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Biomedical subjects

W Bernauer

Publications and source records attributed to W Bernauer.

At least 73 records · Page 4Linked to original sources
PubMed1985

The effect of beta-adrenoceptor blocking agents on evolving myocardial necrosis in coronary ligated rats with and without reperfusion.

The left coronary artery of rats was ligated either permanently, or for a period of 40 or 60 min, with subsequent reperfusion. In experiments with permanent occlusion, the hearts were removed and investigated 5 h after the coronary ligation, or immediately after death in animals which died earlier. The hearts from the reperfusion experiments were investigated 60 min after reopening the occluded artery. The extent of the ischaemic and necrotic areas of the hearts was determined. A quantitative photometric method was developed for this purpose, using "negative staining" with Evans blue for the ischaemic area, and "negative staining" with triphenyltetrazolium chloride for the necrotic area. In experiments in which ligation was permanent, the percentage of the ischaemic area which underwent necrosis increased with the time after coronary occlusion. In reperfusion experiments, myocardial necrosis was detected earlier than in experiments with permanent coronary ligation. The beta-adrenoceptor blocking agents pindolol, propranolol, and metoprolol significantly decreased the percentage of necrosis in experiments with permanent ligation of the coronary artery. The most selective of the beta-adrenoceptor blockers, i.e. metoprolol was tested in the reperfusion experiments. In these experiments, the amount of necrosis was also significantly decreased.

Adrenergic beta-Antagonists↗
PubMed1985

Inhibiting effect of dexamethasone on evolving myocardial necrosis in coronary-ligated rats, with and without reperfusion.

Previous findings suggested that glucocorticosteroids may be able to preserve ischemic myocardial tissue from cellular necrosis. In the present investigation, the left coronary artery in rats was ligated either permanently, or reperfusion was allowed after an occlusion time of 40 min. After 5 h of permanent coronary ligation, or after 60 min of reperfusion, respectively, the hearts were investigated as to the extent of their ischemic and necrotic areas. The ischemic areas were determined by 'negative staining' with Evans blue, and the necrotic areas by 'negative staining' with triphenyltetrazolium chloride. Dexamethasone orthophosphate in both kinds of experiments significantly decreased the percentage of the ischemic area which had undergone necrosis.

Animals↗
PubMed1983

The metabolic role of endogenous catecholamines in acute myocardial infarction: effects of reserpinization and of infused noradrenaline.

A significant decrease of the noradrenaline content of the ischemic as well as non-ischemic parts of the myocardium was found in rats after ligation of the left coronary artery. The eventual role of released noradrenaline in the anaerobic metabolism of the heart was investigated. A highly significant decrease of ATP and glycogen was obtained in the ischemic myocardium 10 min after coronary ligation whereas glucose-6-phosphate (g-6-p) was significantly increased. Catecholamine depletion by reserpine pretreatment did not reduce the loss of ATP, although the hearts had broken down rather higher amounts of glycogen. Glycolytic energy production was obviously inhibited, as the accumulation of g-6-p was significantly greater than in non-reserpinized animals. However when a high breakdown of glycogen was induced by noradrenaline infusion into coronary ligated animals, the g-6-p levels were no higher than those in untreated coronary-ligated rats. The results suggest that the ischemic breakdown of glycogen is independent of endogenous noradrenaline. The metabolic conversion of g-6-p, however, may need sufficient catecholaminergic stimulation to become fully activated.

Adenosine Triphosphate↗
PubMed1982

Comparative investigation of the effects of metoprolol, propranolol, practolol, and verapamil in the acute phase of experimental myocardial infarction.

Myocardial infarction in rats was produced by ligation of the left coronary artery. To ensure exact comparison of drug effect, the extent of the myocardial zone excluded from the coronary circulation was determined in each animal, and the experimental data were related to it. For this purpose, the hearts were perfused with Evans blue, and after the photometric determination of the dye content of the hearts the percentage of ischemic myocardium was calculated. With metoprolol, propranolol, and verapamil a significant increase of the survival times was obtained (min/% of non-ischemic myocardium). Metoprolol and propranolol also significantly increased the survival rates. None of the beta-blockers exerted an antiarrhythmic effect. The arrhythmias were prevented by higher doses of the calcium antagonist verapamil which, however, decreased the survival times. All beta-blocking agents delayed the typical elevation of the ST-segment in the electrocardiogram, and reduced the increase of the activity of the serum creatine kinase. Propranolol and metoprolol antagonized the blood pH decrease obtained after coronary occlusion. Results concerning heart rate, and arterial and central venous pressures are also reported. - The findings with metoprolol, especially, indicate that the essential mechanism in the therapeutic action of beta-blockers is their ability to block the cardiac beta 1-receptors.

Adrenergic beta-Antagonists↗
PubMed1980

Effects of glucocorticosteroids in rats with acute myocardial infarction.

A method was developed which allows exact determination of the extent of the myocardial zone which is excluded from the circulation by ligation of a coronary artery. It consists of the perfusion of the coronary system with Evans blue, and the calculation of the size of the ischemic area after determining the dye content of the heart. Data obtained in animals with experimental myocardial infarction can thus be properly related to the size of the ischemic zone in the heart. Results from different experimental animals can be compared exactly. With this technique the effects of dexamethasone, and cortisol were investigated in rats with ligation of the left coronary artery. With both glucocorticosteroids a significant increase of the survival times and survival rates was obtained. The increase of the serum creatine kinase, characteristic of myocardial infarction, was significantly diminished. The typical elevation of the ST-segment in the electrocardiogram was significantly delayed. Effects on arterial and central venous pressures were recorded which may reflect an improvement in; the condition of the myocardium. Cardiac arrhythmias, occurring typically between 10 and 20 min after coronary artery occlusion were, however, not antagonized, but rather aggravated, by the glucocorticosteroids.

Animals↗
PubMed1979

Digoxin induced release of creatine kinase from isolated guinea-pig hearts.

In isolated perfused guinea-pig hearts, digoxin produced a concentration dependent release of creatine kinase (ATP-creatine-transphosphorylase; CK). A corresponding decrease of the CK activity in the myocardium was obtained. The enzyme release seems to be a sign of glycoside intoxication, as its extent paralleled the severity of digoxin induced arrhythmias. Especially high CK activities were liberated when ventricular fibrillation occurred. Likewise, electrically induced fibrillation, in control hearts, led to enzyme release. However, the digoxin effect was not matched. Reserpine pretreatment antagonized the CK release by electrical fibrillation, whereas it increased excessively the enzyme liberating effect of higher digoxin concentrations. Also, propranolol decreased the enzyme release due to electrical fibrillation. The glycoside induced CK liberation, however, was not diminished, although the ventricular fibrillation was prevented. Increase of the potassium concentration of the perfusion fluid prevented the glycoside induced fibrillation, and reduced the enzyme release. The significance of the enzyme loss from the myocardium, and the mechanisms of enzyme release are discussed.

Adrenergic beta-Antagonists↗
PubMed1978

Pharmacological modification of thromboxane and prostaglandin release in cardiac anaphylaxis.

Isolated perfused sensitized guinea pig hearts release relatively large amounts of radioimmunologically measurable thromboxane B2 (TXB2) as well as smaller amounts of prostaglandin (PGs) after antigenic challenge. Using thin layer chromatography the major PG released was shown to cochromatograph with PGD2, while smaller amounts of immunoreactive PGF2alpha were found. The TX-synthetase inhibitor imidazole (100 microgram/ml) significantly decreased TXB2 release and simultaneously increased PG release during cardiac anaphylaxis. On the other hand, the beta-sympathomimetic drug isoproterenol decreased both TXB2 and PG release from the anaphylactic hearts. While isoproterenol significantly diminished anaphylactic coronary flow reduction, imidazole was without effect in this respect. PGD2 (0.5 microgram/min and 5.0 microgram/min) infused intraaortally into non-sensitized guinea pig hearts reduced coronary flow dose-dependently. These results are compatible with the view that release of TX and PGs might contribute to coronary flow reduction in cardiac anaphylaxis.

Anaphylaxis↗
PubMed1978

Effect of isoproterenol on myocardial creatine kinase activity in rats.

Isoproterenol (0.1-500 mg/kg) decreased the myocardial creatine kinase (CK) activity in rats. The maximum effect was already reached with 10 mg/kg, decreasing the enzyme activity to 58.5% of the control values. The beta-blocking agents propranolol and practolol, and also glucocorticosteroids inhibited the isoproterenol effect. The relative CK isoenzyme composition of the myocardium was not grossly altered by isoproterenol, as shown by DEAE-Sephadex A-50 macrocolumn chromatography. --Serum CK was increased significantly after the administration of the excessive dose of 500 mg isoproterenol/kg.

Animals↗
PubMed1978

The effect of verapamil, isoproterenol, and dexamethasone on enzyme release and viability of coronary obstructed guinea-pig hearts.

In isolated perfused guinea-pig hearts decrease of coronary flow, release of creatine kinase (CK), severe arrhythmias and early standstill were produced by intracoronary application of plastic microspheres. 1 X 10(-9) g verapamil/ml perfusion fluid significantly decreased the CK release from these "ischemic" hearts. With 1 X 10(-8) g/ml a significant increase of the survival times was obtained. Dexamethasone strongly depressed the enzyme release from the coronary obstructed hearts. The survival times, however, were not prolonged. Isoproterenol significantly shortened the survival times. Very low concentrations decreased the CK release, whereas higher concentrations themselves provoked an enzyme release.

Animals↗
PubMed1977

Radioimmunological determination of thromboxane release in cardiac anaphylaxis.

A sensitive and specific radioimmunoassay for thromboxane B2 were detected in perfusates of anaphylactic guinea pig hearts. Indomethacin decreased thromboxane B2 levels in the perfusates to below the detection limit of the radioimmunoassay and concomitantly delayed the onset of coronary vasoconstriction after antigenic challenge.

Anaphylaxis↗
PubMed1976

Release of creatine kinase by antigen, histamine, and catecholamines.

In mepyramine treated, ovalbumin sensitized anaesthetized guinea pigs protracted anaphylactic shock was produced by i.p. injection of antigen, and serum creatine kinase (CK) activities were determined 4, 6, or 17 hrs thereafter. Significant increases above nonsensitized controls were obtained. In nonanaesthetized guinea pigs shock course and serum CK increase were considerably accelerated. Histamine increased the serum CK only when given in high amounts (10 mg/kg) s.c., in the presence or absence of mepyramine. I.p. injection of histamine in mepyramine treated animals had no effect. Adrenaline (1 or 10 mg/kg) given as a s.c. depot in oil produced a significant increase of serum CK, as well as noradrenaline (0.1, 1, or 10 mg/kg). Dibenamine reduced the effect of adrenaline. In isolated perfused guinea pig hearts a significant CK liberation occurred already within the first hour after eliciting anaphylaxis. Nonanaphylactic hearts released CK too, but significant amounts were obtained only in the total 4 hrs after ovalbumin administration. Isolated anaphylactic hearts incubated in Tyrode solution liberated significantly more CK than did nonsensitized control hearts. The findings are discussed in view of a possible myocardial damage in anaphylaxis.

Anaphylaxis↗
PubMed1976

Effect of catecholamines and sympatholytics on survival and circulatory parameters in protracted anaphylactic shock of guinea pigs.

Protracted anaphylactic shock of guinea pigs led to death in over 90% of the animals, and good protection was obtained with an infusion of adrenaline after dibenamine pretreatment. Adrenaline alone, in doses which prevented the anaphylactic fall of arterial blood pressure, had no beneficial effect. Practolol abolished the therapeutic action of the combination of dibenamine/adrenaline. Stimulation of beta-receptors by isoproterenol did not increase the survival rate. With dopamine, however, a significant prolongation of the survival times was obtained.

Anaphylaxis↗
PubMed1976

Influence of adrenaline, dibenamine and dopamine on acidosis, hemoconcentration and lethality in protracted anaphylactic shock of guinea-pigs.

Protracted anaphylactic shock of guinea-pigs was accompanied by a marked decrease in blood pH, and an increase in hematocrit. Death ensued in 58.3% of the animals within 3 hr of observation. Infusion of adrenaline (20 mug/kg/min), after eliciting anaphylaxis, intensified the acidosis, and increased the lethality to 100%. Pretreatment with dibenamine (5 mg/kg) reversed the effect of adrenaline. Dopamine, infused in amounts of 200 mug/kg/min, acted similarly to the combination dibenamine/adrenaline. Hemoconcentration was neither prevented nor intensified by adrenaline. Dopamine, however, reduced significantly the anaphylactic increase in hematocrit.

Acidosis↗
PubMed1975

Myocardial damage during protracted anaphylactic shock in guinea pigs.

In ovalbumin-sensitized, mepyramine-treated guinea pigs protracted anaphylactic shock was elicited by i.v. injection of antigen. Diffuse or focal necrosis of myocardial cells was found in animals which died in protracted shock, as well as perivascular and interstitial edema. The antigen effects could be partially imitated by i.v. infusion of high amounts of adrenaline into nonsensitized guinea pigs. When adrenaline was infused during protracted anaphylactic shock, the catecholamine effects did not add to the histological effects of the antigen. Rather, the morphological alterations in the hearts were reduced, whereas the survival times were not increased, but decreased. - The findings are discussed in view of the nature of protracted anaphylactic shock.

Anaphylaxis↗
PubMed1975

Prostaglandin, slow-reacting substance, and histamine release from anaphylactic guinea-pig hearts, and its pharmacological modification.

Prostaglandins (Pgs), slow-reacting substance of anaphylaxis (SRS-A), and histamine were released from anaphylactic isolated perfused guinea pig hearts. Pgs were to the greatest part of the F2alpha-type. PgE2 was found in traces only. Neither PgA2, nor the metabolites 13,14-dihydro-15-keto-PgF2alpha and 13,14-dihydro-15-keto-PgE2 were detected in the perfusates. Isoproterenol reduced the PgF2alpha output significantly. This effect was increased by the addition of theophylline. Propranolol did not reverse the effect of isoproterenol, but in a high concentration (5 mug/ml) reduced the PgF2alpha output for its own. Indomethacin completely abolished the anaphylactic prostaglandin release. The histamine liberation was significantly decreased only by the combination of isoproterenol and theophylline, and also by a high concentration of propranolol (5 mug/ml). In contrast to the Pg release, the anaphylactic SRS-A and histamine liberation was not abolished by indomethacin, but rather increased. The results are discussed in view of the possible role of the released substances in the functional events of cardiac anaphylaxis.

Anaphylaxis↗
PubMed1975

Catecholamine content of serum and adrenals in protracted anaphylactic shock of guinea pigs.

In ovalbumin-sensitized guinea pigs, the serum catecholamines were significantly increased 20 or 120 min after antigen injection. The highest serum cathecholamine values were obtained in animals which were selected during a severe state of protracted shock, and in those which died in protracted shock. Antihistamine pretreatment reduced the serum noradrenaline, but not the adrenaline values in anaphylaxis. In urethane anesthesia, the anaphylactic serum catecholamine levels (especially noradrenaline) were lower than in nonanesthetized animals. The adrenaline and noradrenaline content of the adrenals in protracted and in acute anaphylactic shock did not differ from control values.

Adrenal Glands↗