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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a combination of novel techniques to assess quantitatively the shape and the filterability of red blood cells (RBC) after exposure to stress conditions (400 mosmol/l, lactacidosis, pH 6.8), the effects of 1-benzyl-3-ethyl-6,7-dimethoxy-isoquinoline hydrochloride (moxaverine-HCl, Kollateral) were tested. The shape of freely suspended RBC was quantified using the tangent count procedure. The filterability (microrheological performance) of leukocyte-free RBC suspensions was determined by computer-assisted conductometry using novel precision metal microsieves with uniform pore diameter of 4.2 micron. Moxaverine, when present in doses between 10(-5) und 10(-2) mol/l while the RBC are stressed, restored both the normal discoid red cell configuration and the microrheological performance when tested under low shear stresses. The data show that moxaverine, a papaverine derivative, hitherto considered as a classical vasodilator exerts protective effects on RBC membrane curvature and whole cell microrheological behavior (performance). The protective effects manifest themselves when the RBC's are exposed to abnormal biochemical conditions such as they might occur in poststenotic areas, where hypoxic ischemia is known to lead to a combination of hyperosmolarity and lactacidosis which modify the RBCs.
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PMID:Influence of moxaverine hydrochloride on membrane curvature and microsieve filterability of red cells after exposure to hyperosmolarity and lactacidosis. 341 14

The effect of S-adenosyl-L-methionine (SAM) on neuronal degeneration induced by transient forebrain ischemia was studied in rats. Bilateral occlusion of the common carotid arteries for 30 min in a 4-vessel occlusion model caused degeneration of CA1 neurons of the hippocampus. When SAM-HCl or SAM sulphate tosylate (SAM-ST, 100 mg/kg as the free form of SAM, i.p.) was administered just after recirculation and every hour for 5 h after recirculation, the degeneration and loss of pyramidal cells were prevented. However, adenosine, a metabolite of SAM, and glycerol, which has the same osmotic pressure as the solution of SAM-ST, did not show any effects on the neuronal damage. The results showed that SAM has a beneficial effect on neuronal damage induced by ischemia.
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PMID:S-adenosyl-L-methionine prevents ischemic neuronal death. 343 68

alpha-Tocopherol and prednisolone exhibited the highest antiischemic activity, while lidocaine and sodium glutamate were less active after administration into isolated perfused rabbit liver tissue subjected to 60-min thermic ischemia. Chlorpromazine.HCl did not affect the biochemical patterns studied in isolated perfused liver tissue.
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PMID:[Effect of anti-ischemic protection on biochemical indices of the isolated perfused liver]. 344 49

In vivo microscopy and histology were used to study the effect of exogenous acid (0.1 N HCl) on the rat corpus mucosal microcirculation and bleeding in hemorrhagic shock. Systemic blood pressure was reduced stepwise by bleeding. Mucosal blood flow showed a significant linear correlation with mean systemic blood pressure. The flow stopped in half of the rats at 25% of control blood pressure, but red blood cells were always present within the microvessels. In contrast, the topical application of 0.1 N HCl accelerated the decrease of blood flow with graded hypotension and caused progressive disappearance of the honeycomblike network of red blood cell-filled superficial mucosal microvessels. After retransfusion, mucosal bleeding occurred in the area in which the blood-filled microvessels had disappeared. Histology revealed that the bleeding extended from the middle of the depth of the mucosa and was associated with tissue necrosis. These results indicate that exogenous acid in hemorrhagic shock causes increased mucosal ischemia and tissue damage with bleeding on retransfusion.
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PMID:Effect of exogenous acid on the rat gastric mucosal microcirculation in hemorrhagic shock. 349 45

The antifibrillatory, antithrombotic and hemodynamic properties of intraventricular prostacyclin (PGI2) application were studied in conscious canine model of sudden cardiac death. In anesthetized dogs, a wire electrode was implanted into the left circumflex coronary artery (LCX) and acute myocardial ischemia was produced by 90 min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. An intracardiac pressure transducer measured ventricular pressure, heart rate, filling pressure and dP/dt. The ECG was obtained from subcutaneous chest needles. Six days later while in ambulatory state, a 180 microA DC current was applied for 4 h to the LCX intimal lining in Tris-HCl (n = 10) and PGI2-treated dogs (50 and 100 ng/kg/min, 11 and 12 dogs, respectively). Myocardial injury and coronary thrombosis induced by electrical stimulation produced ventricular fibrillation in all vehicle-treated dogs at 145 +/- 33 min (mean +/- S.D.). In PGI2-treated hearts only 2 animals fibrillated at 150 +/- 29 min and 180 +/- 52 min following 50 and 100 ng/kg/min of the prostanoid, respectively. Thus, 18/23 PGI2-treated dogs survived 4 h electrical stimulation of the artery. Within the LAD perfusion zone infarction was observed of equal volumes in vehicle and PGI2-treated animals. No ischemia occurred distal to the LCX coronary thrombosis. Ventricular pressure fell in all groups. Heart rate increased in the controls and those animals treated with 50 ng/kg/min PGI2 while 100 ng/kg/min PGI2 increased heart rate by 22 +/- 5% (p less than 0.05). Filling pressure increased in controls but fell in the PGI2-treated hearts. The results indicate that PGI2 can prevent ventricular fibrillation resulting from acute ischemia at a site distant to previous myocardial ischemia with superimposed intimal injury and coronary thrombosis. The PGI2 properties are due to prevention of coronary thrombosis and the occlusion of the artery. Antifibrillatory effects of the prostanoids are suggested.
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PMID:Prostacyclin prevents ventricular fibrillation in a canine model of sudden cardiac death. 352 79

Naloxone HCl (Nx) improves cardiopulmonary performance, reverses cellular hypoxia, and stabilizes lysosomal membranes in shock states. However, no detailed study has yet explored its potential role in renal ischemia, which is inevitable in transplantation and surgical and nonsurgical conditions associated with hypotension and shock. This functional and microanatomical study was carried out on dogs subjected to renal warm ischemia with contralateral nephrectomy. Group I (control; N = 4) had bilateral renal dissection and right nephrectomy. Groups II-IV had their kidney pedicles cross-clamped for 60 min and then reperfused. Group II (N = 9) ischemic kidneys received no treatment. Group III (N = 6) kidneys were flushed with pure Nx HCl (2 mg/kg) during ischemia. Group IV (N = 6) dogs received one iv Nx bolus (2 mg/kg) before clamping and another dose before declamping. Biopsies for adenine nucleotides, histology, and ultrastructure were obtained before ischemia, before reflow, and 15 min and 7 days after reflow. Serum creatinine and blood urea nitrogen were measured daily. Ischemia induced significant renal dysfunction, which was reversed by systemic Nx. Nx offered a remarkable protection against postischemic structural damage. Seventy percent of Group II cortical sections showed grade 4 acute tubular necrosis (ATN), and severe residual damage after a week. Eighty-three percent of Group IV sections showed grade 1 ATN and no residual damage after a week. One week survival was 33% in Group II and 100% in Group IV. Nx can be useful in prevention of acute renal failure in clinical situations with arterial hypotension and shock.
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PMID:Naloxone in renal ischemia: a functional and microanatomical study. 358 32

We investigated whether lipid peroxidation is an important biochemical mechanism in acute gastric mucosal injury induced by acid, base, or postischemic reperfusion. Lipid peroxidation products, i.e., the concentration of conjugated dienes (absorbance at 242 nm), products absorbing at 270 nm, and malondialdehyde were measured in the gastric mucosa of rats killed 30 s or 1, 3, or 6 min after intragastric (ig) administration of 0.6 N HCl or 0.2 N NaOH. No increase in any of the lipid peroxidation products was detected at any of the time intervals. Mucosal lesions, however, were already visible at 30 s. Cumene hydroperoxide (1 ml, 100 mM ig) induced neither mucosal lesions nor lipid peroxidation. In vitro incubation of mucosal homogenates with cumene hydroperoxide (1 or 10 mM) however, rapidly induced elevation of the three parameters of lipid peroxidation. Ischemia induced by clamping the blood vessels of the stomach for 20, 30, and 40 min followed by reperfusion for 10, 30, and 40 min did not induce lipid peroxidation, despite the development of hemorrhagic mucosal lesions. Similarly, in gastric mucosal lesions induced by hemorrhagic shock no lipid peroxidation products were detected. In the small intestine, however, prolonged ischemia (2 h) followed by reperfusion (30 min) resulted in mucosal necrosis and elevation of malondialdehyde levels. These results suggest that lipid peroxidation is not a major pathogenetic mechanism in rapidly developing acute gastric mucosal injury caused by 0.6 N HCl or 0.2 N NaOH, or in the more slowly developing mucosal injury caused by postischemic reperfusion.
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PMID:Role of lipid peroxidation in gastric mucosal lesions induced by HCl, NaOH, or ischemia. 359 47

The effects of intraventricular infusion of prostacyclin (PGI2; 50, 100 ng/kg/min) on hemodynamics, the ECG, coronary thrombosis and myocardial ischemia were studied in chronically equipped, resting conscious dogs and compared to those of intracardiac administration of Tris-HCl as vehicle. Coronary thrombosis was induced by electrical stimulation of an artery over an implanted wire for 6 hr. PGI2 infusion at 100 ng/kg/min decreased blood pressure by 24 +/- 3% (p less than 0.01) for 5 hr, increased heart rate at 1 hr by 28 +/- 4% (p less than 0.05) followed by a decrement, and elevated cardiac output by 41 +/- 3% (p less than 0.05). Filling pressure and dP/dtmax did not change. Treatment with PGI2 prevented ischemic S-T segment alterations in the ECG and arrhythmias observed in controls. The prostanoid infusion reduced coronary thrombus weight from 64 +/- 7.8 mg (mean +/- S.D.) in controls to 10.7 +/- 6.3 mg and 5.2 +/- 7.1 mg (both p less than 0.001) after 50 and 100 ng/kg/min, respectively. It also reduced myocardial ischemia following occlusive coronary thrombosis from 48 +/- 12% of the left ventricle in controls to 8.8 +/- 8.7% (p less than 0.01) and 2.4 +/- 5.2% (p less than 0.001) in the hearts treated with 50 or 100 ng/kg/min PGI2. The results suggest that PGI2 infusion exerts beneficial effects on heart performance by long-lasting blood pressure reduction and elevation of cardiac output caused by dilation of arterial vessels. PGI2 infusion prevents occlusive coronary artery thrombosis in response to intimal damage by anti-thrombotic properties and vasodilation of coronary arteries. This protects the heart from ischemia observed in controls.
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PMID:Influence of prostacyclin on coronary thrombosis and myocardial ischemia in conscious canine experiments. 391 92

Tissue sections of kidneys from 172 patients with various pathologic conditions, such as hydronephrosis, interstitial nephropathies, ischemia, chronic graft rejection and renal cancer, were evaluated by an image analysis technique. Structurally defined kidney alterations were monitored for enzymatic, immunologic and other histochemical changes. Indicator enzymes of the proximal tubule, alanine-aminopeptidase (AAP), alkaline phosphatase (AP), beta-glucoronidase (beta-Gl) and gamma-glutamyltranspeptidase (GGTP), were used as parameters for screening. Enzyme concentrations were found to be significantly decreased in kidney sections of patients with various renal diseases (AP less than 15%, AAP less than 55% and beta-Gl less than 60%) as compared to normal kidney tissues (100%). AAP concentration was measured quantitatively by specific immunofluorescence using an antienzyme antibody. Immunofluorescence of AAP was comparable to that of AAP calculated by the colorimetric technique (substrate: DL-alanine-beta-naphthylamide-HCl) and decreased to less than 50% in altered kidney tissues. Furthermore, kidney cancer (less than 20%) and kidney tissue adjacent to tumours (less than 65%) displayed significantly decreased levels of kidney marker enzyme activity. This study suggests that (1) the diseased kidney is characterized by a defined change in key enzymes of the cell surface and (2) renal cancer exhibits partial depletion of these constituents. Image analysis of the pattern of enzyme activity appears to be a useful tool in the analysis of renal pathology.
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PMID:Quantitative enzymatic, immunologic and histochemical studies of clinically relevant human kidney alterations using image analysis. 611 96

Myocardial protection by dilazep HCl, an antianginal drug and a potent calcium antagonist, against myocardial damage following acute ischemia and reperfusion was studied with respect to myocardial contractility in isolated blood-perfused canine left ventricular muscle. Myocardial function was expressed by percent recovery rate of maximal net developed tension. 1) The coronary infusion of dilazep revealed significant myocardial protection during normothermic ischemic arrest of 45 min and reperfusion. 2) The intravenous administration of dilazep to the support dog and Young's infusion also showed significant myocardial protection during normothermic ischemic arrest of 45 min and reperfusion. Dilazep showed no persistent depression of myocardial contractility due to its calcium antagonistic effect during reperfusion. 3) The combination of intravenous administration of dilazep to the support dog, Young's infusion, and hypothermia showed significant myocardial protection during prolonged ischemia and reperfusion even in hypertrophied ventricle. These results demonstrate that dilazep provides effective myocardial protection during ischemic arrest and reperfusion by preventing abnormal calcium accumulation in myocardial cells during reperfusion. No persistent depression of myocardial contractility during reperfusion may support dilazep's clinical application as a myocardial protective agent in open-heart surgery.
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PMID:Effect of dilazep on myocardial contractility following acute ischemia and reperfusion in isolated blood-perfused canine left ventricular muscle. 645 22


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