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)

A patient with a toxic adenoma, already reduced in size by TSH, presented on the third day after treatment of a common cold by phenylpropanolomine, a severe pain in the thyroid gland. 4 weeks later, the nodule, which measured 3 x 4 cm. had clinically disappeared and the scan returned to normal. The disappearance 5 months later of the antithyroid antibodies confirmed the cure. Catecholamines, stimulating the production of thyroid hormone and producing temporary ischemia of the gland, phenylpropanolamine, a sympathomimetic drug, may have caused hemorrhagic necrosis of the adenoma and its disappearance.
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PMID:[Evanescent toxic thyroid adenoma. Possible role of phenylpropanolamine]. 20 Oct 31

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

Impaired donor heart function after heart transplantation results in the necessity for prolonged catecholamine and ventilatory support of the patient. Subsequently the risk of multiorgan impairment, infection, and rejection will be increased. In this retrospective analysis we tried to identify donor-related risk factors in patients who died early after transplantation. Of 174 patients undergoing heart transplantation from October 1985 through October 1988, 22 (12.6%) died early. Of the total, 39 cases were evaluated retrospectively for donor-related logistic and metabolic factors. All donors were analyzed with respect to the early mortality for age, weight, height, maximum dopamine concentration, thyroid hormone levels, and the duration from brain death until explantation and ischemia. Thirty patients were survivors (group A); nine patients died early (group B). By multiple regression analysis a significant influence (group A vs group B) of donor age, dopamine support, and ischemic time on early mortality could be demonstrated, whereas donor weight and height, hormone levels of triiodothyronine and thyroxine, and duration of brain death showed no correlation. From this limited experience we conclude that use of hearts from older donors with higher catecholamine support and longer ischemic times will result in an increased early mortality. In contrast, no influence of prolonged brain death times and metabolic factors could be demonstrated.
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PMID:Donor heart-related variables and early mortality after heart transplantation. 200 67

A rare case is presented of a woman with spontaneous recovery from hypopituitarism following postpartum hemorrhage. One month after delivery, serum thyroid hormone, TSH, LH and FSH levels were low, and their secretion from the pituitary gland responded poorly to the TRH and LH-RH tests. Pituitary TSH response was normal 3 months after delivery. In the LH-RH test, pituitary LH and FSH response returned to normal at 2 months. Pituitary GH secretion and serum cortisol levels induced by ITT already responded normally one month postpartum. Excessive secretion of pituitary PRL was observed 3 months after delivery and improved gradually thereafter. These results indicate that the secretion of pituitary tropic hormones was sensitive to pituitary ischemia in the following order: TSH, gonadotropin, GH and ACTH. The disturbance of these hormones also persisted in the same order.
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PMID:Spontaneous recovery from hypopituitarism due to postpartum hemorrhage. 250 17

The effect of cerebral ischemia and subsequent recirculation on the nuclear thyroid hormone receptors was investigated. Ischemia was produced by occlusion of the right common carotid artery in the Mongolian gerbil. The thyroid hormone receptors were measured in vitro by a [125I]triiodothyrorine (T3) binding assay with isolated nuclei and Scatchard analysis. A rapid increase of the total number of binding sites for T3 appeared within 30 min of ischemia and reached over 40% by 3 h. During the same 3-h period, the relative binding affinity was reduced by 25%. Upon recirculation after 30 min or 3 h of ischemia, a rapid reversal of measured T3 binding sites occurred, which progressed to 20-30% below the control value by the recirculation period of 3 h. If the ischemic period was only 30 min, the nuclear T3 binding capacity recovered toward the control level and the affinity constant returned normal after recirculation for 24 h. When the ischemic period was extended to 3 h, there was progressive loss of receptor sites, and no tendency for recovery of the affinity constant was observed. These results demonstrated a prompt alteration of a specific nuclear regulatory component in cerebral ischemia, which may indicate the importance of such changes within the nuclear regulatory mechanism for reversibility of cerebral function following ischemic insult.
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PMID:Nuclear binding sites for triiodothyronine in the gerbil brain following ischemia and recirculation. 632 44

Cardiopulmonary bypass results in a "euthyroid sick" state. Recently, interest has focused on the relationship between low serum triiodothyronine levels and postoperative cardiovascular hemodynamics. The present study was undertaken to more clearly define the acute effects of triiodothyronine on myocardial mechanics and energetics after hypothermic global ischemia using an ex-vivo canine heart preparation to model the clinical condition. Experiments were performed on isolated hearts subjected to hyperkalemic arrest with 90 minutes of hypothermic (10 degrees C) ischemia. Isolated hearts were cross-perfused by euthyroid support dogs in which triiodothyronine levels spontaneously decreased by 65% to 75% (p < 0.01) after the initiation of cross-perfusion. In nine heart preparations, triiodothyronine (Triostat) was given as a bolus dose (0.2 micrograms/kg) after 1 hour of baseline data collection with a subsequent measurable rise in serum triiodothyronine levels (p < 0.01). In six postischemic hearts, reverse triiodothyronine was given as a 0.2 micrograms/kg bolus. Triiodothyronine was also administered to a group of eight nonischemic, continuously perfused isolated hearts. Intrinsic myocardial contractility was assessed by analysis of the preload recruitable stroke work area, energetic efficiency from the myocardial oxygen consumption-pressure-volume area relationship, and coronary vascular resistance from analysis of coronary flow and perfusion pressure. Acute administration of triiodothyronine to postischemic hearts improved the preload recruitable stroke work area from 9.5 +/- 1.42 to 14.9 +/- 2.03 x 10(7) erg/ml, a 56% increase from baseline (p < 0.001), but had no effect on the preload recruitable stroke work area of the nonischemic hearts. The inotropic response resulting from triiodothyronine treatment did not alter the myocardial oxygen consumption-pressure-volume area relationship. Triiodothyronine treatment was associated with significantly decreased coronary resistance and increased coronary flow through a range of diastolic loading conditions in the postischemic hearts. The biologically inactive thyroid hormone metabolite reverse triiodothyronine was without effect on any of the measured parameters. On the basis of these results, we conclude that the low triiodothyronine state of cardiopulmonary bypass can be reproduced in this isolated heart model and that acute triiodothyronine treatment results in a unique inotropic action manifest only in the postischemic reperfused myocardium and is accomplished without oxygen wasting effects.
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PMID:Triiodothyronine improves left ventricular function without oxygen wasting effects after global hypothermic ischemia. 787 6

Left ventricular hypertrophy (LVH) is an important independent risk factor for cardiovascular morbidity and mortality. Initially LVH improves contractility and pump function; however, over time a sequence of events occurs including disintegration of myofibrils, interstitial fibrosis, adenosine triphosphate depletion, and altered gene expression. Eventually the hypertrophied myocardium outgrows its capillary bed, subendocardial ischemia develops, and the heart fails. Hemodynamic (pressure) and nonhemodynamic signals (catecholamines, angiotensin II, thyroid hormone) have been identified that stimulate hypertrophic growth of the myocardium. Evidence is also accumulating that the induction of immediate early genes such as c-fos and c-myc may participate in the development of LVH.
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PMID:Cellular and signaling mechanisms of cardiac hypertrophy. 793 62

Thyroid hormone is an important interventional agent shown to be beneficial in a variety of models of acute renal failure (ARF). While its usefulness is clear, its mechanism of action remains unknown. Although there are a multitude of thyroid-inducible proteins and enzymes, the one singled out in these studies as of potential mechanistic significance in the protective effect of thyroid in ARF is ornithine decarboxylase (ODC). This enzyme catalyzes the entry step in the biosynthesis of polyamines, which possess several potential roles in fostering renal repair and recovery. Ischemic ARF was induced in rats by renal arterial clamp and functional assessment was made by inulin clearance 24 h after injury. Both T4 (10 micrograms/100 g) and T3 (1 and 10 micrograms/100 g) resulted in significant improvement in inulin clearance when compared to ischemia alone, while reverse T3 was without effect. The activity of ODC was reduced 70% at 24 h in the kidney cortex but T3 restored the level to near control. Pretreatment of rats with difluoromethylornithine (DFMO), and irreversible inhibitor of ODC, resulted in nearly complete inhibition of this enzyme in the cortex and medulla, and blocked the increase in activity induced by T3. From the functional standpoint, DMFO did not worsen the severity of ischemic ARF but completely blocked the protective effect of T3. These data strongly suggest roles for ODC stimulation and, presumably, the consequent augmentation of polyamine biosynthesis, in the mechanism by which thyroid hormone enhances recovery from ARF.
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PMID:Thyroid hormone induction of ornithine decarboxylase in ischemic acute renal failure. 793 52

Cardiopulmonary bypass is associated with a reduction in plasma thyroid hormone concentrations in patients undergoing cardiac surgery. However, studies of the effects of cardiopulmonary bypass on thyroid function are limited and many studies report conflicting data concerning only the period of cardiopulmonary bypass. In this study, we tried to clinically determine the effects of cardiopulmonary bypass on concentrations of thyroid hormones by comprehensive thyroid function tests in 10 patients before and after surgery, and observed the benefits of triiodothyronine supplementation after global ischemia on myocardial function experimentally in guinea pigs. In patients undergoing surgery, concentrations of total triiodothyronine and free triiodothyronine decreased progressively on the institution of cardiopulmonary bypass and remained below normal levels until 24 hours postoperatively. In the guinea pig hearts studied in a Langendorf perfusion apparatus, T3 supplementation enhanced percentage recovery of ventricular contractile force, heart work and heart rate with respect to other groups receiving no T3 supplementation or T3 supplementation without any ischemic interval.
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PMID:The effects of thyroid hormones on the heart following global ischemia. A clinical and experimental study. 796 49

Administration of thyroid hormone, triiodothyronine (T3), causes numerous cardiovascular effects such as increases in stroke volume, cardiac output, heart rate, and myocardial contractility, and decreases in systemic vascular resistance. Along with other stressors, cardiopulmonary bypass (CPB) has been associated with reduced levels of T3. We examined the effects of T3 on early postischemic myocardial recovery in rabbit hearts subjected to crystalloid perfusion to simulate a low T3 state, and in pig hearts following global ischemia due to CPB. Studies using the former system showed that T3 administration results in significantly improved developed pressure after reperfusion of mildly ischemic hearts compared to controls, without producing inotropic effects. In more severely stunned rabbit hearts, physiologic and 10 times physiologic doses of T3 produced significantly improved (p < 0.05) stroke work end-diastolic length compared to placebo treatment. T3 treated pigs undergoing CPB and subjected to 30 minutes of global normothermic ischemia experienced significantly enhanced recovery of left ventricular contractility compared to controls at 90 and 120 minutes post reperfusion. Neither placebo nor T3 affected myocardial adenosine triphosphate levels. These data show that T3 enhances recovery from myocardial stunning without producing acute inotropic effects.
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PMID:Effects of triiodothyronine on stunned myocardium. 846 28


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