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

The efficacy of surface cooling and intraluminal antiseptic solutions for short term preservation of intestinal segments in preparation for free tissue transfer were investigated. Five segments of the small intestine and five segments of the colon were allocated to each group as follows: group 1, ischemia at 37 degrees C.; group 2, ischemia at 6 to 12 degrees C., and group 3, ischemia at 6 to 12 degrees C. plus povidone-iodine intraluminally. Histologic grading of segments allowed assessment of the efficacy of short term protection against ischemic changes. Surface cooling effectively prevented histologic evidence of ischemia. No additional benefit was observed using povidone-iodine intraluminally. Significant changes in tissue water content and evidence of bacterial invasion were not observed.
 ...
PMID:Effects of cooling and intraluminally administered antiseptics on surgically induced ischemia of the intestine in dogs. 47 99

Acute ischemia was created by placing a tourniquet on the extremity or on a clamp on the kidney limb for a period corresponding to the critical metabolism level in the test tissue study. Restoration of circulation in the ischemic kidney led to the excessive accumulation of glucose high-molecular polymer of the glycogen type. The character of its branching in the molecule determined by the iodine complex spectrum pointed to the changes in the processes of glycogen biosynthesis. Lactate of the ischemic kidney could be used for the glycogenesis requirements. This anomalous glycogen was shown to be actively uptaken by the kidney tissue. Glycogen accumulation in the muscle tissue following acute ischemia failed to exceed the normal level, and its structure was unchanged.
 ...
PMID:[Glycogen metabolism in ischemic organs]. 70 66

Liver and spleen phagocytic clearance of blood-borne microparticulate tissue debris and products of intravascular coagulation after trauma and surgical injury is an important mechanism to limit the deposition of debris in the pulmonary vascular bed. Plasma fibronectin (pFn) modulates this clearance process. We evaluated the effect of a localized peripheral ischemia and reperfusion injury on liver and spleen phagocytic function. Male rats (250 to 350 g) underwent 4 hours of tourniquet-induced bilateral hindlimb ischemia, followed by 18 hours of reperfusion after release of the tourniquet. Rats subjected to ether anesthesia alone or anesthesia followed by groin incision without ischemia were the control and sham groups, respectively. Reticuloendothelial (RE) phagocytic function was assessed at 15 minutes and 18 hours after the start of reperfusion by the in vivo liver and spleen removal of blood-borne iodine 125 (125I)-test microparticles, which were coated with gelatin (denatured collagen) to enhance their interaction with pFn. Liver and spleen particle uptake in control and sham rats was similar. In contrast, after 4 hours of ischemic injury with 15 minutes of reperfusion, we observed a 30% to 40% decrease (p less than 0.05) in liver and spleen particle uptake as compared with sham controls with partial restoration of this removal mechanism by 18 hours. This depression in liver and spleen phagocytic function was associated with a significant (p less than 0.05) increase in the deposition of the 125I-test particles in the lung. RE depression was not due to a deficiency of pFn; indeed, a marked elevation (588 +/- 12 micrograms/mL versus 1,083 +/- 40 micrograms/mL) of pFn was observed by immunoassay over the 18-hour reperfusion interval. Comparative bioassay of humoral (opsonic) versus cellular (Kupffer's cell) activity revealed that Kupffer's cells in livers from controls or ischemia-reperfusion rats exhibited normal phagocytic function when incubated in plasma harvested from either control or 4-hour ischemic rats. The opsonic activity of plasma harvested after ischemia and reperfusion was also more than adequate, consistent with the immunoassay analysis. Thus, the impaired liver and spleen clearance mechanism after peripheral ischemia and reperfusion injury did not appear to be due to either a macrophage cellular deficit or a lack of pFn. This clearance depression may be mediated by splanchnic malperfusion, which is known to develop after peripheral ischemia and reperfusion and associated soft tissue injury.
 ...
PMID:Liver and spleen phagocytic depression after peripheral ischemia and reperfusion. 141 24

Reperfusion-induced vascular endothelial cell dysfunction may exacerbate skeletal muscle damage after an ischemic insult. Although concurrent endothelial and skeletal muscle injury has been documented after ischemia and reperfusion, their temporal relationship has not been well characterized. An isolated rat hindlimb model was used to measure the effect of progressive ischemia and reperfusion on both endothelial cell function and skeletal muscle damage. Endothelial cell dysfunction as reflected by changes in permeability was measured by protein clearance techniques with use of albumin labeled with iodine 125 (125I-albumin). Skeletal muscle damage was assessed by tissue uptake of technetium 99m pyrophosphate (99mTc-pyrophosphate). The soleus muscle was used for evaluation of endothelial and skeletal muscle damage throughout the study. Significant increases in vascular permeability preceded skeletal muscle damage. The protein leak index increased after 60 minutes of ischemia and reperfusion (7.5 +/- 1.2 vs 4.1 +/- 0.9 control), whereas the muscle injury index did not change until 120 minutes of ischemia and 60 minutes of reperfusion (10.5 +/- 0.6 vs 4.5 +/- 0.5 control). Significant graded increases in both indexes were noted with longer intervals of ischemia. Electron microscopy revealed ultrastructural evidence of endothelial and skeletal muscle damage after 120 minutes of ischemia and 60 minutes of reperfusion but not after 60 minutes of ischemia and reperfusion. These studies indicate that microvascular injury precedes skeletal muscle damage after ischemia and reperfusion. This temporal relationship may have important implications in designing strategies to minimize ischemia-reperfusion injury.
 ...
PMID:The temporal relationship between endothelial cell dysfunction and skeletal muscle damage after ischemia and reperfusion. 153 68

The purposes of this study were to characterize the temporal relationship of distant organ dysfunction after mesenteric ischemia/reperfusion (I/R), and to ascertain if the neutrophil is critical to this process. Normal and neutrophil-depleted rats (vinblastine sulfate, 0.75 mg/kg intravenously) underwent 45 minutes of superior mesenteric artery occlusion and after 0, 6, and 18 hours of reperfusion, blood was sampled and liver and lungs were harvested. Iodine 125 albumin leak was used as a marker for pulmonary and liver injury, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) was used as an index of hepatic mitochondrial redox state. Gut I/R at 6 hours increased 125I-albumin lung/blood ratio (gut I/R, 0.077 +/- 0.006; control, 0.045 +/- 0.004) and 125I-albumin liver/blood ratio (gut I/R, 0.120 +/- 0.007; control, 0.077 +/- 0.003), while AcAc/3-OHB decreased significantly (gut I/R, 0.420 +/- 0.040; control, 0.880 +/- 0.120). Neutrophil depletion eliminated these changes at 6 hours (blood AcAc/3-OHB, 0.720 +/- 0.100; 125I liver/blood, 0.068 +/- 0.006; 125I lung/blood, 0.046 +/- 0.007). We conclude the following: (1) intestinal I/R produces simultaneous liver and lung injury; (2) injury was present at 6 hours but is reversed at 18 hours; and (3) the I/R-induced liver and lung injuries were neutrophil mediated.
 ...
PMID:Liver injury is a reversible neutrophil-mediated event following gut ischemia. 154 95

We have previously shown that gut ischemia/reperfusion (I/R) causes simultaneous liver and lung dysfunction and that neutrophils play a critical role in this process. The purpose of this study was to ascertain whether xanthine oxidase (XO) was likewise operational. Normal and XO-inactivated rats (given a tungsten-enriched, molybdenum-depleted diet for 3 weeks) underwent 45 minutes of occlusion of the superior mesenteric artery, and control rats were subjected to a sham laparotomy. After zero and six hours of reperfusion, blood was sampled and livers and lungs harvested. Iodine-125-labeled albumin leak was used as a marker for pulmonary and liver capillary permeability barrier function, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) levels as an index of hepatic mitochondrial redox state. Gut ischemia/six hours of reperfusion (I/R) increased the 125I albumin lung/blood ratio and the 125I albumin liver/blood ratio; AcAc/3-OHB levels decreased significantly. Xanthine oxidase activation eliminated the observed lung and liver capillary leak as well as the hepatic metabolic derangement induced by gut I/R. In conclusion, the simultaneous lung and liver dysfunction produced by gut I/R is mediated by XO.
 ...
PMID:Simultaneous liver and lung injury following gut ischemia is mediated by xanthine oxidase. 161 31

Focal cerebral ischemia was produced by occluding the left middle cerebral artery in 769 rats. Permeability of the blood-brain barrier to small or large molecules was evaluated qualitatively using Evans blue or sodium fluorescein and quantitatively using the transfer indexes of iodine-125-labeled bovine serum albumin or [14C]sucrose. Water content was determined using wet and dry weights and sodium and potassium contents using flame photometry. Cortical tissue in the middle cerebral artery territory was sampled less than or equal to 14 days after occlusion. A significant increase in the albumin transfer index was first found 12 hours after occlusion, and the index remained approximately the same until water content peaked 3 days after occlusion. In contrast, the sucrose transfer index increased gradually, significantly correlated with increases in the water and sodium contents. Tissue staining by sodium fluorescein was more extensive than that by Evans blue. As edema fluid decreased gradually 4-10 days after occlusion, the albumin and sucrose transfer indexes increased markedly. These findings indicate that disruption of the blood-brain barrier to small molecules is accompanied by accumulation of edema fluid during the later stages of ischemia. Opening of the barrier to serum protein is probably related to the resolution of edema.
 ...
PMID:Brain edema and cerebrovascular permeability during cerebral ischemia in rats. 169 34

Excessive activation of excitatory amino acid receptors has been implicated in the neuronal degeneration caused by ischemia, hypoglycemia, and prolonged seizures. We have observed directly the time course and regional vulnerability of hippocampal neurons to glutamate receptor-mediated injury in organotypic hippocampal cultures, a preparation which combines accessibility and long-term survival with preservation of regional differentiation and neuroanatomic organization. Cultures were incubated with the fluorescent dye propidium iodide which selectively enters and stains cells only after membrane damage. After 5 to 10 min of a 30-min exposure to kainate (100 microM), large neurons in the hilus of the dentate were first to become brightly fluorescent. Propidium staining subsequently appeared in the other regions of the hippocampus and increased to a maximum over the first 6 h of recovery. NMDA (10 microM) caused propidium staining that was limited to CA1 and the dentate gyrus of the cultures, sparing CA3, consistent with the regions of highest NMDA receptor density in vivo. Glutamate (1 mM) caused a delayed, progressive pattern of staining that began in CA1 (2 to 4 h after exposure), then extended to include CA3 and finally the dentate gyrus over the next 24 h. Release of LDH activity into the media was slower and less sensitive than propidium staining. Histologic degeneration was limited to neurons 24 h after agonist exposure and was consistent with the propidium staining. NMDA, kainate, and glutamate each produced a unique pattern of neuronal injury. Most notably, glutamate had low potency as a toxin and its pattern of neuronal injury was not reproduced by NMDA.
 ...
PMID:Direct observation of the agonist-specific regional vulnerability to glutamate, NMDA, and kainate neurotoxicity in organotypic hippocampal cultures. 171 7

This study was designed to probe the hypothesis that oxygen-derived free radicals are involved in initiation of the no-reflow phenomenon. We developed a reproducible model of no reflow in the rat hind limb. Laser Doppler studies confirmed that the hind limbs perfused well after 2 or 4 hours of ischemia, but perfusion ceased in the first 10 minutes after 6 hours of ischemia. Venous blood samples and biopsy specimens of skin and muscle were taken after 2 and 4 hours of ischemia to study tissue injury. Blood samples were evaluated for xanthine oxidase (XO), xanthine dehydrogenase, and creatine phosphokinase (CPK) activities. Conjugated dienes and iodine 125-labeled albumin extravasation were quantified in tissue samples. Groups of animals were treated with inhibitors of XO (allopurinol), antioxidant enzymes (superoxide dismutase plus catalase), and free radical scavengers (dimethyl sulfoxide and dimethyl thiourea) to assess the roles of free radicals in ischemia-reperfusion injury in the hind limbs. After 4 hours of ischemia followed by reperfusion, plasma XO activity rose threefold over preischemia levels (p less than 0.05). Xanthine dehydrogenase activity did not change; conjugated diene levels in muscle rose twofold; CPK levels rose sixfold, and 125I albumin extravasation rose twofold (p less than 0.05). Pretreatment with the XO inhibitor allopurinol reduced XO activity to negligible levels and significantly attenuated conjugated diene levels, CPK levels, and albumin extravasation. Albumin extravasation was also significantly attenuated by pretreating animals with superoxide dismutase together with catalase, dimethyl thiourea, and dimethyl sulfoxide. In all animals pretreated with allopurinol or superoxide dismutase and catalase, reperfusion persisted after 6 hours of ischemia. These data suggest that, in ischemia followed by reperfusion, tissue injury is related to oxygen products derived from XO activity.
 ...
PMID:Xanthine oxidase: its role in the no-reflow phenomenon. 173 87

The synthetic acetylcholine analogue ethyl-3-(2,2-dimethyl-2-ethyl-hydrazinium) propionic iodide (EDIHYP) exerts a powerful antiarrhythmic action in cardiac ischemic, reperfusion, and adrenergic lesions, as well as in infarction and postinfarction cardiosclerosis, as evidenced by animal experiments. The study was undertaken to examine the electrophysiological mechanism of EDIHYP s action on isolated rat heart cardiomyocytes. It was shown that the agent substantially reduced the resting potential, as well as action potential amplitude and duration in total ischemia and resultant reperfusion. The antiarrhythmic changes provided a multiple decrease in the duration of ventricular tachycardia and cardiac fibrillation in reperfusion. Thus, the fact that EDIHYP has a direct action on the bioelectrical activity of cardiomyocytes may play an important role in its antiarrhythmic effect in the whole body.
 ...
PMID:[Bioelectrical mechanism of the anti-arrhythmia effect of a synthetic acetylcholine analog EDIHYP]. 177 21


1 2 3 4 5 6 7 8 9 10 Next >>