion of the recovery process. rCBF showed good recovery throughout the recirculation period. Pentobarbital (20 mg/kg, i.v.) facilitated the recovery of PR during the early period of recirculation, but secondary suppression of PR, associated with the decline of rCBF, was evident. These results suggest that the ameliorative effect of nizofenone on the recovery of neuronal functions is due to its ability to protect neurons against ischemic anoxia and to prevent interruption of postischemic circulation, and also the good recovery of rCBF is due to its ability to protect vasculature against ischemic anoxia.
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PMID:[Effect of nizofenone on pyramidal response, electrocorticogram and regional cerebral blood flow following recirculation after complete global brain ischemia in cats]. 651 84

We previously reported that whole-brain free fatty acids (FFA) rose almost linearly for up to 1 h after decapitation of unanesthetized rats and was significantly attenuated by pentobarbital anesthesia. However, our values for total FFA and arachidonic, stearic, oleic, and palmitic acids were severalfold higher than those obtained by previous investigators. Based upon the suggestion that this may be due to FFAs released from di- and triglycerides in the quantitation of FFAs, we have now analyzed and improved our procedures for TLC separation of FFA and reassessed the accumulation of FFA in whole brain during decapitation ischemia in unanesthetized and pentobarbital-anesthetized rats. FFA levels in whole brain after 0.5 min of ischemia were one-half to one-fourth the levels previously reported after 1 min of ischemia. The rise in FFA between 0.5 and 60 min of ischemia was 9-fold for total FFA, and between 7 and 12-fold for each of the FFAs quantitated. Pentobarbital significantly attenuated the rise of all FFAs with, however, greater effects on oleic and palmitic acids than previously reported.
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PMID:Reassessment of brain free fatty acid liberation during global ischemia and its attenuation by barbiturate anesthesia. 682 83

Uteroplacental ischemia is associated with uterine renin release in pregnant nephrectomized rabbits. In the present study, uterine and renal renin release after uteroplacental ischemia were investigated in 10 Australian white rabbits at 24 to 28 days' gestation. Pentobarbital was administered, and both uterine arteries were ligated close to their origins. Blood samples were taken for plasma renin activity (PRA) determinations from the femoral artery, uterine vein, and right renal vein before ligation and at 30 and 60 minutes after ligation. Mean arterial blood pressure (MAP) was monitored throughout. In five additional pregnant rabbits renal blood flow (RBF) was measured with an electromagnetic flowmeter. The preligation uterine vein-artery PRA difference was not significant (1.9 +/- 1.1 ng/ml/hr). Postligation uterine vein-artery PRA was 11.4 +/- 3.2 at 30 minutes and 6.6 +/- 1.9 ng/ml/hr at 90 minutes (p less than 0.02). Preligation renal vein-artery PRA was 32.3 +/- 10.5 ng/ml/hr (p less than 0.02) and did not change significantly after ligation. MAP remained stable and RBF was unchanged after uterine artery ligation. These observations confirm the finding that the kidney is the primary source of renin in the normal pregnant rabbit and demonstrate that following acute uteroplacental ischemia there is significant uterine renin release even when the kidneys are intact.
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PMID:Uterine and renal renin release after ligation of the uterine arteries in the pregnant rabbit. 698 78


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