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)

Under the aspect of systemic diseases and their manifestation in the gut the following conclusions can be drawn: 1. The skin is the mirror of the intestinal tract; not only in primary gastroenterological disorders one should look for dermatological complications, but should also think in chronic skin lesions of concomitant intestinal alterations. 2. In all patients with collagen diseases a gastrointestinal involvement is very common. 3. In all endocrine disorders except in hypothyroidism diarrhea is a very common finding. 4. Infiltrations of gastrointestinal tract can be demonstrated in many cases by gastric, small bowel or rectal biopsy. 5. In all forms of dysgammaglobulinemia giardiasis is very common. 6. In right heart failure protein-losing enteropathy should be considered, in left ventricular insufficiency bowel ischemia.
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PMID:[Manifestations of systemic diseases in the gastrointestinal tract]. 96 97

Myxedema megacolon is rare; usually, it manifests with abdominal distention, flatulence, and constipation. Herein we describe a 72-year-old man who had intermittent diarrhea, bloating, and abdominal pain for more than a year. Cultures of stool specimens for Clostridium difficile enterotoxin were variably positive and negative. Colonoscopic biopsy specimens were thought to be consistent with chronic ischemia. Thyroid function tests showed severe hypothyroidism; the patient's symptoms resolved with thyroid hormone replacement. We hypothesize that gross dilatation of the colon, attributed to myxedema, was followed by intestinal ischemia and complicated by recurrent episodes of pseudomembranous colitis. A review of the relevant literature is provided. This unusual manifestation of myxedema should be considered in the differential diagnosis when a patient has diarrhea, bloating, and abdominal pain.
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PMID:An unusual case of myxedema megacolon with features of ischemic and pseudomembranous colitis. 154 53

The protective effect of hypothyroidism against lethal ventricular tachyarrhythmias (VT) in the subacute phase of experimental myocardial infarction (MI) was investigated in 10 thyroidectomized dogs using a conscious model of sudden coronary death. Four weeks after surgical ablation of the thyroid, and having established biochemical hypothyroidism, anterior MI was produced by 120 min of occlusion-reperfusion of the left anterior descending coronary artery. In the subacute phase of MI, the inducibility of VT was investigated using programmed ventricular stimulation (PVS), and the effects on spontaneous development of ventricular fibrillation (VF) were studied by production of posterolateral ischemia at a site remote from the area of the previous infarction. Ischemia was produced by the passage of anodal direct current through a silver wire electrode implanted in the left circumflex coronary (LCX) artery. The results were compared to those from a cohort of 20 existing euthyroid controls that had undergone an identical experimental protocol. No differences were found in heart rate and other electrocardiographic parameters such as the PR, QRS, and QT (paced at 2.5 Hz) and the QTc interval between the hypo- and euthyroid groups. During PVS in the subacute phase of anterior MI, the measured threshold voltage and ventricular refractory periods were similar in both groups. The incidence of inducibility of VT was 100% in the euthyroid animals compared to 60% in the hypothyroid dogs, suggesting an antiarrhythmic effect of hypothyroidism. The incidence of sustained vs. nonsustained VT was similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothyroidism renders protection against lethal ventricular arrhythmias in a conscious canine model of sudden death. 172 67

Hypothyroidism is associated with profound left ventricular dysfunction. Brain-dead organ donors and patients undergoing cardiopulmonary bypass are chemically hypothyroid with significantly reduced circulating free triiodothyronine (T3). To test the hypothesis that T3 enhances left ventricular function in a hormonally deficient environment, a total of 36 healthy New Zealand White rabbit hearts were studied using a modified Langendorff preparation with Krebs-Henseleit perfusate and intra-ventricular balloon. In 9 normal rabbit hearts a cumulative dose-response curve with logarithmically increasing doses of T3 was obtained. The vehicle solution for T3 dissolution served as control (n = 9). Left ventricular function was assessed from peak developed pressure at baseline and after T3 administration. Triiodothyronine had no effect in normal hearts on peak developed pressure or end-diastolic pressure. In 18 rabbits, the acute effect of T3 administration after ischemia was investigated. Preischemic left ventricular function was measured to serve as baseline, and hearts were subjected to 37 degrees C global ischemia. Triiodothyronine (n = 9) or vehicle (n = 9) was infused during reperfusion, and left ventricular peak developed pressure was measured at 30 and 60 minutes of reperfusion. Recovery of function (expressed as percent return of left ventricular peak developed pressure) was significantly improved within 15 minutes of reperfusion (65.0% +/- 2.1% versus 80.2% +/- 4.1%) and remained significantly improved throughout the reperfusion period (p less than 0.05 by analysis of variance). These data suggest that although T3 possesses no inotropic properties, it significantly improves postischemic left ventricular function. The rapidity of the functional improvement suggests that these effects may be due to plasma membrane-mediated mechanisms.
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PMID:Triiodothyronine-enhanced left ventricular function after ischemic injury. 206 45

A 55-year-old man, previously treated for primary hypothyroidism, was admitted for evaluation of atypical chest pain. On physical examination, the pulse rate was 60 and blood pressure was 132/84 mmHg. Heart sounds were normal and no murmur was heard. Abdominal palpation showed no abnormal finding, and bruit was not heard. The electrocardiogram was normal and stress-induced ischemia was not found. The chest X-ray showed no sign of pulmonary hyperaemia or mass lesion, and central shadow was normal (CTR = 44%). During right heart catheterization, the pressures were normal in the cardiac chambers, pulmonary artery, and wedge position. A significant increase in oxygen saturation was disclosed at pulmonary artery level (10%) and the upper site of the inferior vena cava (22%). Coronary arteriography found coronary artery fistulas from the left main trunk, the left anterior descending artery, the left circumflex, and the right coronary artery to the pulmonary trunk. The left and right ventriculograms were normal. The digital subtraction angiography of celiac artery showed hepatic arteriovenous fistula. Ultrasonography and computed tomography found no mass lesion of the liver. Since combination of the bilateral coronary artery with pulmonary artery fistula, and hepatic arteriovenous fistula is very rare, the present case is worth noting for the investigation of the pathogenesis of congenital arteriovenous fistulas.
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PMID:[A case of bilateral coronary artery to pulmonary artery fistulas associated with hepatic arteriovenous fistula]. 261 12

Alpha-adrenoceptors mediating positive inotropic effects are well established in the heart of various species including human heart. The mechanism by which alpha-adrenoceptor stimulation increases force of contraction is not known. cAMP is unlikely to be involved as a mediator. Evidence has been presented that an increase in magnitude and duration of the slow Ca++ inward current may be partly responsible for the positive inotropic effect. In addition, stimulation of alpha-adrenoceptors may increase Ca++ sensitivity of the contractile proteins. Stimulation of alpha-adrenoceptors by endogenous catecholamines may serve as a reserve mechanism under various conditions of impaired beta-adrenergic influence, e.g. hypothyroidism, bradycardia or ischemia. Furthermore, alpha-adrenoceptors may be involved in the genesis of reperfusion arrhythmias in ischemic heart.
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PMID:[Alpha-adrenoceptors in the myocardium: incidence and functional significance]. 300

The cause of hypothyroidism after subtotal thyroidectomy for primary thyrotoxicosis is not precisely understood. Activity is not just related to the size of the thyroid remnants, and ischemia of the remnants has been suggested as a factor which might contribute to the development of hypothyroidism. A prospective study has been carried out to look for evidence that ischemia is implicated. In 55 patients undergoing subtotal thyroidectomy for primary thyrotoxicosis, the inferior thyroid artery (ITA) was ligated on one side but preserved on the opposite side. All of the patients had postoperative isotope scans. We predicted that, if ITA ligation produced significant ischemia of the remnant, then the remnant with the intact ITA ought to show greater activity on the postoperative scan. This was not the case. The remnant with the intact ITA was dominant in only 15 of 55 patients, the remnant with the ligated ITA was dominant in the same proportion, 15 of 55 patients, while in the remaining 25 patients, activity was equally distributed between the two remnants. The results of this study provides no evidence to support the contention that nonligation of the inferior thyroid arteries will reduce ischemia of the thyroid remnants and thereby discourage postoperative hypothyroidism.
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PMID:The effect of ligation of the inferior thyroid artery upon thyroid remnant function. 336 61

The effect of hypothyroidism on ischemic acute renal failure was studied in rats. Ten days after thyroidectomy with parathyroid reimplantation, rats underwent right uninephrectomy followed by occlusion of the left renal artery for 60 min. Plasma creatinine was lower in thyroidectomized than control rats 24 hr after ischemia; 1.3 +/- 0.5 vs. 3.2 +/- 0.6 mg%; P less than 0.05. Twenty-four hours after ischemia, inulin clearance was higher in thyroidectomized than control animals (0.40 +/- 0.06 vs. 0.17 +/- 0.03 mliter/min; P less than 0.01), despite an initially lower inulin clearance in thyroidectomized animals (0.81 vs. 1.1 +/- 0.07 mliter/min; P less than 0.05). Administration of the antithyroid drug prophylthiouracil for 14 days also resulted in lower plasma creatinine after ischemia. Kidneys from thyroidectomized animals showed less histologic damage 24 hr after ischemia. Renal cortical content of the lipid peroxidation product malondialdehyde was increased less in thyroidectomy than control kidneys after 60 min ischemia plus 15 min reflow (0.08 +/- 0.02 vs. 0.42 +/- 0.1 nmole/mg protein; P less than 0.005). Renal cortical glutathione content was higher in thyroidectomized animals by approximately 36%, 650 +/- 46 vs. 479 +/- 32 nmole/mg protein (P less than 0.02). In normal rats, glutathione infusion also increased renal cortical glutathione content and resulted in lower plasma creatinine 24 hr after renal artery ischemia. Therefore, hypothyroidism resulted in functional and histologic protection against injury after ischemia. Post-ischemic renal lipid peroxidation was reduced in thyroidectomized animals, perhaps the result of increased scavenging of reactive oxygen species (oxygen free radicals and H2O2) by glutathione.
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PMID:Hypothyroidism protects against free radical damage in ischemic acute renal failure. 374 32

The mechanisms by which brain cells die after brief episodes of cerebral ischemia are not fully understood. In certain brain regions this damage may not be apparent for days. Hypothyroidism is known to decrease cerebral metabolism. We postulated that this slowing in cerebral metabolism may be neuroprotective after transient cerebral ischemia. To test this hypothesis, a total of 10 gerbils had thyroidectomies performed 2 weeks prior to ischemia. Six gerbils served as euthyroid controls. All animals were exposed to 5 min of transient ischemia and sacrificed 7 days after the insult. Silver degeneration staining was used for histological evaluation. Hippocampal damage [subiculum (P < 0.001), CA1 (P = 0. < .001), CA3 (P < 0.05), and CA4 (P < 0.001)] was significantly less in the hypothyroid animals. There was also significantly less damage in the cerebral cortex (P < 0.05) and thalamus (P < 0.05) in the hypothyroid animals. The exact mechanism of this protection is not fully understood but could be secondary to a decrease in the metabolic activity, or a reduced generation of free radicals (as is seen with protection from ischemia in kidney and liver under hypothyroid conditions). Further studies are required in order to gain a better understanding of the protective effects of hypothyroidism on cerebral ischemia.
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PMID:Hypothyroidism protects the brain during transient forebrain ischemia in gerbils. 791 Oct 86

Hypothyroidism protects the brain from the effects of transient forebrain ischemia in gerbils. The mechanism for this protection is not fully understood. In this study we looked at the release of glutamate during ischemia in gerbils exposed to surgical hypothyroidism (n = 7), chemical hypothyroidism (n = 8), and surgical hypothyroidism thyroxine-treated (n = 3) and compared them to control euthyroid animals (n = 8). The duration of ischemia was 10 min. Glutamate release was measured with in vivo microdialysis. Microdialysis analysis began 2 h after the placement of the probes (to stabilize the baseline) and collections were obtained in 10-min samples. During ischemia, there was an increase in the release of glutamate that returned to the baseline within 20 min following the insult. In animals made hypothyroid surgically and chemically, the extent of glutamate release was significantly lower than that in the controls. The release of glutamate in the surgically hypothyroid thyroxine-treated animals was similar to that in controls. The attenuated glutamate release could be a mechanism of protection during ischemia in hypothyroid gerbils.
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PMID:Decreased glutamate release during hypothyroidism may contribute to protection in cerebral ischemia. 791 76


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