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 role of the sympatheticoadrenal and kallikrein-kinin systems in the pathogenesis of hemodynamic disorders was studied in 29 dogs with acute experimental occlusion of the terminal part of the aorta. Data confirming the close dependence of the indices of central hemodynamics on the activity of the sympatheticoadrenal and kallikrein-kinin systems are presented. Close positive correlative connection between activation of the sympatheticoadrenal and kallikrein-kinin systems was revealed. The possible mechanisms of the correction of hemodynamic disorders in severe degree of ischemia by means of agents blocking the kallikrein system are discussed.
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PMID:[Role of the sympathetic-adrenal and kallikrein-kinin systems in regulating central hemodynamics in acute experimental occlusion of the terminal portion of the aorta]. 30 71

To evaluate the effect of prostaglandin inhibition on the renal blood flow of the ischemic kidney, we administered indomethacin to 10 anesthetized dogs with renal artery stenosis and contralateral nephrectomy. Following the operation to produce renal ischemia, there was an increase of blood pressure associated with an increase of renin and the prostaglandins F1 (PGF1), and E (PGE). The administration of indomethacin to the intact, normotensive animals caused the anticipated decrease of prostaglandin E, renin, and renal blood flow. However, in the hypertensive dogs, indomethacin caused a paradoxical 45 per cent increase in the renal blood flow, despite a 44 per cent decrease of prostaglandin E. PGF1, PGE, renin, and erythropoietin exhibited the anticipated decreased levels. The study suggests that prostaglandins may not be the sole important factor in the regulation of renal blood flow in the presence of ischemia. Other important factors likely include the renin-sensitive angiotensin, the adrenergic, and the kallikrein-kinin systems.
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PMID:Paradoxical increase of renal blood flow in anesthetized hypertensive dog treated with indomethacin. 48

The role of serotonin, histamine, and the kallikrein-kinin system in acute arterial occlusion during ischemia was studied from the standpoint of multivariate correlation analysis. The mechanisms of their participation in the genesis of pathophysiological disorders in the organism in acute arterial occlusion are discussed. The important role of serotonin and the kallikrein inhibitor in this pathological condition is shown.
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PMID:[Use of correlation analysis of clinical biochemical indices for a study of the pathogenesis of acute arterial obstruction]. 51 67

Bradykinin, a nine-amino-acid peptide formed from a large precursor polypeptide (kininogen) by the action of the enzyme kallikrein (kininogenase), is the initial mediator of inflammation, and, in particular, bradykinin induces pain and alters vascular permeability. Bradykinin is one of the first compounds produced at the site of tissue injury and subsequently initiates a cascade of reactions that produce the cardinal features of inflammation. We will explore the role that bradykinin plays in various types of neuronal injury. In particular, we will focus on the role that bradykinin and other kinins play in brain and spinal cord trauma, in the pathophysiology of subarachnoid and intraparenchymal hemorrhage and ischemia, and in the initiation of nociceptive pain. This role suggests that bradykinin antagonists may be clinically useful in the therapeutic management of neurosurgical patients.
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PMID:Bradykinin and neuronal injury. 158 16

Bradykinin (BK) is known to be involved in the inflammatory process causing various tissue reactions such as peripheral vasodilation and increased vascular permeability. The aims of this study was to investigate the involvement of the kallikrein-kinin system (K-K system) in the generation and progression of cerebral edema following an ischemic incident. First, after infusion of BK into the internal carotid artery, the cerebral water content was measured and electron microscopic observations were made to investigate changes of permeability using the horseradish peroxidase (HRP) tracer method. Secondly, the plasma and tissue BK levels, cerebral water content and energy metabolites (ATP, lactate and pyruvate) were measured at scheduled intervals. This was achieved using the cerebral ischemia model induced in spontaneously hypertensive rats (SHR) in which the common carotid artery were occluded (BLCO) with clips in both sides. The plasma and tissue BK were measured by radioimmunoassay. Furthermore, aprotinin and soybean trypsin inhibitor (SBTI), which specifically inhibit the K-K system, were applied to the same model and the effects on cerebral edema and metabolism were tested. At three hours after infusion of BK, cerebral edema was observed on the infused hemisphere and an increase of pinocytosis in the vessels was observed in the electron microscopic study. The chronological observation of cerebral water content revealed that it started to increase after BLCO, reaching a peak level at 30 min after reperfusion, before decreasing slightly. The plasma BK levels also showed an increase at the end of BLCO and reached a peak level at 30 min after reperfusion, decreasing thereafter. The tissue BK levels elevated significantly at 30 min after reperfusion and returned to control levels at 60 min. The ATP levels decreased remarkably after BLCO, and then increased after 30 min of reperfusion. The lactate levels increased during ischemia and became higher at 30 min after reperfusion and then decreased. The pyruvate levels did not change during this time period. In the treated group, aprotinin showed significantly lower levels of cerebral water content compared to the control. This group also showed lower lactate accumulation and preservation of ATP levels than the control. SBTI also had significantly lower water content than the control, but there was no difference in the metabolites. These results showed that BK augments the progression of brain edema and that the BK level corresponded with progression of ischemic brain edema and the suppression of BK decreased edema formation. These novel findings indicate a close relationship between BK and ischemic brain edema.
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PMID:[Studies on the involvement of bradykinin in the formation of ischemic brain edema]. 169 63

The paper discusses if it is advisable to use kallikrein-kinin system inhibitors earlier. A total of 122 patients with acute ischemia and infarction of the myocardium were studied. Contrykal and heparin infused in the prehospital period, followed by hospital treatment are optimal to prevent vascular wall lesions, maximally retain retrograde blood flow, and substantially reduce the size of myocardial infarction. Therapy with protease inhibitors proved to be most beneficial within the first 2 hours of the disease, as evidenced by a profound improvement in the clinical course of myocardial infarction, a decrease in ECG and precordial mapping signs of ischemia, a positive change in myoglobin and MB creatine phosphokinase levels, and a significant reduction in the rehabilitative period.
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PMID:[Rationale for using kinin system inhibitors in patients with acute ischemia and infarction of the myocardium during the prehospital phase]. 171 6

The effects of aprotinin on canine myocardium subjected to cardioplegia and global ischemia for 4 hours and then reperfused for 1 hour were investigated. Lysosomal and mitochondrial enzymes and cyclic nucleotides (adenosine cyclic monophosphate and guanosine cyclic monophosphate) were measured in coronary sinus blood. Aprotinin was given intravenously before cardiopulmonary bypass at total doses of 10 X 10(3) kallikrein units per kilogram (group A, six dogs) and 20 X 10(3) KU/kg (group B, six dogs). In group A, three dogs survived but with poor cardiac function; all dogs in group B survived and had better cardiac function. Lysosomal (N-acetyl-beta-D-glucosaminidase) and mitochondrial (aspartate aminotransferase) enzymes in coronary sinus blood at 60 minutes of reperfusion were significantly (p less than 0.05) lower in group B than in group A. In both groups, guanosine cyclic monophosphate was significantly (p less than 0.01) lower during reperfusion than before cardiopulmonary bypass; however, the values were significantly (p less than 0.05) higher in group B than in group A. Serum adenosine cyclic monophosphate was lower during reperfusion than before bypass in both groups, but it recovered during reperfusion in group B. Myocardial adenosine triphosphate was well preserved in both groups but creatine phosphate was decreased (p less than 0.01) in group A. These results suggest that aprotinin at a dose of 20 X 10(3) KU/kg may be effective in preserving myocardial viability and function after prolonged cardioplegia.
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PMID:Role of protease inhibition in myocardial preservation in prolonged hypothermic cardioplegia followed by reperfusion. Effect of aprotinin in an experimental model. 245 28

The renin-angiotensin system (RAS) has long been perceived as basically humoral. Since recent findings in molecular biology extended this view to local, possibly independent, tissue-RAS, both the RAS and the kallikrein-kinin cascade are understood as mixed local-systemic interacting systems, which explains local and systemic effects of converting enzyme (CE) inhibitors well. The key enzyme of both systems, CE, catalyzes the activation of the vasopressor and possibly trophic peptide, angiotensin II, and also inactivates the vasodilatory and, according to our observations, cardioprotective bradykinin. Thus, it is consistent that CE-inhibitors lower blood pressure, reduce cardiac hypertrophy, improve metabolic state and attenuate arrhythmias, particularly in ischemic hearts. It is evident from animal experiments that the tight binding favours new oral CE inhibitors, such as ramipril, not only for prevention but also for treatment of tissue injuries due to hypertension or ischemia.
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PMID:[Pharmacologic modification of the converting enzyme--local and systemic effects on the heart and blood vessels]. 285 Jun 85

Among the mediators for development of endotoxic shock, plasma kallikrein and prostanoids have been suggested to play an important role. The role of kallikrein and PGF2 alfa in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring inactive and active kallikreins and PGF2 alpha in superior mesenteric vein, right ventricle and aorta during shock induced by occlusion of the superior mesenteric artery. After removal of the clamp in dogs subjected to occlusion for 1 hour, the mean arterial blood pressure fell rapidly within 5 min and gradually increased over the next 60 min, with return to the control values. The plasma concentrations of PGF2 alfa in superior mesenteric vein, right ventricle and aorta increased three- to fivefold within 5 min of reperfusion. Thereafter the PGF2 alfa levels fell, so that at 60 min after declamping they did not significantly differ from the control values. No significant changes were observed in the levels of inactive and active kallikreins. The results suggest that PGF2 alfa released by intestinal tissues may contribute to the development of shock caused by intestinal ischemia.
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PMID:Changes in plasma kallikrein and PGF2 alfa concentrations during circulatory shock. Studies with superior mesenteric artery occlusion in anesthetized dogs. 292 98

Traumatology deals with two different types of shock - the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthine-xanthine oxidase system) and activation of the humoral axis - of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a "locus minoris resistentiae" for further development of endotoxemia, bacteremia, septic shock and multi-organ failure without a typical septic focus. By this "septic challenge" further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.
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PMID:[Current findings in the pathogenesis of the shock process in traumatology]. 328 34


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