Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:[Studies on the involvement of bradykinin in the formation of ischemic brain edema]. 169 63

Immunohistochemical localization of prostaglandin (PG) F2 alpha synthesized during recirculation following experimental forebrain ischemia was studied in Mongolian gerbils. The bilateral carotid arteries were clamped for 5 minutes, and the brains were frozen in situ after 5 minutes of recirculation. Sham-operated gerbils not subjected to arterial occlusion served as controls. Cryostat sections containing dorsal hippocampus 10 microns in thickness were incubated in rabbit anti-PGF2 alpha serum and stained with avidin-biotin-peroxidase complex after fixation in carbodi-imide and Zamboni's solution. In specimens from control animals, blood vessels were faintly stained with anti-PGF2 alpha serum, while neurons and glial cells were less intensely stained or unstained. Specimens from reperfused gerbils demonstrated strongly positive staining for PGF2 alpha in blood vessels, neurons (especially hippocampal pyramidal neurons), and glial cells. Staining for PGF2 alpha in the reperfused animals was substantially diminished by pretreatment with indomethacin (10 mg/kg, i.p.). The results indicate that recirculation after forebrain ischemia results in an increase in PGF2 alpha in neurons, glial cells, and blood vessels.
 ...
PMID:Immunohistochemical localization of prostaglandin F2 alpha in reperfused gerbil brain. 169 90

The purpose of this study was to determine whether normal fibrinogen contributes to the development of myocardial reperfusion injury by acting as a substrate in vivo for neutrophil adhesion. This was tested in a dog model of acute myocardial infarction that used pentobarbital anesthetized dogs subjected to 90 min regional myocardial ischemia and 5 h reperfusion. Dogs were treated with 1 unit/kg Ancrod (venom from the Malayan pit viper, Agkistrodon rhodostoma) or vehicle i.v. 60 min after left circumflex coronary artery occlusion. Therapeutic defibrination was verified in Ancrod-treated dogs by measurements of clottable fibrinogen, alpha-2 antiplasmin and plasminogen, by the activated partial thromboplastin time and by immunoelectrophoresis. Fibrinogen was depleted to below detectable limits of the assay (less than 0.05 mg/ml) after treatment with Ancrod. The defibrination effect was accomplished by the expected activation of the fibrinolytic system: alpha-2 antiplasmin was decreased by 10% and plasminogen activity was decreased by 30% with Ancrod treatment. There were no measureable differences between the two treatment groups in heart rate, mean arterial blood pressure, rate pressure product or circumflex coronary blood flow throughout the 90 min of regional ischemia or during the 5 h of reperfusion. The relative severity of ischemia between the two treatment groups was similar when assessed with radiolabeled microsphere measurement of myocardial blood flow. The accumulation of neutrophils (measured by myeloperoxidase activity) within the myocardium after reperfusion was not reduced by prior depletion of fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Therapeutic defibrination with ancrod does not protect canine myocardium from reperfusion injury. 170 37

Isolated segments of cat small intestine were subjected to 3 hr of ischemia followed by 1 hr reperfusion (I/R). Mucosal biopsies were obtained for measurement of myeloperoxidase (MPO) activity, an index of tissue neutrophil count, and leukotriene B4 (LTB4) production. Animals were pretreated with either cyclosporin A (CsA) or FK506, which are potent immunosuppressants. Both agents significantly attenuated the neutrophil infiltration induced by I/R. FK506, but not CsA, reduced the elevated mucosal LTB4 production normally observed following reperfusion. The results of this study suggest that FK506 and CsA may be important agents in modulating neutrophil infiltration in acute inflammatory conditions.
 ...
PMID:Effects of cyclosporin A and FK506 on ischemia/reperfusion-induced neutrophil infiltration in the cat. 171 12

In order to determine thresholds for irreversible cellular injury in the rat retina, timed acute no-flow ischemic episodes of 30-180 min duration were produced by elevation of intraocular pressure (IOP) above systolic pressure. Quantitation of irreversible degeneration and cell loss following a 2-week post-ischemic interval was performed by computer-assisted measurements from histologic sections. Alterations of thickness of retinal layers and linear cell density were determined for ischemia of selected durations (30, 60, 80, 90, 120 and 180 min). Different thresholds were evident for inner and outer retinal damage. Neurons of the inner nuclear layers showed extensive loss with episodes at 60 min. Decrease in the thickness of the inner plexiform layer provided the best index of this inner nuclear damage. The outer retina was more resistant, with photoreceptors showing extensive damage only after 90 min in conjunction with pigment epithelial metaplasia and degeneration. Two-hour episodes produced full-thickness degeneration with loss of pigment epithelium and sparing of the peripheral retina. Greater sensitivity of the inner retina suggested problems with restoration of the retinal circulation. Horseradish peroxidase infusions did reveal central microcirculatory defects in retinal wholemounts of some specimens with episodes longer than 60 min. Refinements of the methods resulted in outcomes sufficiently reproducible for quantitative assessment of acute ischemic injury. The rat retina provides an economical basic tissue model of acute ischemic injury affecting neurons, glia, and microvasculature. Quantitation of this injury promises great utility in testing agents with potentially protective effects on acute ischemic injury.
 ...
PMID:Quantitation of ischemic damage in the rat retina. 174 56

This study examined regional patterns of increased vascular permeability and morphological indicators of acute neuronal injury following normothermic and mildly hyperthermic forebrain ischemia. Rats underwent 20 min of four-vessel occlusion during which intraischemic brain temperature was maintained at either 37 degrees C or 39 degrees C. At 45-min recirculation, the blood-brain barrier (BBB)-tracer horseradish peroxidase was injected and rats were perfusion-fixed at 1-h recirculation for light and electron microscopic analysis. In normothermic and hyperthermic rats, sites of increased vascular permeability were spatially correlated with dark shrunken type IV neurons. Neuronal alterations within cortical, hippocampal, striatal, and thalamic areas ranged from mild cytoplasmic vacuolation and mitochondrial swelling to severe cytoplasmic shrinkage and increased density. Although dark shrunken neurons were routinely associated with permeable blood vessels in both temperature groups, dark neurons were not detected in regions demonstrating an intact BBB. Following normothermic brain ischemia, the appearance of dark shrunken neurons was restricted to the cerebral cortex and striatum. In both temperature groups, luminal leukocytes were detected within otherwise well-perfused forebrain microvascular beds. Our studies suggest a close interrelationship between postischemic microvascular abnormalities, including increased vascular permeability, and morphological indicators of acute neuronal injury following brain ischemia.
 ...
PMID:Interrelationships between increased vascular permeability and acute neuronal damage following temperature-controlled brain ischemia in rats. 188 38

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction. 190 90

The distribution patterns of ionic Lanthanum (La3+; mol. wt. 139) were evaluated after 15, 30 and 60 min of middle cerebral artery occlusion in perfused-fixed rats. Blood-brain barrier (BBB) permeability to Evans blue (EB) and horseradish peroxidase (HRP; mol. wt. 40,000) in vivo was also evaluated. Brain tissue specific gravity was measured. An increase in brain water content was found as early as 30 min following occlusion. HRP and EB extravasation was not observed. La3+ crossed the interendothelial clefts of venules and capillaries at 30 and 60 min and was seen in both extracellular and intracellular brain compartments at 60 min. La3+ extravasation was seen in nonedematous areas bordering the regions of water accumulation. Our findings suggest that the early phase of incomplete continuous ischemia is accompanied by changes in BBB permeability and the interendothelial clefts of venules and capillaries seem to represent one of the early sites of ischemic damage.
 ...
PMID:Blood-brain barrier permeability to micromolecules and edema formation in the early phase of incomplete continuous ischemia. 192 66

Superoxide radicals produced during acute intestinal ischemia are biochemically related with the presence of hydrogen peroxyde. In this study we have investigated the distribution of peroxidase-catalase activity, histochemically determined, in the ischemic ileal wall. In the rat, complete arterial and venous occlusion produced a progressive increase in extra-vascular peroxidase-catalase activity with a maximum corresponding to the ileal wall. Probably the tissue peroxidase-catalase activity is related to massive degranulation of polymorphonucleates.
 ...
PMID:Intestinal ischemia: morphological features--II. 196 11

The effects of daltroban, a specific thromboxane receptor antagonist, were investigated in a model of myocardial ischemia consisting of 1.5 h of coronary artery occlusion followed by reperfusion for 4.5 h in anesthetized cats. Daltroban (1 mg/kg) was infused as a bolus 10 min prior to reperfusion of the left anterior descending (LAD) coronary artery. Daltroban infusion resulted in a significantly lower necrotic area expressed as a percentage of the myocardial area-at-risk compared to the MI + vehicle group. However, daltroban failed to retard increases in myeloperoxidase activity in the ischemic myocardium, indicating no reduction in neutrophil accumulation. Moreover, left anterior descending coronary artery ring preparations isolated from daltroban treated MI cats exhibited endothelial dysfunction following ischemia reperfusion. Thus, daltroban significantly protected the myocardium from reperfusion injury without protecting the coronary endothelium or retarding neutrophil accumulation.
 ...
PMID:Daltroban, a thromboxane receptor antagonist, protects the myocardium against reperfusion injury following myocardial ischemia without protecting the coronary endothelium. 196 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>