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)

This report concerns itself with additional experimental evidence to support the immunologic concept for the pathogenesis of Bell's palsy, using the mast cell as an index of immunological activity. In a previous experimental study, we postulated that degranulation of mast cells activated by complement or specific allergens with release of histamine and other substances may be the mechanism leading to nerve edema, ischemia, and paralysis. In this study we observed a loss of granulated mast cells in the more severely damaged facial nerves of immunized dogs after the intrafallopian canal injection of various substances, in contrast with the relative abundance of these cells in nerves that showed little or no evidence of injury. In addition, we demonstrated that cromolyn sodium, a mast cell degranulation inhibitor, when infused intravenously at the time of the intrafacial canal injection of horse serum, very effectively lessened the degree of experimental paralysis and histologic nerve injury.
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PMID:Immunological concept for Bell's palsy: further experimental study. 86 31

To examine the influence of preexistent diabetes mellitus on left ventricular performance and coronary blood flow responses to acute ischemia, mild normoglycemic diabetes was induced in nine mongrel dogs after three doses of alloxan, (20 mg/kg, iv), at monthly intervals. Hemodynamic measurements and coronary blood flow (85Kr clearance) were obtained before and after the onset of ischemia. This was produced by occlusion of the proximal left anterior descending coronary artery via a balloon-type catheter in nine intact anesthetized diabetic dogs and 10 nondiabetic dogs. During the 1st hour of ischemia in the diabetic group, the end-diastolic pressure rose from 7 +/- 1.1 (mean +/- SE) mm Hg to 23.8 +/- 2.3 without a significant increase of end-diastolic volume. In controls end-diastolic pressure rose from 8.6 +/- 1.1 mm Hg to 15.3 +/- 1.4, and end-diastolic volume was significantly increased, so that the ratio of end-diastolic pressure and volume was significantly higher in the diabetic group (P less than 0.005). Although indices of contractility did not differ, stroke volume and work reductions were significantly greater in diabetics, despite the fact that coronary blood flow was reduced to a similar extent. Size of the ischemic areas appeared comparable as judged by distribution of dye injected distal to the occlusion. Since potassium loss and sodium gain in the inner and outer layers of ischemic tissue did not differ between the two groups, the intensity of ischemia seemed similar. Glycogenolysis was unimpaired in the diabetic ischemic muscle but triglyceride levels remained elevated. Morphologically the diabetic myocardium was characterized by a diffuse accumulation of periodic acid-Schiff-positive glycoprotein in the interstitium, which was thought to limit diastolic filling of the ischemic ventricle and to contribute to the substantial reduction of ventricular performance.
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PMID:Myocardial function and coronary blood flow response to acute ischemia in chronic canine diabetes. 87 Feb 38

When reproducing ischemia of the myocardium in acute experiments on rabbits and in tests with the isolated rabbit's heart an elevated permeability of the myocardial histo-blood barriers (HBB) to sodium sulphacyl in the region of ischemia and its boundary zone was established. Upon introduction of isadrine (2 mg/kg and 2-10-6 M) and anapriline (1 and 2.5 mg/kg; 2-10-6 and 10-5M) the permeability of the HBB to sodium sulphacyl within the ischemia zone and in areas of the myocardium contiguous to it diminished. The permeability of the myocardial HBB in the intact zone did not change under the effect of the drugs. In in vitro experiments with erythrocytes by using the fluorescent test and methods for determination of the osmotic resistance the drugs were found to display the membranotropic activity. From the in vitro tests it follows that anapriline and isadrine exercise no antiprotease action.
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PMID:[Effect of isadrine and anapriline on permeability of myocardial histo-hematic barriers in conditions of acute ischemia]. 90 37

The effect of warm ischemia on the transmembrane transport of potassium in dog kidney slices was studied by measurement of the uptake of 42K. The requirement for steady-state conditions concerning the intracellular potassium concentration was thereby studied. The total potassium content in the slices was found to be constant between 120 and 180 min incubation at both 25 and 37 degrees C. The cell water calculated from the total tissue water and 14C-inulin space in the dog kidney slices amounted to 38 ml-100 g wet weight-1 at 37 degrees C and 45 ml-100 g wet weight-1 at 25 degrees C and was found to remain constant for the incubation interval 120--180 min. The major part of the tissue uptake of 42K could be described by one single mono-exponential function under these conditions. The transmembrane influx at 37 degrees C calculated by using a modified Keynes formula amounted to 1.70 mmol K+-kg wet weight-1-min-1 after no warm ischemia and to 0.89 mmol K+-kg wet weight-1-min-1 after 2 h warm ischemia. The corresponding values for incubation at 25 degrees C were 1.26 and 0.77 mmol K+-kg wet weight-1-min-1, respectively. In the slices incubated at 25 degrees C, the potassium content was higher and the sodium content lower than in slices incubated at 37 degrees C.
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PMID:Transmembrane fluxes of potassium in dog kidney slices. A quantitation of the effect of warm ischemia. 92 4

In 12 patients affected by acute myocardial infarction complicated only by ventricular extrasystoles, verapamil was highly effective in the control of the arrhythmias. This result is in agreement with the experimental finding that ischemia inactivates partially or totally early Na+ inward currents, so that fast fibers become slow fibers. The efficacy of verapamil stresses the importance of these fibers which have acquired a slow response in the genesis of arrhythmias due to acute coronary attacks and opens interesting therapeutical prospects.
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PMID:[The antiarrhythmic effects of verapamil in acute myocardial infarction. Considerations on the possible action mechanism (author's transl)]. 92 57

1. Changes of structural proteins in experimental and human myocardial infarction were studied by the determination of myosin- and actomyosin-ATPase activities and gel electrophoretic analysis in the presence of sodium dodecyl sulfate (SDS). 2. In animal experiments using dogs, the relative amounts of myosin and alpha-actinin decreased at 24 to 48 hours after coronary ligation, became lowest at 72 hours, and remained at this level for 2 weeks and returned to almost normal value at 28 days. 3. Myosin- and actomyosin-ATPase activities decreased rapidly during 24 to 48 hours after ligation with temporary increase in their activities in the initial stage of ischemia and followed the similar time course as that of the amounts of myosin and alpha-actinin. 4. SDS gel electrophoretic analysis of structural proteins of infarcted tissues of the human hearts obtained from 5 cadavers showed also marked decrease of the contents of myosin and alpha-actinin with relative preservation of actin, tropomyosin and troponin-T.
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PMID:Changes of cardiac structural proteins in myocardial infarction. 92 15

In order to determine the validity of clinical-chemical parameters for the prognosis of hepatic failure, 28 pigs were subjected to liver ischemia for 40--160 minutes duration. The following parameters were studied: GOT, GPT, gamma-GT, LAP, LDH, GlDH, AP and isoenzymes, total bilirubin, potassium, sodium and chloride. In a statistical comparison in the surviving animals, an unexplainable increase in GlDH activity was observed. In the other clinical-chemical parameters none was seen to be of use for the prognosis for either life or death in acute hepatic failure.
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PMID:[Acute hepatic coma. Experimental study on the predictive value of clinical-chemical findings for the prognosis of acute hepatic coma]. 96 33

The effects of the dimethyl quarternary analog of propranolol, UM-272, on myocardial infarct volume were studied in the canine heart. Myocardial infarction was produced by occlusion of the left circumflex coronary artery for 60 minutes followed by reperfusion and quantitation of infarct volume 24 hours later. Groups of dogs were either untreated or pretreated with UM-272 with an initial loading dose of 5.0 mg/kg (group A) or 2.5 mg/kg (group B) 30 minutes before occlusion of the left circumflex coronary artery. Both group A and group B animals received additional doses of 2.5 mg/kg of UM-272 every 90 minutes for a period of 6 hours so that the total respective doses were 15 and 12.5 mg/kg. Control animals received comparable volumes of 0.9% sodium chloride solution. All animals were followed throughout the 6-hour procedure with continuous electrocardiographic recordings which were used to assess the effects of acute myocardial ischemia upon disturbances in cardiac rhythm and the effects of drug treatment. Dogs which survived the procedure were given tetracycline i.v. the next day and sacrificed 1 hour later by an overdose of pentobarbital sodium. The hearts were removed and the left ventricle was sliced and examined first under ultraviolet light to localize the ischemic zone by noting the tetracycline fluorescence. The ventricular slices were next incubated in nitro blue tetrazolium which stains normal myocardial tissue, thus allowing one to quantitate the volume of infarcted myocardium by excising and weighing the nonstained and stained muscle separately. The untreated control group had an infarct volume of 23.8 +/- 3.2 g/100 g of left ventricle. The treated animals in groups A and B had respective infarct volumes of 2.3 +/- 0.8 g/100 g (P less than .001) and 7.0 +/- 3.3 g/100 g (P less than .025) of left ventricle. During the acute phase of ischemia and reperfusion, arrhythmias and alterations in the ST-segment, R-wave amplituted and development of pathologic Q-waves were more prominent in the untreated animals and almost totally absent in the treated animals. UM-272 produced a dose-dependent decrease in heart rate as well as a decrease in developed isometric tension. Pretreatment with UM-272 did not prevent the derangement of function in the ischemic zone nor did it permit a return of function upon reperfusion, even though it reduced the degree of cellular damage resulting from 60 minutes of regional ischemia. A possible mechanism for the protective effect of UM-272 may be through its ability to reduce myocardial contractility and heart rate, both of which would reduce myocardial oxygen consumption and thus produce a more favorable balance between myocardial oxygen supply and myocardial oxygen demand.
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PMID:Ischemic changes in the canine heart as affected by the dimethyl quaternary analog of propranolol, UM-272 (SC-27761). 97 88

An acute circulatory renal failure (ARF) was induced in 18 rabbits by temporary ischemia of the remaining kidney 8 days after unilateral nephrectomy and subcuteaneous autotransplantation of renomedullary tissue.--Mortality in the postischemic course was 50% in treated animals but 100% in the control group (n = 18) without autotransplantation. In the postischemic period plasma urea concentration was significantly lower (p smaller than 0.005) in the surviving transplanted animals and excretion of sodium and water significantly higher (p smaller than 0.005) as compared with the control group. Plasma renin values which were significantly lower than thos of the control(p smaller than 0.005) had decreased significantly even as compared with the initial values. These results indicate that hormonal substances are produced in interstitial cells of renomedullary autotransplants exerting a distinct protective effect against experimental acute renal failure. Decreased plasma renin activity may point to an inhibition of circulating and/or intrarenal renin by lipids originating from the transplants. Changes in sodium and water excretion indicate effects of circulating prostaglandins
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PMID:Experimental oliguric acute renal failure: protective effects of renomedullary autotransplants. 109 74

In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...
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PMID:Abnormalities in the regional circulations accompanying congestive heart failure. 110 32


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