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 surface membrane of proximal tubular cells is organized into distinct apical and basolateral membrane domains. The establishment and maintenance of these biochemically, structurally and physiologically distinct domains involves a multi-stage process involving cell-cell, cell-ECM interactions, and polarized targeting mechanisms. Ischemia, via cellular ATP depletion, results in a series of structural, biochemical and functional alterations that lead to loss of proximal tubular cell surface membrane polarity. Of central importance is the rapidly-occurring, duration-dependent disruption and dissociation of the actin cytoskeleton and associated surface membrane structures. This results in numerous cellular alterations including loss of cell-cell contact, cell-extracellular matrix adhesion and surface membrane polarity. Redistribution of surface membrane proteins and lipids into the alternate domain results in the cells inability to function properly. Repair of these disorders involves re-establishment of the actin cytoskeleton and apical and basolateral surface membrane domains. Recent information indicates growth factors may play a role in hastening this repair process.
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PMID:Surface membrane polarity of proximal tubular cells: alterations as a basis for malfunction. 874 61

Acute coronary syndromes are responsible for more than half a million hospital admissions each year in the United States alone. Plaque rupture is the precipitating pathophysiologic event. The degree of narrowing of plaques that rupture is not necessarily severe, in the range of 30% to 70% diameter stenosis. Plaques containing large lipid pools with only thin fibrous caps are most at risk. The site of rupture is most often at the shoulder of the plaque, where stress is highest. Clusters of macrophages are often seen at these points. Most plaque ruptures heal without causing symptoms, perhaps leaving a narrowing somewhat more severe than before. Plaque ruptures that expose larger areas of thrombogenic intramural debris to flowing blood in areas of high turbulence are most likely to provoke more extensive thrombosis. Risk factors, particularly smoking and hypercholesterolemia, cause increased thrombin deposition at the site of deep arterial injury. Thrombin deposition causes local coronary vasoconstriction that may contribute to the development of ischemia. Whether plaque rupture with thrombosis causes infarction, unstable angina, or no symptoms at all depends on the site of the lesion, its severity, and whether the jeopardized myocardium is served by collaterals. Aspirin, heparin, and, potentially, the newer agents provide benefit in each of the acute coronary syndromes.
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PMID:Pathophysiology and initial management of the acute coronary syndromes. 887 45

Despite the availability and use of effective methods for limiting infarct size with thrombolytic agents and primary angioplasty, patients experiencing a myocardial infarction (MI) are at increased risk for a second cardiac event in the post-MI period (e.g., reinfarction, heart failure, and sudden death). For this reason, postinfarction risk management is crucial. An extensive data base has firmly established the efficacy of beta blockers in reducing cardiovascular risk following acute MI. The full advantages of angiotensin-converting enzyme (ACE) inhibitors have only recently begun to emerge as the result of a growing understanding of the mechanisms of adverse outcomes following MI. The importance of lipid-lowering agents, in particular the "statins," should be considered in all post-MI patients, especially since recent studies have conclusively shown improved survival and reduced rates of MI and coronary artery bypass surgery in this population with this therapy. Aspirin is now considered a standard part of the early management of the acute infarct patient as well as for secondary prevention in post-MI patients. At present, chronic anticoagulation with warfarin should be reserved for selected patients. The nondihydropyridine calcium antagonists diltiazem and verapamil can be considered for post-MI use only in patients in whom beta blockers are contraindicated and who have preserved systolic function and/or those without clinical heart failure. In contrast, the dihydropyridine calcium antagonists, particularly nifedipine, have no role in secondary prevention. Although long-term benefits are minimal, nitrates continue to be useful in post-MI patients with residual ischemia (angina or silent ischemia), heart failure (systolic or diastolic), or postinfarction hypertension. Antiarrhythmic agents, except amiodarone, are relatively contraindicated in post-MI patients. Recent data show that vitamin E reduces the rate of nonfatal MI. Its role in cardiovascular death and overall mortality remains to be clarified. Despite their demonstrated value, agents used in secondary prevention generally appear to be underutilized. In addition, when pharmacologic therapies are administered for secondary prevention, they are often prescribed at lower doses than those tested and proved in trials. A greater appreciation for the efficacy and safety profiles of these agents could lead to more widespread use and more pronounced reductions in morbidity and mortality among post-MI patients.
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PMID:Pharmacologic therapies after myocardial infarction. 890 Mar 39

Our study evaluated the relationship between the endogenous production of prostacyclin and the antiarrhythmic effect of ischemic preconditioning against ischemic and reperfusion-induced tachyarrhythmia. Langendorff perfused rat hearts underwent 30 min regional ischemia with reperfusion. Preconditioning was induced by a single episode of 5 min ischemia and 15 min reperfusion. Prostaglandin 6-keto F1 alpha (a stable metabolite of prostacyclin) was determined in the coronary effluent. In the control group the incidence of tachyarrhythmia was 31% during ischemia and 67% during reperfusion. Preconditioning did not affect ischemic arrhythmias but attenuated arrhythmias a reperfusion (8%, p < 0.01) and was associated with increased release of prostacyclin prior to reperfusion. Aspirin abolished the antiarrhythmic effect of preconditioning against reperfusion tachyarrhythmias. However, no relationship was found between suppression of prostacyclin production and the occurrence of arrhythmia in individual hearts. Thus, our findings suggest that metabolites of arachidonic acid via the cyclooxygenase pathway are involved in the protective effect of ischemic preconditioning against reperfusion-induced tachyarrhythmias.
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PMID:Prostaglandins and the antiarrhythmic effect of preconditioning in the isolated rat heart. 890 80

Impaired parasympathetic control of heart rate is associated with increased incidence of cardiac dysrhythmias and ischemia. Anticholinergic drugs suppress parasympathetic control and could be detrimental in the early postoperative period in high-risk patients. In this double-blind randomized trial, 30 ASA physical status I and II patients undergoing minor surgery received either atropine 20 micrograms/kg and neostigmine 50 micrograms/kg (Group A), glycopyrrolate 8 micrograms/kg and neostigmine 50 micrograms/kg (Group G), or placebo (Group P) for reversal of neuromuscular blockade. Two indices of parasympathetic modulation of heart rate, spontaneous baroreflex sensitivity, and high-frequency heart rate variability, were assessed. At 2 h after reversal, Group A showed persisting impairment of baroreflex sensitivity with respect to Group P (7.12 +/- 0.86 vs 12.71 +/- 1.38 ms/mm Hg, P = 0.022) as well as decreased high-frequency heart rate variability (280.8 +/- 30.1 vs 569.2 +/- 115.2 ms2/Hz, P = 0.015). Groups A and G showed a borderline decrease in normalized high-frequency variability at 2 h (P = 0.05 for Groups A and G versus Group P). Anticholinergic drugs with neostigmine cause impairment of parasympathetic control of heart rate which persists into the early postoperative period. The effects of glycopyrrolate appear to be of shorter duration; this drug may thus be preferable in patients at risk of cardiovascular complications.
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PMID:The effects of reversal of neuromuscular blockade on autonomic control in the perioperative period. 898 16

In the 10 years since our previous review of this topic, the acute coronary syndromes (Q wave myocardial infarction [QMI], non-Q wave MI [NQMI], and unstable angina) have been more clearly categorized. Many of the differences delineated between QMI and NQMI still hold: a less extensive infarction and a lower in-hospital mortality, but a larger degree of jeopardized myocardium leading to a higher incidence of reinfarction and recurrent angina. The pathophysiology of NQMI appears to be similar to that of unstable angina except for the greater incidence and extent of thrombus formation and coronary artery occlusion with NQMI. Prognostic studies have shown that ST depression and anterior infarct location are associated with a greater risk for posthospital clinical events than the findings of ST elevation and other infarct locations. Symptom-limited stress testing using electrocardiogram and thallium-201 imaging are now recommended before discharge or in the early postdischarge period, with coronary arteriography recommended for evidence of residual ischemia. Aspirin and low dose heparin should be administered on admission after NQMI to decrease further thrombus formation, and aspirin continued in the posthospital period. Diltiazem administration is recommended in NQMI without evidence of pulmonary congestion to prevent recurrent nonfatal acute myocardial infarction. Percutaneous transluminal coronary angioplasty and surgical revascularization should be reserved for patients with NQMI with residual ischemia.
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PMID:The non-Q wave myocardial infarction revisited: 10 years later. 912 24

The objective is demonstrate that subarachnoid anesthesia with 2% isobaric lidocaine at low doses (0.5 mg/kg) is safe and effective for outpatient arthroscopic surgery of the knee. This was a prospective study of 150 ASA I-III patients undergoing arthroscopic knee surgery as outpatients under subarachnoid anesthesia. With no prior vascular filling, we provided blockade by administering 2% isobaric lidocaine at a dose of 0.5 mg/kg through a Sprotte 25G needle without vasoconstrictor. We assessed effectiveness and degree of sensory-motor blockade, cardiovascular repercussions, recovery time (until reversal of blockade, ambulation, micturition and discharge) as well as side effects observed. The mean dose of lidocaine used was 33.44 +/- 4.16 mg. The sensory-motor blockade achieved provided optimum conditions for prevention of ischemia and the practice of the surgical procedure in all cases. Surgery lasted a mean 38 +/- 10 min. Hemodynamic changes were not clinically significant and no patients additional fluids, atropine or vasopressors. Time from start of blockade until ambulation, micturition and discharge from the recovery unit were 123 +/- 8.3, 175 +/- 12.4 and 194 +/- 13.4 min, respectively. Micturition was spontaneous in all cases. Complications recorded were cephalea and backache. In conclusion, subarachnoid anesthesia at low doses of 2% isobaric lidocaine provides excellent conditions for practicing arthroscopic surgery of the knee on outpatients, with minimum side effects.
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PMID:[Subarachnoid anesthesia with minimal doses of lidocaine in ambulatory arthroscopic surgery of the knee]. 928 Sep 99

Experimental occlusion of a brain-supplying artery triggers tissue ischemia and subsequent inflammatory events that are initiated at the blood microvessel interface. Cytokine production and molecular adhesive events occur in the early moments following cerebral blood flow reduction, which underlie the transition from ischemic to inflammatory injury. Events both within the microvascular lumen and in the immediately surrounding tissue are involved. Cytokines, including TNF-alpha, IL-1 beta, IL-6, and PAF, are produced from the ischemic parenchyma and contribute to the endothelial cell expression of P-selectin, ICAM-1, and E-selectin. Platelet activation occurs paris passu and probably involves alpha-granule P-selectin to mediate PMN leukocyte-platelet interactions. Other integrin heterodimers are also involved in the early microvascular responses to ischemia. The response of the basal lamina and ECM is somewhat slower, entailing yet unproven mechanisms that most probably include the proteolytic processes of leukocyte transmigration. The modifications to microvascular structure are likely to affect both endothelial and astrocyte relationships, promote erythrocyte extravasation and hemorrhage, and contribute to tissue injury. Remodeling of the microvasculature, apparent in other tissues, involves a number of these processes. However, the enzymatic participants and regulating mechanisms are coming under study: the unraveling of regulatory mechanisms of adhesion receptor expression and their modulation, and the companion roles of integrins as mediators of structural integrity and intercellular signaling.
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PMID:Microvascular responses to cerebral ischemia/inflammation. 929 40

Progesterone stimulation of the estradiol (E2)-primed human endometrium initiates DZ of the stromal cells around the spiral arterioles. Under continued steroid stimulation, DZ spreads wave-like to establish the decidual cell as a major cell type of the luteal phase and pregnant endometrium. Because of their widespread distribution throughout the endometrium and concentration at perivascular sites, decidual cells are spatially and temporally positioned to mediate the opposing requirements of maintaining hemostasis during endovascular trophoblast invasion, yet promoting menstrual hemorrhage in the absence of implantation. The experimental results summarized in this review indicate that the paradoxical properties manifested by endometrial stromal/decidual cells are controlled by several proteins with either hemostatic or ECM-degrading or vasoactive activity, and that their expression is altered in response to changes in levels of circulating ovarian steroids during the menstrual cycle. These conclusions are drawn primarily from studies with a well-characterized in vitro model of DZ using monolayers of stromal cells derived from specimens of predecidualized endometrium. Thus, progestins modify the expression of several DZ-related markers in the cultured stromal cells, and E2 enhances these effects despite the lack of response to E2 alone. These responses are consistent with the differential actions displayed by E2 and progesterone in vivo, by which E2 primes the endometrium for the decidualizing effects of progesterone by elevating progesterone receptor levels. Accordingly, during steroid-induced in vitro DZ, a marked increase in the expression of stromal cell TF and PAI-1 and reciprocal inhibition of tPA activity suggest mechanisms to account for the absence of hemorrhage during invasion of the endometrial vasculature by implanting trophoblasts. In contrast to steroid-induced DZ, the events of menstruation are initiated in response to a decline in circulating levels of ovarian steroids. Accordingly, subjecting in vitro decidualized stromal cells to steroid withdrawal results in pronounced reversal in the expression of all of the end points listed above. Consequently, the local hemostatic environment is transformed into a hemorrhage-promoting milieu. Taken together with vascular injury resulting from ischemia induced by spiral artery vasoconstriction, the net effect is attainment of two prerequisites for menstrual hemorrhage, vascular injury and inadequate hemostasis.
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PMID:Decidual cell regulation of hemostasis during implantation and menstruation. 932 39

Angina pectoris due to coronary artery disease is a common manifestation of myocardial ischemia. Reduction of oxygen demand (beta-blockers) and relief of coronary vasoconstriction (calcium blocker or nitrate) are additive approaches to controlling ischemia. Risk factor reduction may improve coronary vascular physiology, and ASA reduces the likelihood of thrombosis and myocardial infarction. It is still unclear whether reduction of angina reduces cardiac morbidity and/or mortality. In the Asymptomatic Cardiac Ischemia Pilot Study (ACIP) and Total Ischemic Burden Bisoprolol Study (TIBBS) trials, data suggest benefit from reducing myocardial ischemia. Thus control of angina pectoris is a major goal of the treatment of coronary artery disease.
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PMID:Optimal treatment of stable angina. 939 90


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