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)

At the present time ergotism is due primarily to excessive use or abuse of ergot preparations for migraine headaches. The diagnosis may be made with the evidence of vascular ischemia in the presence of a history of migraines and its treatment with this drug. The therapy for the vasospasm is directed chiefly at the discontinuation of the ergot preparation, with further treatment aimed at the relief of symptoms or prevention of complications. A case is presented of lower extremity ischemia with impending gangrene of both feet in a patient with a history of chronic schizophrenia. Arteriograms revealed symmetrical vasospasm in the lower extremities as well as spasm of the superior mesenteric artery and its intestinal branches. This is believed to be the first documented case of mesenteric vasospasm due to ergotism. Treatment was instituted with low molecular weight dextran, tolazoline, and reserpine with rapid and complete resolution. Caution is advised in the use of ergot preparations in neuropsychiatric disorders.
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PMID:Mesenteric and peripheral vascular ischemia secondary to ergotism. 83 86

Two patients with retroperitoneal fibrosis demonstrated symptoms of peripheral vascular ischemia. Arteriolysis to free the distal aorta and iliac vessels was successful in both patients. Aortography in the posteroanterior view was equivocal, but the accompanying urologic abnormalities and a history of methysergide ingestion helped establish the etiology of the ischemia. The most direct approach to the treatment of the vascular obstruction caused by retroperitoneal fibrosis is complete arteriolysis. Most previous reports indicate that it is relatively easy to establish a dissection plane between the fibrotic plaque and the vessel wall. We found that the fibrotic process invaded the vessel wall. Accordingly, the surgeon must anticipate a difficult, tedious dissection when performing arteriolysis for the treatment of vascular compression secondary to retroperitoneal fibrosis.
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PMID:Peripheral ischemia due to retroperitoneal fibrosis. 87 Nov 93

Ischemia and reperfusion alter the reactivity of large coronary arteries, but the effect of ischemia and reperfusion on the coronary microcirculation has been less well defined. Elevated circulating levels of vasopressin are associated with cardiopulmonary bypass and numerous other clinical states in which vascular ischemia and reperfusion may occur. We examined the effects of ischemia with and without reperfusion on the responses to vasopressin of both large coronary arteries and coronary arterial microvessels. Studies were performed on vessels from control dogs (n = 8), dogs undergoing 1 hour of ischemia only (n = 8), and dogs undergoing 1 hour of ischemia followed with 1 hour of reperfusion (n = 9). Rings of proximal obtuse marginal coronary arteries distal to the site of circumflex coronary artery occlusion were studied in isolated organ chambers. Coronary microvessels (110 to 220 microns in diameter) were studied in a pressurized (20 mm Hg), no-flow state with a microvessel imaging apparatus and electronic dimension analyzer. Microvessels were preconstricted with the thromboxane A2 analog U46619. Responses of large vessel rings were studied in the nonpreconstricted state and after preconstriction with prostaglandin F2 alpha. Large vessel response to vasopressin was minimal and not altered by ischemia with or without reperfusion. In contrast, ischemia markedly affected the coronary microvascular response to vasopressin (10 to 1000 microU/ml). Control coronary microvessels constricted minimally to vasopressin (4% +/- 2% of the baseline diameter), while microvessels after either ischemia alone or ischemia followed by reperfusion constricted 22% +/- 5% and 21% +/- 3%, respectively (p less than 0.05 versus control for both). Hemoglobin, which inactivates the endothelium-derived relaxing factor, augmented microvascular constrictions to vasopressin in all groups to a similar extent. Relaxations to the endothelium-independent agent nitroglycerin were not altered by ischemia. Constrictions of the coronary microcirculation to vasopressin in conditions such as cardiopulmonary bypass or myocardial ischemia, in which circulating levels of vasopressin are increased, may predispose to persistent myocardial ischemia in the perioperative setting.
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PMID:Altered effects of vasopressin on the coronary circulation after ischemia. 149 97

This patient demonstrates that peripheral vascular ischemia and gangrene may complicate the use of intraarterial vasopressin in the absence of catheter-related phenomena such as microemboli or catheter dislodgement. Discontinuation of vasopressin effectively reverses ischemic changes. Sympathetic blocking agents or direct-acting vasodilators may accelerate the reversal of the vasopressin induced ischemia. In the patient with a history of previous extremity cold injury, vasopressin may precipitate severe ischemia or gangrene by its direct effect at the arteriolar level in an extremity with already increased sympathetic vascular tone. Peripheral circulatory status must be assessed frequently during vasopressin infusion especially in patients with a history of frostbite.
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PMID:Upper extremity gangrene secondary to superior mesenteric artery infusion of vasopressin. 697 39

One of the ulcerogenic mechanisms by which ethanol induces mucosal lesions in the stomach is the depression of gastric mucosal blood flow (GMBF). The goal of this study was to determine whether lesion formation is the result of vascular ischemia alone or ischemia combined with congestion. The aims of this study were to answer this question by evaluating the relationship between GMBF, oxygen saturation (ISO2) and hemoglobin volume (IHb) in the gastric mucosa under the influences of ethanol and prostaglandin E2 (PGE2) in the ischemic and congestive states, using a laser Doppler flowmeter and tissue spectrum analyzer. Ligation of the gastric celiac artery or vein markedly decreased the GMBF and the ISO2 level. The former procedure also reduced but the latter increased the IHb level. Ethanol administration produced effects similar to venous ligation, i.e. vascular stasis with ischemia. There was a negative correlation between GMBF and severity of lesion formation after ethanol administration. However, at the lesion site all the hemodynamic parameters were significantly reduced, indicating that a necrotic condition had occurred. PGE2 preincubation (25 micrograms) elevated GMBF, ISO2 and IHb levels. It also alleviated the reduction of blood flow induced by ethanol and increased the recovery rate of GMBF and ISO2 after the release of arterial or venous ligation. It is concluded that the decrease in blood flow due to ethanol is probably caused by constriction of venules rather than arterioles inside the mucosa, and this effect could lead to vascular congestion. PGE2 probably dilates both arterioles and venules in the gastric mucosa and thereby increases the blood flow in the gastric mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of hemodynamic changes in rat stomachs by laser Doppler velocimetry and reflectance spectrophotometry. Effects of ethanol and prostaglandin E2 under ischemic and congestive conditions. 770 51

In 14 in situ canine renal transplants, intracellular phosphorus metabolites were evaluated by phosphorus-31 magnetic resonance spectroscopy (31P-MRS), performed using surface coils to investigate the usefulness of this technique for assessing renal viability in situ. Group I control kidneys (n = 5) were autografts, as were Group II (n = 5) kidneys: the latter group were subjected to surgically induced vascular ischemia and thrombosis. Group III kidneys (n = 4) were rejecting allografts. Renal flow and function, as measured by 99mTc-DTPA, and findings on histologic examination were correlated with 31P-MRS spectra. Group I kidneys showed excellent viability on both 99mTc-DTPA studies and biopsy evaluation, and their 31P-MRS-derived ratios of phosphomonoesters/inorganic phosphate (PME/Pi) and adenosine triphosphate/Pi (ATP/Pi) were high (1.32 +/- 0.23 and 0.90 +/- 0.36, respectively). In contrast, Group II kidneys demonstrated poor flow and function, histologic evidence of severe ischemia from venous and arterial thrombosis, and significantly (P < 0.005) less viability than controls, as monitored by 31P-MRS PME/Pi (0.58 +/- 0.30) and ATP/Pi (0.20 +/- 0.13) ratios. Group III kidneys also demonstrated poor flow and function with 99mTc-DTPA, and the associated histologically injury was noted to be caused by accelerated rejection and severe vascular damage. PME/Pi (0.24 +/- 0.22) and ATP/Pi (0.10 +/- 0.01) ratios were also significantly (P < 0.005) less than those in controls, reflecting nonviability. The 31P-MRS-derived PME/Pi and ATP/Pi ratios enable a qualitative noninvasive assessment of blood flow-dependent renal viability, but with currently used localization techniques the differentiation between severe ischemia and severe acute rejection was not possible.
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PMID:Assessment of in situ renal transplant viability by 31P-MRS: experimental study in canines. 838 89

The findings of several authors suggest that alterations in cochlear vascular physiology may contribute to noise-induced hearing loss. Although the influence of noise on cochlear microcirculation is controversial, recent investigations have identified a number of microvascular alterations during noise exposure. Researchers, using intravital microscopy, a technique which offers the advantage of continuous in vivo observation of cochlear lateral wall vessels, have observed alterations in red blood cell velocity and capillary vasoconstriction within the cochlea during exposure to noise. These alterations were sufficient to induce localized periods of stasis, alterations in vascular permeability, and local ischemia. It is possible that such noise-induced vascular ischemia may result in reduced auditory sensitivity.
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PMID:Cochlear vascular changes in response to loud noise. 858 26

Diabetes is a major risk factor for coronary and peripheral artery diseases. Although diabetic patients often present with advanced forms of these diseases, it is not known whether the compensatory mechanisms to vascular ischemia are affected in this condition. Accordingly, we sought to determine whether diabetes could: 1) impair the development of new collateral vessel formation in response to tissue ischemia and 2) inhibit cytokine-induced therapeutic neovascularization. Hindlimb ischemia was created by femoral artery ligation in nonobese diabetic mice (NOD mice, n = 20) and in control C57 mice (n = 20). Hindlimb perfusion was evaluated by serial laser Doppler studies after the surgery. In NOD mice, measurement of the Doppler flow ratio between the ischemic and the normal limb indicated that restoration of perfusion in the ischemic hindlimb was significantly impaired. At day 14 after surgery, Doppler flow ratio in the NOD mice was 0.49+/-0.04 versus 0.73+/-0.06 for the C57 mice (P< or =0.005). This impairment in blood flow recovery persisted throughout the duration of the study with Doppler flow ratio values at day 35 of 0.50+/-0.05 versus 0.90+/-0.07 in the NOD and C57 mice, respectively (P< or =0.001). CD31 immunostaining confirmed the laser Doppler data by showing a significant reduction in capillary density in the NOD mice at 35 days after surgery (302+/-4 capillaries/mm2 versus 782+/-78 in C57 mice (P< or =0.005). The reduction in neovascularization in the NOD mice was the result of a lower level of vascular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western blot and immunohistochemistry. The central role of VEGF was confirmed by showing that normal levels of neovascularization (compared with C57) could be achieved in NOD mice that had been supplemented for this growth factor via intramuscular injection of an adenoviral vector encoding for VEGF. We conclude that 1) diabetes impairs endogenous neovascularization of ischemic tissues; 2) the impairment in new blood vessel formation results from reduced expression of VEGF; and 3) cytokine supplementation achieved by intramuscular adeno-VEGF gene transfer restores neovascularization in a mouse model of diabetes.
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PMID:Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF. 1002 94

Studies suggest that pulmonary vascular ischemia-reperfusion injury (IRI) can be attenuated by increasing intracellular cAMP concentrations. The purpose of this study was to determine the effect of IRI on capillary permeability, assessed by capillary filtration coeficient (Kfc), in lungs retrieved from non-heart-beating donors (NHBDs) and reperfused with the addition of the beta(2)-adrenergic receptor agonist isoproterenol (iso), and rolipram (roli), a phosphodiesterase (type IV) inhibitor. Using an in situ isolated perfused lung model, lungs were retrieved from NHBD rats at varying intervals after death and either ventilated with O(2) or not ventilated. The lungs were reperfused with Earle's solution with or without a combination of iso (10 microM) and roli (2 microM). Kfc, lung viability, and pulmonary hemodynamics were measured. Lung tissue levels of adenine nucleotides and cAMP were measured by HPLC. Combined iso and roli (iso/roli) reperfusion decreased Kfc significantly (p < 0.05) compared with non-iso/roli-reperfused groups after 2 h of postmortem ischemia. Total adenine nucleotide (TAN) levels correlated with Kfc in non-iso/roli-reperfused (r = 0.89) and iso/roli-reperfused (r = 0.97) lungs. cAMP levels correlated with Kfc (r = 0.93) in iso/roli-reperfused lungs. Pharmacologic augmentation of tissue TAN and cAMP levels might ameliorate the increased capillary permeability observed in lungs retrieved from NHBDs.
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PMID:Maintenance of cAMP in non-heart-beating donor lungs reduces ischemia-reperfusion injury. 1140 88

The angiogenic effect of vascular endothelial growth factor (VEGF) has typically been assessed by indirect methods, including microsphere injection and angiography. Here, we use 3-D scanning electron microscopy (SEM) to directly visualize patterns of angiogenesis after a single bolus administration of VEGF in a model of peripheral vascular ischemia. Hind limb ischemia was induced by subcutaneous turniquet implantation in adult Wistar rats. The control group (group A, n = 10) was left untreated, group B (n = 10) received a single dose of VEGF (50 microg) injected in the peroneus muscle. LASER Doppler was applied for blood flow measurements. Animals were sacrificed on day 14 after ischemia induction and vascular casting was performed. Angiogenetic events such as 'tiny lateral sprouts', arcus formations', confluences and the angle of sprouting were assessed by SEM. Significant capillary sprouting was observed in both groups. VEGF-treated limbs demonstrated higher degrees of capillary growth (P = 0.01) and flow recovery (P = 0.028). 3-D-SEM showed sprouts to be more frequent in group B. Tiny lateral sprouts, which always left the mother vessel at an angle of 90 degrees and which were of small diameter and lacked imprints of endothelial cell nuclei, were more frequent in the VEGF-treated group (P = 0.018). Arcus formation was significantly higher in the treated group (P = 0.02). We have developed a simple and effective experimental model of ischemia. For the study of angiogenic phenomena, 3-D imaging of the microvasculature offers a direct and conclusive method for the study of angiogenic events.
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PMID:Restoration of blood flow and evaluation of corresponding angiogenic events by scanning electron microscopy after a single dose of VEGF in a model of peripheral vascular disease. 1254 64


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