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)

There are numerous literature reports of oral contraceptive-induced (estrogen and progesterone) ischemic bowel disease. However, Premarin-induced (equine conjugated estrogen) intestinal ischemia has rarely been reported. We describe three cases of Premarin-induced ischemic colitis. In contrast to oral contraceptive-induced ischemic colitis, Premarin-induced ischemia is restricted to the colon, has not required surgical therapy, can have a chronic or chronic intermittent course, may be reversible despite continued usage of Premarin, and may present with nonspecific abdominal and colonic symptoms.
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PMID:Premarin-induced ischemic colitis. 796 54

We treated 10 postmenopausal women with stable angina, positive exercise test, and documented coronary artery disease with oral conjugated equine estrogen (0.625 mg/day of Premarin) or placebo for 4 weeks, in random order, with crossover after a 4-week washout period. Exercise tests, performed after each treatment period while the patients were taking their usual antianginal drugs showed no differences; thus, short-term estrogen does not improve exercise-induced ischemia compared with placebo.
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PMID:Estrogen replacement therapy and exercise performance in postmenopausal women with coronary artery disease. 959 21

The present study was conducted to assess whether Premarin, a water-soluble estrogen sulfate, can act via estrogen receptors (ERs) to rescue mice from heat-induced lethality. Unanesthetized, unrestrained mice were exposed to ambient temperature of 42.4 degrees C to induce heatstroke (HS). Another group of mice was exposed to room temperature (24 degrees C) and used as normothermic controls. They were given isotonic sodium chloride solution, Premarin (0.1 - 1.0 mg/kg of body weight, i.p.), or Premarin (1 mg/kg of body weight, i.p.) plus the nonselective ER antagonist ICI 182, 780 (0.25 mg/kg of body weight, i.p.) 1 h after the termination of heat stress. Their physiologic and biochemical parameters were continuously monitored. Mice that survived on day 4 of heat treatment were considered survivors. When the vehicle-treated mice underwent heat, the fraction survival and core temperature at +4 h of body heating were found to be 0 of 12 and 34.4 degrees C +/- 3 degrees C, respectively. Administration of Premarin (1 mg/kg) 1 h after the cessation of heat stress rescued the mice from heat-induced death (fraction survival, 12/12) and reduced the hypothermia (core temperature, 37.3 degrees C). The beneficial effects of Premarin in ameliorating lethality and hypothermia can be abolished by simultaneous administration of ICI 182, 780. Both IL-10 (an anti-inflammatory cytokine) and estradiol in the serum were increased significantly in heat-stressed mice administered Premarin compared with vehicle-treated HS group. Heat-induced apoptosis, as indicated by terminal deoxynucleotidyl-transferase-mediated alpha UDP-biotin nick end-labeling staining, in the spleen, liver, and kidney were significantly reduced by Premarin. The increased levels of cellular ischemia (e.g., glutamate, lactate-to-pyruvate ratio, and nitrite) and damage (e.g., glycerol) markers and iNOS expression in the hypothalamus during HS were decreased significantly by Premarin therapy. The levels of proinflammatory cytokines (e.g., IL-1 beta and TNF-alpha) and renal and hepatic dysfunction markers in plasma that are up-regulated in heat stressed mice were significantly lower in Premarin-administered mice. The data indicate that Premarin may act via ERs to rescue mice form HS-induced lethality.
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PMID:Premarin can act via estrogen receptors to rescue mice from heatstroke-induced lethality. 1849 35

A need exists for the effective treatment of individuals suffering from spinal cord injury (SCI). Recent advances in the understanding of the pathophysiological mechanisms occurring in SCI have resulted in an expansion of new therapeutic targets. This review summarizes both preclinical and clinical findings investigating the mechanisms and cognate pharmacologic therapeutics targeted to modulate hypoxia, ischemia, excitotoxicity, inflammation, apoptosis, epigenetic alterations, myelin regeneration and scar remodeling. Successful modulation of these targets has been demonstrated in both preclinical and clinical studies with agents such as Oxycyte, Minocycline, Riluzole, Premarin, Cethrin, and ATI-355. The translation of these agents into clinical studies highlights the progress the field has made in the past decade. SCI proves to be a complex condition; the numerous pathophysiological mechanisms occurring at varying time points suggests that a single agent approach to the treatment of SCI may not be optimal. As the field continues to mature, the hope is that the knowledge gained from these studies will be applied to the development of an effective multi-pronged treatment strategy for SCI.
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PMID:Recent advances in the pharmacologic treatment of spinal cord injury. 2483 53