Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 modulatory role of the platelet-activating factor (PAF) antagonist WEB-2086 (30 microM) on the response to antigen-induced (trinitrophenyl-haptenized ovalbumin) and global ischemia (30 and 60 min)-induced changes in the response to antigen was studied in isolated hearts from actively sensitized rats. In sensitized normoxic hearts, both antigen (0.8 mg) and PAF (100 pmol) induced a short-term increase followed by a long-term decrease in coronary flow (CF). The antigen- but not the PAF-evoked increase in CF was accompanied by a substantial release of histamine. WEB-2086 enhanced the vasodilator effect and abolished the vasoconstrictor effect of 100 pmol of PAF but neither modified the coronary vascular effects of antigen nor the antigen-induced histamine release. Ischemia for 60 min followed by 30 min of reperfusion increased the diastolic left ventricular pressure but a 30-min period of ischemia and reperfusion had no effect on baseline cardiac function. WEB-2086 had no effect on ischemia-induced changes in cardiac function. A 30-min period of global ischemia enhanced the antigen-induced decrease in CF and systolic left ventricular pressure (SLVP). A 60 min period, however, suppressed the antigen-induced effects on CF and SLVP as well as antigen-induced histamine release. WEB-2086 partly protected the heart against the enhanced antigen-induced decrease in CF and SLVP after a 30-min period of global ischemia but no modulatory role of WEB-2086 was observed after 60 min of global ischemia. Our conclusions are that (a) PAF is not involved in rat cardiac anaphylaxis since WEB-2086 was proven to be inactive; (b) cardiac ischemia and cardiac anaphylaxis have interrelated mechanism of action since ischemia changed the anaphylactic response, which indicates that coincidence of these two pathological events could influence the clinical outcome; and (c) PAF is possibly involved in rat cardiac ischemia since WEB-2086 partly protected the heart against the enhanced antigen-induced decrease in CF and SLVP after 30 min of ischemia and reperfusion.
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PMID:Modulation of antigen- and ischemia-induced effects by the platelet-activating factor antagonist WEB-2086 in isolated sensitized rat hearts. 128 Jul 43

Acupuncture activates the defense systems. It influences specific and nonspecific cellular and humoral immunities; activates cell proliferation, including blood, reticuloendothelial, and traumatized cells; and activates leucocytosis, microbicidal activity, antibodies, globulin, complement, and interferon. It modulates hypothalamic-pituitary control of the autonomic and neuroendocrine systems, especially microcirculation, response of smooth and striated muscle, and local and general thermoregulation. Immunostimulant points include LI-4, LI-11, ST-36, GB-39, SP-6, GV-14, BL-11, BL-20, BL-23, BL-24, BL-25, BL-26, BL-27, BL-28, and CV-12. Some, such as BL-47, are immunosuppressive. Antifebrile points include GV-14 and ST-36. Reactive reflex SHU points, MU points, and earpoints are useful in organic diseases. In immunomediated diseases, some or all of these points can be used with other points, especially local points and points of the major symptoms or points of the affected body part, area, function, or organ. Applications of acupuncture include treatment of inflammation and trauma; stimulation of tissue healing in burns, ulcers, indolent wounds, ischemia, necrosis, and gangrene; infections; postinfection sequelae; fever; autoimmune disease; allergies; anaphylaxis and shock; and treatment or prevention of side effects from cytotoxic chemotherapy and ionizing radiation. Acupuncture therapy may inhibit neoplastic cells. Examples of acupuncture use in immunomediated conditions in small animals are given.
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PMID:Acupuncture for immune-mediated disorders. Literature review and clinical applications. 158 55

Ginkgolides are unique twenty-carbon terpenes, occurring naturally only in the roots and leaves of Ginkgo biloba. The molecules incorporate a tert-butyl group and six 5-membered rings, and are specific and potent antagonists of platelet-activating factor (PAF), a potent inflammatory autacoid. Studies in animal models with the most potent ginkgolide, BN 52021, and other specific PAF antagonists have demonstrated that PAF plays an important role in pathologies such as asthma, shock, ischemia, anaphylaxis, graft rejection, renal disease, CNS disorders and numerous inflammatory conditions. Ginkgolides are now being developed as therapeutic agents and very promising results have been obtained in clinical trials on shock, organ preservation and thermal injury. In addition to ginkgolides, several other types of natural PAF antagonists have been identified from various medicinal plants. These compounds have not only helped to explain the pharmacological basis of several traditional medicines, but have also provided man with a valuable new class of therapeutic agents.
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PMID:Ethnopharmacology and the development of natural PAF antagonists as therapeutic agents. 188 Nov 52

An anaphylactic reaction in the isolated perfused heart is characterized by a drastic coronary constriction, arrhythmias, and an impairment of contractility. In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to ascertain the electrocardiographic and cardiovascular changes during systemic hypersensitivity reactions. In addition, an attempt was made to differentiate cardiac from respiratory events. In guinea pigs, sensitization was produced by s.c. administration of ovalbumin together with Freund's adjuvant solution. Fourteen days after sensitization, the effects of an i.v. infusion of ovalbumin were tested in the anesthetized guinea pigs, which were ventilated with room air or 100% oxygen. A second administration of the antigen induced the development of cardiovascular collapse, leading to death within 12 min. Within 3 min, cardiac output decreased by 90% and end-diastolic left ventricular pressure increased significantly, indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in the form of atrioventricular block. Left ventricular contractility declined continuously within the first 4 min. Finally, after 4 min, blood pressure steadily decreased. During ventilation with room air, severe hypoxia developed, with arterial PO2 decreasing from 94 mmHg to 14 mmHg after 3 min. However, under ventilation with 100% oxygen, a dissociation between cardiac damage and respiratory distress occurred. Myocardial ischemia and signs of cardiac failure preceded the development of hypoxia by a significant time interval. It is to be concluded that cardiac damage is a primary event in anaphylactic shock. Furthermore, the electrocardiographic signs of ischemia are interpreted as a result of coronary artery spasm.
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PMID:Systemic anaphylaxis--separation of cardiac reactions from respiratory and peripheral vascular events. 221 74

The platelet activating factor (PAF), a low molecular phospholipid, plays an important role in inflammation, anaphylaxis, and shock state development. In the isolated perfused guinea pig heart, PAF induces a decrease in coronary flow and cardiac contractility and atrioventricular conduction disturbances. Furthermore, PAF mediates a powerful bronchoconstrictory action causing a severe impairment in respiratory function. In the present study an attempt was made to separate cardiac from respiratory events during PAF-induced shock in vivo. PAF was injected intravenously (0.1-10 micrograms/kg) into anesthetized guinea pigs ventilated with room air or 100% oxygen. Administration of 10 micrograms/kg PAF was uniformly lethal: already within 2 min, cardiac output decreased by 60% and end-diastolic left ventricular pressure increased markedly indicating cardiac failure. ECG recordings showed signs of acute myocardial ischemia. Arrhythmias occurred in terms of atrioventricular conduction delay. Blood pressure initially increased, then declined continuously to below baseline within 10 min. All animals died within 25 min. Ventilation with room air was paralleled by development of severe hypoxia. However, under ventilation with 100% oxygen a dissociation between PAF-mediated cardiac and respiratory effects occurred. It is concluded that the PAF-induced shock is primarily based on direct cardiac damage. Furthermore, the ECG signs of ischemia are most likely due to coronary spasms.
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PMID:Cardiovascular reactions and respiratory events during platelet activating factor-induced shock. 238 16

Arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to test the development of lipoxygenase metabolites of arachidonic acid in cerebral ischemia, we measured free arachidonic acid and slow reacting substance of anaphylaxis (SRS-A) and leukotriene C4 in the brain tissue. Moreover, we studied the influence of inhibitor of SRS-A release on postischemic cerebral edema. Severe forebrain ischemia in rats was induced by the modification of the method described by Pulsinelli and Brierley. Both vertebral arteries were electrocauterized through the alar foramen and then bilateral common carotid arteries were clamped by aneurysmal clips and mean arterial pressure was reduced to 80-90 mmHg. EEG activity was isoelectric throughout the period of carotid clamping. After forebrain ischemia had been maintained for 30 minutes, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Following the desired ischemic or postischemic periods, the brains were frozen in situ with liquid nitrogen. The brains were then chiselled out during irrigation with liquid nitrogen and stored at -80 degrees C until analysis. The brain extracts were analysed by high performance liquid chromatography for free arachidonic acid, by bioassay using the ileum of guinea pig for SRS-A and by radioimmunoassay for leukotriene C4. Brain water content was calculated with dry weight method. Inhibitor of SRS-A release, tranilast, was given intraperitoneally, 100 mg/kg 30 minutes before induction of ischemia and 50 mg/kg immediately before recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tissue leukotrienes in cerebral ischemia and the effect of inhibitor of SRS-A release on postischemic cerebral edema]. 246 14

Human plasma leukotriene C4 (LTC4) levels of cerebral infarcted patients showed a significant increase and plasma vitamin A (VA) levels showed a significant decrease compared to the normal plasma obtained from age-matched control. Therefore, the effect of VA on leukotriene (LT) levels and the progress of cerebral edema were investigated in VA deficient Wistar rat brains. Incomplete global cerebral ischemia was induced by occluding the bilateral common carotid arteries (BLCO) with clips. Wistar rats were made VA deficient by feeding them a vitamin A deficient diet for 5 weeks on a specific pathogen free status. After 3 hours of BLCO the blood was reperfused by removing the clips. After each period of reperfusion, the rat brain was fixed by freezing in situ and used for assaying leukotrienes, vitamin A, and water content. Slow reacting substance of anaphylaxis (LTC4 + LTD4 + LTE4) levels showed an increase at the end of BLCO in the VA deficient group and the high levels persisted for 30 min and then decreased to the control level. Brain water contents were elevated significantly at the 30 min phase of reperfusion. With VA administration, the water contents tended to be lower than in the VA deficient group at any phase. Histologically, after ischemia and reperfusion, evans blue extravasation and marked spongioid formations around small vessels were observed in the VA deficient rats only. These facts indicate that VA functions to stabilize cell membranes and suppress ischemic cerebral damage.
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PMID:[The effect of vitamin A on leukotriene production in the ischemic rat brain]. 260 50

A 31-year-old man with allergic rhinoconjunctivitis and asthma experienced an episode of anaphylaxis following an injection of allergens during hyposensitization. His anaphylactic episode was remarkable because of a relative sinus bradycardia at the beginning of his reaction. This case is reported to highlight the importance of not confusing the anaphylactic syndrome with vasovagal syncope even when a tachycardia is initially absent. The possible pathophysiologic role of right coronary vasospasm resulting in the Bezold-Jarish reflex or sinoatrial node ischemia is discussed.
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PMID:Anaphylaxis associated with relative bradycardia. 273 57

Leukotrienes have been implicated as mediators of ischemia and shock. Recent evidence has been obtained supporting the four major criteria of acceptance of leukotrienes as mediators of shock, namely (a) increased concentration in body fluids during shock states, (b) ability to exert significant pathophysiologic effects which aggravate ischemia and shock, (c) amelioration of the shock state by leukotriene synthesis inhibitors and leukotriene receptor antagonists, and (d) production of a shock-like state by exogenous administration of leukotrienes. In conclusion, both LTB4 and the peptide leukotrienes (e.g. LTC4, LTD4 and LTE4) also known as the slow reacting substance of anaphylaxis (SRS-A) can be considered as mediators of ischemia and shock. Although difficulties exist with measuring leukotrienes in circulating blood and in obtaining long lasting selective blockers of leukotriene synthesis, innovative experiments measuring leukotrienes in bile and other body fluids and in employing specific leukotriene receptor antagonists have helped in assessing the significance of the leukotrienes in shock states. Additional studies are necessary to evaluate these findings in perspective, and to compare and contrast the role of leukotrienes to that of other vascular mediators including prostaglandins and thromboxanes, as well as non-eicosanoids including serotonin, histamine, angiotensin II and vasopressin, all of which can play a mediator role in ischemia and shock states. Further clarification of these issues promises to open exciting new chapters in shock research.
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PMID:Leukotrienes as mediators of ischemia and shock. 300 83

Cardiac myolysis was observed in guinea pigs sensitized with vesicular stomatitis virus (VSV), following challenge with this antigen. The phenomenon developed within 1 h of challenge, appearing as islands in the myocardium. The speed and focal nature of the damage point to obstruction of blood flow as a cause of the myolysis. The myolysis was not a toxic effect of the virus itself, but probably a consequence of cardiac anaphylaxis. It occurred only after challenge, and was abolished in 71% of the animals by pretreatment with a mixture of the lipoxygenase-cyclooxygenase inhibitor, BW755C and H1 histamine receptor antagonist, diphenhydramine. Treatment with BW755C alone before challenge prevented myolysis from developing in 46% of the animals. Challenge in vitro with VSV to the perfused, spontaneously beating, sensitized isolated guinea pig heart increased sulfidopeptide-leukotriene (LTC4, LTD4, LTE4) production from undetectable levels (0.5 ng LTD4-equivalent/heart/15' to 13 ng LTD4-equivalent/heart/15'. At the same time, there were derangements in cardiac rate, contractility and coronary outflow typical of cardiac anaphylaxis. The reduction in coronary outflow rate during cardiac anaphylaxis is due largely to the powerful vasoconstrictor effect of LT, as well as perhaps platelet-activating-factor. Thus it is speculated that there is a causal relationship between LT release, vasoconstriction, ischemia and myolysis in the heart, following VSV challenge to sensitized guinea pigs.
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PMID:Immunological challenge with virus initiates leukotriene C4 production in the heart and induces cardiomyolysis in guinea pigs. 302 94


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