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)

The effect of experimentally induced uniocular trauma was investigated in the adult albino rabbit by means of iris fluorescein angiography. Paracentesis, blunt trauma, occlusion of all four vortex veins or of the two long posterior ciliary arteries, or local instillation of nitrogen mustard, were performed in a number of animals, some of which received systemic aspirin preoperatively. Iris angiograms of the injured and the contralateral eye were performed immediately after the traumatic insult. The injured eye always showed an increased permeability to fluorescein. Except for paracentesis, the ipsilateral response often included ischemia of the iris. The contralateral eye always showed an increase in fluorescein permeability into the aqueous. In some cases, sector ischemia of the contralateral iris was seen. Aspirin inhibited some ipsilateral responses but had no effect on the consensual reactions. It is concluded that ipsilateral trauma almost invariably causes a contralateral reaction in the rabbit eye, which is more severe if the injury creates ischemia of the iris. Since these reactions are inefficiently blocked by aspirin, they are not prostaglandin-mediated. The interocular pathway involved may be neural or vascular in nature.
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PMID:Anterior segment reactions after experimental trauma to rabbit eyes. 31 Nov 67

The eventual depth of tissue necrosis after burning is not immediately apparent. In all burn wounds, there exists a zone of stasis which shows progressive microvascular deterioration. These progressive changes have been prevented by methylprednisolone acetate, indomethacin, and ASA. All of these agents are known to inhibit prostaglandin synthesis. These data suggest that prostaglandins have a role in the progressive dermal ischemia after thermal trauma and that their effect can be prevented by specific antiprostaglandins.
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PMID:Preventing the prostaglandin effect on dermal ischemia in the burn wound. 40 Dec 78

Cardiac output and blood flow to different regions and layers of the stomach were determined by the microsphere distribution technique. Aspirin tablets were placed in the stomach of anesthetized cats by gastrotomy. In some animals the arterial pressure was reduced to about 60 mmHg for 30 min by bleeding. The gastric mucosal blood flow decreased markedly during the bleeding. Three hours after reinfusion of the blood gastric mucosal erosions were present at the site of contact of the tablet with the mucosa. In most of the non-bled animals no mucosal lesions were found 4 1/2 after aspirin application. No mucosal damage occurred in animals subjected to bleeding without aspirin treatment. It is concluded that the aspirin damage to the gastric mucosa increases under hemorrhagic shock because of mucosal ischemia in the shocked animals.
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PMID:Aspirin damage to ischemic gastric mucosa in shocked cats. 49 67

Radioactive microspheres were used to measure blood flow in the cat stomach during exposure to saline, 0.075 M HCl, and then 15 and 30 min after exposure to 20 or 40 mM aspirin in HCl. At the end of the experiment, the stomach wall was divided into ulcerated regions and adjacent nonulcerated areas. When exposed to saline, both regions had similar blood flow: 27 +/- 5 and 25 +/- 5 ml.min-1.100 g-1 (means +/- SE). Addition of acid caused a significant increase in blood flow to 41 +/- 7 ml.min-1.100 g-1 only at those sites that eventually ulcerated in the presence of aspirin. In the adjacent nonulcerated regions, blood flow was 31 +/- 5 ml.min-1.100 g-1 and was not significantly greater than the flow recorded during saline exposure. Aspirin caused ulcer site blood flow to increase dramatically to 89 +/- 12 and 122 +/- 18 ml.min-1.100 g-1 after 15 and 30 min, whereas the adjacent nonulcerated tissue rose to 40 +/- 6 and 44 +/- 5 ml.min-1.100 g-1, respectively. The ulcer site hyperemia with acid alone suggests higher mucosal permeability in these regions allowing back-diffusion of acid and injurious agents. The present data obtained in the cat do not support the notion that ischemia plays a role in initiating nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers, but rather that acute NSAID ulcers are associated initially with a hyperemia.
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PMID:Effect of aspirin on ulcer site blood flow in cat stomachs. 151 25

The incidence of ischemic cardiac events is highest in the early morning hours (symptomatic and asymptomatic cardiac ischemia, myocardial infarction, and sudden death). Quantitatively, however, most of them occur during the rest of the day; therefore, an ideal therapy should be established in the early morning hours and be efficient all day long. We recommend that nitrates should be taken as early as possible after a dose-is-free interval during the night. Patients taking beta-blockers do not show a circadian rhythm of the incidence of ischemic cardiac events. Compliance can be improved with the never long-acting agents. Therapy should be tailored individually for each patient. It is not yet known whether calcium blockers influence the circadian rhythm. The efficacy of the never preparations is comparable to the older ones. Aspirin can be taken at any time of the day because of its long duration of action.
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PMID:[Consequences of circadian variability for the treatment of ischemic heart disease]. 153 52

Mesenteric ischemia reflexly activates the cardiovascular system. In addition, mesenteric ischemia and reperfusion generate reactive oxygen species. However, the ability of these short-lived reactive oxygen species to generate cardiovascular reflexes is unknown. We therefore investigated cardiovascular reflexes induced by serosal application of hydrogen peroxide (H2O2) to the gallbladder, stomach, or duodenum in anesthetized cats. Serosal application of hydrogen peroxide (44 mumols) to the gallbladder (n = 14) significantly (p less than 0.05) increased mean arterial blood pressure (MAP) by 37 +/- 6 mm Hg, left ventricular dP/dt by 1,893 +/- 416 mm Hg/sec, heart rate by 6 +/- 1 beats per minute, and systemic vascular resistance from 0.34 +/- 0.01 to 0.42 +/- 0.04 peripheral resistance units. The cardiovascular effects were dose-dependent over a range of 0.4 pmol to 132 mumols H2O2. Celiac and superior mesenteric ganglionectomy abolished H2O2-induced cardiovascular effects. Dimethylthiourea (10 mg/kg), a reactive oxygen species scavenger, significantly (p less than 0.05) attenuated 44 mumols H2O2-induced increases in MAP from 36 +/- 3 to 2 +/- 2 mm Hg. Deferoxamine (10 mg/kg) also significantly attenuated 44 mumols H2O2-induced increases in MAP from 40 +/- 7 to 19 +/- 10 mm Hg, but iron-loaded deferoxamine did not. Aspirin (50 mg/kg) did not attenuate H2O2-induced excitation of the cardiovascular system. These data suggest that H2O2 activates abdominal visceral afferents to reflexly stimulate the cardiovascular system by a mechanism involving hydroxyl radicals. Thus, reactive oxygen species could modulate systemic vascular tone by stimulating abdominal visceral afferents during mesenteric ischemia and reperfusion.
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PMID:Hydrogen peroxide-induced cardiovascular reflexes. Role of hydroxyl radicals. 162 88

Results of our prospective, randomised pilot trial to evaluate the clinical effects and the angiographic correlates of early thrombolysis in patients with unstable angina are reported. Sixty-seven patients had coronary angiography 10 +/- 8 (median 7) hours after an episode of transient chest pain at rest with reversible ischaemic changes on the electrocardiogram. Patients with left main disease (4), or diffuse coronary disease and unidentified ischemia-producing lesions (13) were excluded, as were those without severe (greater than or equal to 70%) stenosis (10). Intracoronary thrombus was identified at angiography in 7 patients (17%) and complex coronary lesions in 5 (12%) of the remaining 40 patients who were randomised to either intracoronary streptokinase 250,000 IU followed by intravenous heparin along with conventional treatment (20 patients), or to conventional treatment alone (20 patients). All patients received Aspirin. No differences between the streptokinase and the conventional treatment groups were observed with respect to demographic and clinical characteristics at admission to the study. During observation in the intensive care unit for 3 +/- 1 days, 8 patients (40%) with streptokinase and 10 (50%) with conventional treatment were free from angina and infarction (p = 0.75; 95% confidence interval for the difference in response rates = -20 to 40%). There were no bleeding complications and no patient died. Patients enrolled in our study had fewer coronary thrombi at angiography than currently reported. Our data did not show that adjunct treatment with streptokinase and heparin is superior to conventional treatment alone in these patients.
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PMID:Intracoronary streptokinase in unstable angina: a prospective randomised study. 180 19

Today many patients admitted with an acute coronary syndrome are already taking aspirin. Because they have symptoms despite antithrombotic therapy, these patients are presumed to be at higher risk for subsequent clinical events. In a pilot trial of antithrombotic therapy in patients with unstable angina at rest or non-Q wave infarction, 93 patients admitted within 48 h of pain were prospectively followed up for 12 weeks. On admission, 29 patients (31%) were already taking daily aspirin; 64 (68%) were receiving no antiplatelet agent. After enrollment all patients received antithrombotic therapy with either aspirin or heparin according to protocol regardless of prior aspirin use. The two groups (prior users versus nonusers of aspirin) were similar with regard to age, gender, coronary risk factors, prior antianginal medication, duration of symptomatic coronary disease, presentation with non-Q wave infarction and extent of electrocardiographic changes on admission. Quantitative analysis of coronary arteriograms (on a 0 to 10 scale) showed similar myocardium-in-jeopardy scores (JS). Follow-up events (recurrent ischemia [Isch], infarction [MI] and revascularization [Revasc]) were: (formula: see text) Aspirin users experiencing rest angina are similar to other patients with ischemic rest pain. The "resistant to aspirin" group does not constitute a subgroup that is at higher risk for cardiac events or revascularization.
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PMID:Clinical and angiographic characteristics and outcome of patients with rest-unstable angina occurring during regular aspirin use. 193 46

Sudden fissuring of an atherosclerotic plaque has been suggested as the primary trigger of transient spontaneous ischemia in both the coronary and cerebral circulation. Measurements of urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2, as well as results of Aspirin trials, have suggested that episodic platelet activation at the site of this acute vascular lesion is mediated, at least partly, by enhanced thromboxane (TX) A2 biosynthesis. Thus, episodic increases in metabolite excretion have been detected in unstable angina. Aspirin (75-325 mg/day) prevents about one third of all fatal and nonfatal thrombotic events in this setting. That a similar "dynamic" thrombotic process occurs during the early phase of acute myocardial infarction is suggested by thromboxane metabolite measurements and by the results of the ISIS-2 trial showing a similar impact of short-term Aspirin therapy to that seen in unstable angina. Percutaneous transluminal coronary angioplasty is associated with transiently enhanced TXA2 biosynthesis and Aspirin-suppressable periprocedural thrombotic complications. On the other hand, both non-insulin-dependent diabetes mellitus and type IIa hypercholesterolemia are associated with a relatively reproducible and persisting abnormality of TXA2-dependent platelet function. This association is likely to reflect a systemic rather than localized stimulus to platelet activation and a continuous rather than episodic alteration. Low-dose (50 mg/day) Aspirin can largely suppress thromboxane metabolite excretion in both diseases. Thus, low-dose Aspirin and/or selective prostaglandin H2/TXA2-receptor antagonists may be important tools to test the hypothesis that TXA2-dependent platelet activation represents an important transducer of the enhanced thrombotic risk associated with these metabolic abnormalities.
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PMID:Thromboxane biosynthesis in cardiovascular diseases. 226 Jan 37

Over a 24-month period, 291 patients were consecutively admitted to the West Haven Veterans Administration Medical Center with new ischemic neurological symptoms. Of these, 90 patients (31%) developed ischemic neurological symptoms while taking aspirin (aspirin treatment failure). Of those in whom aspirin treatment failed, 66 patients had ischemic symptoms in the distribution of the carotid artery. Aspirin treatment failed in 21 patients with severe carotid stenosis (greater than 75% stenosis). Eleven of these 21 patients had cerebral infarctions while taking aspirin, and 7 of these 11 infarcts occurred without the prior warning of transient ischemic attacks. Aspirin treatment failed in 45 patients with lesser degrees of carotid stenosis. Transient ischemic attack without permanent ischemia was the most common manifestation of failure in these patients. Infarction occurred in only 12 of these 45 patients and in only 4 patients did infarction occur without warning. We conclude that patients with symptomatic high-grade carotid stenosis (greater than 75%) in whom aspirin treatment failed are likely to suffer an infarct without warning as the first sign of treatment failure (P less than 0.033). We suggest that this subgroup of patients should be considered for alternative forms of therapy.
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PMID:Patterns of failure of aspirin treatment in symptomatic atherosclerotic carotid artery disease. 233 76


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