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 case report of subacute, reversible ischemic colitis associated with use of oral contraceptives (OCs) is reported. A 19-year-old woman was admitted to the hospital with chief complaints of abdominal cramps, nausea, vomiting, diarrhea, and rectal bleeding of 2 days' duration. Past medical history and family history were noncontributory. The patient was receiving no medication other than Norinyl 2 (2 mg of norethindrone and .1 mg of mestranol), which she had been taking for 6 months. 2 days before admission the patient had taken 100 mg of dimenhydrinate and 2 ExLax tablets (90 mg of phenolphthalein) for constipation. Colonic roentgenograms revealed impaired mesenteric circulation and bowel ischemia; OC-induced ischemic bowel disease was diagnosed. Patient symptoms subsided within 96 hours of discontinuing the OC and initiating supportive therapy (including intravenous fluid infusion, nasogastric suction, analgesics, and antiemetics). When a repeat barium enema was performed, it showed resolution of the ischemia. In a short review following the case report, these drugs were indicted in causation of colitis-like syndrome: amoxicillin, ampicillin, cephazolin, chloramphenicol, chlorpropamide, clindamycin, cloxacillin, cotrimoxasole, cyclophosphamide, digitalis, ergotamine tartrate, flucytosine, fluorouracil, gold salts, laxative and cathartic abuse, mercurous chloride, methyldopa, penicillin V, and tetracycline. Ischemic bowel disease secondary to OC use is a rare but important complication because of its significant morbidity and potential mortality, and because of the widespread use of the drugs. The case report emphasizes the need to consider the differential diagnosis of acute vascular insult with bowel ischemia when acute abdominal pain progressing to bloody diarrhea occurs in young women taking OCs.
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PMID:Oral contraceptive-induced ischemic bowel disease. 48 72

From Wistar rats, data are presented which indicate that inbred females a) have a greater ability to clear particulate matter from the blood stream than do males of the same strain; b) are significantly more resistant to two different forms of lethal circulatory stress (e.g., intestinal ischemia and whole-body trauma) than are males; and c) exhibit a greater resistance to undergo reticuloendothelial system (RES) phagocytic depression after both forms of lethal trauma than do males. Estradiol treatment of males, using either acute, massive (1 or 10 mg/kg) or multiple, low dose (10 or 100 mug/kg) regimens, confers trauma resistance on such animals. Such estradiol treated male rats exhibit hyperactive RES's. These estradiol-treated males, when subjected to either lethal ischemia or trauma, fail to demonstrate the early RES phagocytic depression seen in untreated controls. Untreated female as well as estradiol-treated male rats exhibit significantly higher arterial blood pressures post-trauma than do untreated male rats. Direct microscopic observation of rat mesenteries indicr whole-b0dy trauma, the untreated females as well as the estradiol-treated males exhibit significantly less dilatation of microscopic capacitance vessels (i.e., venules) than do untreated male rats. The data reported herein could be used to suggest that estrogenic hormones may play pivotal roles in a) the amelioration of an organism's reaction to systemic stress; and b) control of macrophage and peripheral vascular functions.
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PMID:Sex and estrogens in protection against circulatory stress reactions. 97 Apr 65

Primary dysmenorrhea occurs mostly in young women with a painful bleeding pattern. In a recent study, 72% of 19-year-old women had light, 19% had medium to severe, and 8% had severe symptoms. Secondary dysmenorrhea means pathological organic alterations of the genital tract: uterus myomatosus, endometrial polyps, endometriosis, and retroflexed uterus. IUDs can also generate this condition. A certain imbalance of estradiol and progesterone results in defective prostaglandin formation in the endometrium (too much PGF2alpha and too little PGI2) as well as in abnormal and increased uterine contractility and diminished endometrial, blood supply with concomitant painful ischemia. Increased prostaglandin synthesis leads to inflammatory processes and the traumatization of the endometrium (high PGF2alpha level), but IUDs also often cause secondary dysmenorrhea. Treatment calls for the normalization of prostaglandin formation in the uterus by dietary change by increasing fatty acid intake (fish oils and plant fats), and also by the systematic addition of exogenic gestagens (Duphaston 10 mg/day po. Orgametril 5 mg/day), and by the use of the progesterone-releasing IUDs (Biograviplan and Progestasert) that lessen the contractility of the myometrium by reducing PGF2-alpha synthesis. If pregnancy is to be avoided hormonal ovulation inhibitors as optimal, since their effectiveness is over 90% (Cilest, Femovan, Marvelon, and Ortho-Novum 2 mg). If contraception is not sought, nonsteroidal antiphlogistics are recommended: ibuprofen (400 mg 3-4 times/day), naproxen (250 mg 4-5 times/day), flufenamic acid (200 mg/day tid), mefenamic acid (500 mg 3 tid or 250 mg qid), aspirin (650 mg every 4-6 hours), indomethacin (25 mg tid, although it is relatively toxic). Magnesium is a natural calcium antagonist that can influence the intracellular calcium concentration in the myometrium. THe calcium blocker nifedipin (20-40 mg po) and beta-sympathomimetics (Partusisten) also mitigate uterine contractions, but the latter can produce more side effects as a consequence of interfering in the vegetative nervous system.
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PMID:[Drug therapy of dysmenorrhea]. 289 19

A case of mesenteric vascular occlusion is detailed. The 30-year-old female had abdominal pain, bloody diarrhea, and small bowel changes seen on x-ray. She had begun taking the oral contraceptive Ovral (.5 mg norgestrel, .05 mg ethinyl estradiol) 3 years prior to hospital admission. Symptoms began to disappear when her oral contraception was discontinued on the ninth hospital day. Over the next 5 days abdominal signs and symptons subsided progressively. A follow-up small bowel series showed complete disappearance of previous abnormalities. In the differential diagnosis of acute abdominal pain progressing to bloody diarrhea, especially in young women or oral therapy, acute vascular insult with small bowel ischemia must be considered.
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PMID:Reversible mesenteric vascular occlusion associated with oral contraceptives. 470 Oct 37

In Belgium, physicians at Heilig Hart Kliniek in Roeselare removed half of the colon of a 22-year-old woman suffering from obstructing Crohn's disease of the terminal ileum. 2 weeks after leaving the hospital she had diarrhea and abdominal cramps and neither fecal culture nor Clostridium difficile toxin were positive. 2 weeks later she experienced the same symptoms, but the diarrhea was now profuse watery diarrhea mixed with blood. The physicians performed a biopsy of the colonic segment at both ends of the left colon which revealed signs of ischemic colitis (obvious congestion, acute extravasation of blood, and focal desquamation of epithelial cells). So they ordered parenteral feeding for 24 hours, after which she had no more symptoms. She began oral feeding with no complications. When the physicians learned that after discharge she began using the combined oral contraceptive (OC) Trinovum and 2.5 mg dihydroergotaminemesilate to treat migraine, they told her to stop taking the ergotamine alkaloid and recommended that she not use the OC. She agreed to stop using the migraine medication but started using the OC again. 4 months after the biopsy she no longer has side effects. The woman had multiple risk factors of ischemic colitis development: OC use and use of an ergotamine alkaloid. The potentially vasoconstrictory and thrombogenic factors may have irritated underlying vascular injury and the tendency of focal mesenteric thrombosis which is often present in people with Crohn's disease. Therefore, the physicians deducted that OC use and use of ergotamine alkaloid were responsible for the ischemia. In conclusion, ergotamine alkaloid use in association with OC use is contraindicated in women who have predisposing factors, e.g., thrombogenic disease or coagulation abnormalities.
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PMID:Ischemic colitis in a patient with Crohn's disease taking an oral contraceptive and an ergotamine alkaloid. 838 3

Arterial dysfunction and disease affect a majority of women during their life time. Ovarian hormones inhibit the development of atherosclerosis and play an integral role in the maintenance of normal arterial function. Estrogens act in the liver to improve and maintain lipid profiles and also act in the walls of arteries and in cardiac myocytes to maintain function and prevent disease. Death from cardiovascular disease is reduced in women receiving estrogen replacement therapy (ERT). Ten-year follow-up studies of women with advanced coronary artery disease (CAD) show a marked reduction in fatalities among the women receiving estrogens compared with untreated women. Sublingual estradiol-17 beta compared with placebo results in improved exercise tolerance and reduced ischemia during exercise in women with CAD. Estradiol-17 beta infused into the coronary arteries in women with CAD leads to improved arterial function. Estrogen deficiency has been reported in women with angina pectoris who have normal coronary arteries, and these women respond to estrogen treatment. HRT implies the use of ERT with the addition of a progestin. Progestins oppose the actions of estrogens. Counter-effects of lipid metabolism appear to be minimal with progestins currently in use. Oppositional effects of progestins on hemodynamic actions of estrogens may be significant, as progestins appear to induce vasoconstriction of estrogenized vessels.
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PMID:Cardiovascular disease in women: implications of hormone replacement therapy. 882 4

Cardiovascular effects of estrogens and particularly that of estradiol involve protection of the heart against ischemia. These effects were believed to be mainly indirect, mediated via changes in the blood and blood vessels. In the present paper a direct action of estradiol on the heart is demonstrated. Estradiol stimulates (p < 0.001) the Na,K-ATPase activity of cardiac sarcolemmal membranes by stimulating in an allosteric manner, the activation of the enzyme by potassium. The latter activation involves also an increase in affinity to potassium of the potassium binding sites on the enzyme molecule, but remains without any effect on the capacity and KD value of specific ouabain binding to the Na,K-ATPase. Estradiol is also antagonizing the depression of Na,K-ATPase activity that may be caused by ischemia and it is stimulating (p < 0.01) the ouabain-sensitive uptake of 86Rb into the heart cells. Our results indicate, that in addition to the known indirect effects of estradiol on the heart, the hormone also stimulates the activity and improves the kinetics of interaction of cardiac sarcolemmal Na,K-ATPase with ATP as well as with Na+ and K+ ions. This direct action may also account for the cardioprotective effects of estradiol.
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PMID:Estradiol modulates the sodium pump in the heart sarcolemma. 940 52

Brain ascorbate levels in young adult female rat are lower than those in males. Loss of ascorbate during ischemia is also less in females, suggesting lower oxidative stress. After ovariectomy, however, ischemia-induced loss equals that in males. In the present study, we determined ascorbate levels in maturing male and female rat brain to establish when the gender difference in content arises. We further investigated whether 17beta-estradiol and/or progesterone treatment modulate levels and ischemia-induced loss in ovariectomized females and compared these data with those from normal females in proestrus and estrus. Gender differences in brain ascorbate content were absent before puberty and persisted only in cortex in aging rats. Chronic estradiol treatment, whether alone or in combination with progesterone, prevented an ovariectomy-induced ascorbate increase in hippocampus and caused levels in cortex and cerebellum to fall below those of randomly sampled normal females. These same low levels were found during proestrus and estrus. Estradiol replacement after ovariectomy prevented enhanced ischemia-induced ascorbate loss in hippocampus, but not in cortex or cerebellum. Ischemia-induced losses in proestrus and estrus were similar to those in normal controls. Progesterone had little effect in any region. These data indicate that ascorbate content and redox balance in female brain are influenced postpubertally by estrogens in a region-selective manner.
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PMID:Estrogen-dependent modulation of rat brain ascorbate levels and ischemia-induced ascorbate loss. 972 11

We studied the effect of 2-week treatment with estradiol 17beta on myocardial glutathione concentration in dogs and isolated perfused rat heart subjected to brief coronary ischemia and reperfusion. Estradiol protected against ischemia/reperfusion-induced myocardial systolic shortening and malonylaldehyde production and increased myocardial glutathione concentration and glucose-6-phosphate dehydrogenase enzyme activity. Reduction of myocardial glutathione with buthionine sulfoximine to levels seen in the absence of estrogen reversed the protective effect of estradiol against myocardial dysfunction and lipid peroxidation associated with ischemia/reperfusion. These results suggest that the antioxidant effect of estradiol in ischemia/reperfusion may be mediated by regulation of myocardial glutathione metabolism.
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PMID:17-Beta estradiol regulation of myocardial glutathione and its role in protection against myocardial stunning in dogs. 973 60

Clinical studies demonstrate that estrogen replacement therapy in postmenopausal women may enhance cognitive function and reduce neurodegeneration associated with Alzheimer's disease and stroke. This study assesses whether physiologic levels of estradiol prevent brain injury in an in vivo model of permanent focal ischemia. Sprague-Dawley rats were ovariectomized; they then were implanted, immediately or at the onset of ischemia, with capsules that produced physiologically low or physiologically high 17beta-estradiol levels in serum (10 or 60 pg/mL, respectively). One week after ovariectomy, ischemia was induced. Estradiol pretreatment significantly reduced overall infarct volume compared with oil-pretreated controls (mean+/-SD: oil = 241+/-88; low = 139+/-91; high = 132+/-88 mm3); this protective effect was regionally specific to the cortex, since no protection was observed in the striatum. Baseline and ischemic regional CBF did not differ between oil and estradiol pretreated rats, as measured by laser Doppler flowmetry. Acute estradiol treatment did not protect against ischemic injury. Our finding that estradiol pretreatment reduces injury demonstrates that physiologic levels of estradiol can protect against neurodegeneration.
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PMID:Estradiol protects against ischemic injury. 980 15


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