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)

Tritiated leucine was injected into the vitreous of rhesus monkey eyes to make it available for protein synthesis by the ganglion cells. The short posterior ciliary arteries were cut three hours later or several weeks prior to the leucine injection. A reduction of labeled protein within the retrolaminar optic nerve was seen in all eyes so treated. Autoradiography revealed a diffuse reduction of axoplasmic transport into these optic nerve heads. There was consistent evidence of focal obstruction of labeled protein at the interface between the lamina scleralis and retrolaminar optic nerve. Vacuoles appeared in the most severely affected areas. These histologic changes were followed by gliosis in the areas of ischemic damage. Glaucomatous cupping of the optic nerve head was not seen within six weeks following the induced ischemia.
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PMID:The effect of interruption of the short posterior ciliary arteries on slow axoplasmic transport and histology within the optic nerve of the rhesus monkey. 5 49

(1) Using isolated, blood-perfused atrium preparation of dogs, the effect of ischemia on sinus rate was studied in ten preparations. Cessation of atrial perfusion usually induced gradual deceleration of the sinus rate which was not blocked by atropine. Occasionally, brief and slight sinus acceleration was initially observed in three of ten atrium preparations. This positive chronotropic effect was not blocked by a beta-adrenoceptor blocking agent, propranolol. (2) In every preparation, just after release of occlusion, there was an initial profound sinus deceleration, occasionally followed by oscillatory changes in sinus rate. (3) The chronotropic response pattern induced by temporary occlusion and release of the sinus node artery was not influenced by propranolol, phenoxybenzamine or atropine treatment. (4) These results suggest that ischemia exerts its principal effect directly on the sino auricular node pacemaker cells, rather than on neighboring nerve endings.
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PMID:Chronotropic responses to experimental ischemia of the canine sino auricular node. 6 Sep 77

Whole excis ed rat hearts were treated with 5, 10, or 15% (v/v) dimethyl sulfoxide/glycerol and then some were frozen in liquid nitrogen while the balance remained unfrozen. Freezing and thawing rates were approximately 30degreesC/min. Ventricular tissue was examined for histological damage, glycogen depletion, and enzyme sites, using histological, histochemical, and electron microscopy techniques. Early signs of cellular degeneration and ischemia were observed in all unfrozen groups; depletion of glycogen reserves, fuchsinophilic staining, vacuolization and granulation of the sarcoplasm were noted. Results from frozen groups were similar, but ultrastructural damage was more severe and extensive. Alkaline phosphatase and succinic dehydrogenase sites were abundant in unfrozen specimens and absent or markedly reduced in frozen specimens which also exhibited widespread nonspecific staining throughout intercellular spaces.
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PMID:Cryoprotectant-treated myocardium evaluation. 6 Nov 4

A vital dye solution injected intra-arterially stains only the viable parts in intestine of questionable viability. After various periods of ischemia, the viability of rat intestinal loops was assessed by three methods: on clinical basis; by detection of reactive hyperemia using an electronic thermometer; and by intra-arterial dye injection. The accuracy in viability prediction was 36, 69, and 84 per cent, respectively. The intraarterial dye injection method proved to be a simple, easy, and inexpensive way to accurately predict the viability of ischemic rat intestine.
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PMID:Prediction of intestinal viability by intra-arterial dye injection: a simple test. 6 17

The most commonly recognized cause of mesenteric venous thrombosis following splenectomy is hypercoagulation secondary to reactive thrombocytosis. A case is reviewed in which hypercoagulation followed splenectomy for idiopathic thrombocytopenic purpura (ITP) in spite of persistent thrombocytopenia. Episodic mesenteric venous occlusion occurred due to antithrombin III deficiency. This hypercoagulable state may be the cause of primary acute mesenteric venous occlusive disease. Symptoms and signs suggesting thrombosis in the portal circulation demand immediate coagulation studies since even in the thrombocytopenic patient thrombotic proglems can occur. Surgical intervention is the treatment of choice for segmental small bowel ischemia; warfarin therapy is indicated when there is evidence of antithrombin III deficiency.
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PMID:Antithrombin III deficiency causing postsplenectomy mesenteric venous thrombosis coincident with thrombocytopenia. 6 57

Following superior mesenteric artery occlusion and revascularization in dogs all animals died in a circulatory collapse state. However, pretreatment by aminoguanidine, the strong and specific inhibitor of diamine oxidase, accelerated the circulatory break-down significantly and increased the venous plasma histamine concentrattions up to levels which also in normal dogs are effective in the circulatory system. Furthermore, the haematocrit increased significantly more in the aminoguanidine-treated animals than in the dogs treated by saline. No changes in plasma diamine oxidase activity were observed in saline-treated animals during intestinal ischemia and following revascularization. In aminoguanidine-treated animals no enzymic activity could be measured. The results were interpreted by a protective role of intestinal diamine oxidase in intestinal ischemia. Enhancement of the enzymic activity in patients, for instance by heparin, may be helpful in mesenteric infarction disease.
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PMID:Diamine oxidase activity and histamine release in dogs following acute mesenteric artery occlusion. 6 85

Left atrial-to-aortic (La-A) assistance is effective in supporting the failing circulation. This study evaluated its effect in salvaging ischemic myocardium in both large and small infarct models. In a control group, good correlation was shown between measurements of infarct size by ST-segment mapping at 20 minutes, triphenyl tetrazolium chloride staining at 5 hours, and the distribution of radioactive microspheres (P less than 0.01). A servo controlled assist pump was used which controlled pump speed according to the left atrial pressure. This allowed greater degrees of bypass for prolonged periods with reduced risk of air embolism. La-A assistance reduced systolic left ventricular pressure, and reduced the pressure time index (P less than 0.05). La-A assistance did not reduce infarct size measured by ST-segment mapping in a large infarct model when instituted before occlusion or 20 minutes after occlusion. Triphenyl tetrazolium chloride staining, however, showed less severe and homogenous damage in the assisted group as compared to controls. Electron microscopy confirmed the patchy nature of the ischemia. In a small infarct model, La-A assistance reduced nST from 6.3 +/- 0.8 to 3.8 +/- 1.5 and ST from 4.9 +/- 0.6 to 2.7 +/- 0.9 (P less than 0.05). The endocardial to epicardial ratio in the ischemic area fell from 0.69 +/- 0.05 to 0.43 +/- 0.05 in the control group (P less than 0.05) and a similar fall occurred in the assisted groups. La-A assistance is thus effective in reducing myocardial ischemia in a small infarct model, but appears to be less effective in a large infarct model.
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PMID:The effect of left atrial-to-aortic assistance on infarct size. 6 5

Lesions in skeletal muscle resulting from ischemia caused by peripheral vascular disease in two patients were essentially identical to the early muscle lesions of Duchenne muscular dystrophy (DMD) patients and carriers of that disease, as well as to the early muscle lesions of experimental animals with aorta ligations plus a small dose of 5-hydroxytryptamine (serotonin). The one similarity is harmonious with, although does not necessarily advance, the ischemia hypothesis of DMD, and the other supports the ischemia mechanism proposed in the animal model.
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PMID:Focal lesions of muscle in peripheral vascular disease. 6 85

It has been suggested that glaucomatous field loss may progress on the basis of ischemia of the optic nerve head alone after the intraocular pressure has been controlled. Bishydroxycoumarin (Dicumarol) has been reported to be of benefit in such situations. A review of 551 consecutive glaucoma records did not support this theory. Apparent progression of field loss at intraocular pressures of 20 mm Hg or less was either due to artifacts in field testing or to a pressure that was still too high. A pilot study suggested that bishydroxycoumarin was of no benefit in these situations.
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PMID:An evaluation of anticoagulation in glaucoma therapy. 7 Oct 7

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


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