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Biomedical subjects

D Lehr

Publications and source records attributed to D Lehr.

At least 19 recordsLinked to original sources
PubMed1998

Prospective analysis of patient management in severe head injury.

Severe head injury with and without peripheral trauma is the most frequent cause of death and of severe disability up to 45 years. Outcome is determined by two major factors, the extent and nature of the irreversible primary brain damage, and the evolving secondary sequelae, which contrary to the former are responsive in principle to therapeutic intervention. An improvement of outcome from severe head injury can be expected only from an increased efficiency of the measures to prevent secondary brain damage. A research consortium "Neurotrauma" was formed by the University of Munich in collaboration with almost all city hospitals in Munich, Augsburg, Murnau, Ingolstadt, Vogtareuth and Southern Bavaria, providing care for neurotrauma patients. These hospitals together with the associated organizations carry out a system analysis on the management, logistics, organization, patient referral, etc. In severe head injury. Data acquisition is e.g. also concerned with outcome-relevant time periods of emergency care measures in the pre-clinical phase until hospital admission, conclusion of diagnostic procedure, and of the initial clinical care. Current results and experiences with establishment of this comprehensive research organization are presented, where no less than 31 hospitals. Institutions and organizations, and a study group of more than 40 physicians, students and statisticians are collaborating. Emerging data appear to be suitable to further improve pertinent aspects of the patient management as a basis to lower the incidence of secondary brain damage from severe head injury.

Adult↗
PubMed1994

A possible beneficial effect of selenium administration in antiarrhythmic therapy.

OBJECTIVE: The following review of the literature on the importance of Selenium (Se) in myocardial homeostasis and of the pharmacology of this trace metal, represents an attempt to search, without prejudice to other possible explanations, for a rationale of a beneficial effect of Se substitution as an adjuvant to antiarrhythmic therapy. BACKGROUND: For several years, in the early 1980s, I had to deal with the problem of a serious ventricular arrhythmia (non-sustained and sustained ventricular tachycardia) which was remarkably resistant to a battery of the most potent antiarrhythmic agents. Eventually, dramatic improvement, lasting for a period of 8 years, was achieved with Flecainide, which, however, left unsolved the episodic occurrence of disabling ventricular bigemini. Over the most recent period of 1 year and 8 months, there was a sudden and unexplained return to unbroken normal sinus rhythm. Among the multiplicity of possible reasons for this fortunate development, the concurrent introduction of Se substitution appeared as the most obvious, though very tentative explanation. Substitution of this trace metal preceded the extinction of ventricular bigemini by 1 week and actually represented the sole modification of otherwise reasonably standardized conditions of antiarrhythmic therapy, life style and diet.

Adult↗
PubMed1990

Hemodynamic changes after an intensive short-term exercise and nutrition program in hypertensive and obese patients with and without coronary artery disease.

PURPOSE: To assess the effectiveness of the Pritikin diet and exercise program on cardiovascular hemodynamics using the noninvasive technique of Thoracic Electrical Bioimpedance (TEB). MATERIAL AND METHODS: Twenty subjects divided in two groups, according to their body habitus and hemodynamic disturbances. These data were compared to a group of 10 healthy individuals not involved in the program. Hemodynamic parameters were collected at admission and at the end of the intensive 26-day program of exercise and nutrition. RESULTS: In obese and hypertensive subjects not on medication we observed that cardiac index increased from 3.27 +/- 0.4 to 3.58 + 0.5 L/min/m2; mean arterial pressure decreased from 100 +/- 8.5 to 94.8 +/- 7.9 mmHg while systemic vascular resistance index decreased from 2362 +/- 391 to 1934 +/- 357 dynes. sec. cm-5/m2; p less than 0.05 (Data obtained in supine position). Also documented was a improvement in ventricular performance after postural changes from upright to supine based on indices of left ventricular performance, uniquely obtained by the TEB technique. From admission to discharge, changes were: Ejection fraction 48% to 53%; Peak flow index 295 to 316 ml/s/m2 and Index of contractility 40 to 47 s-1, explained by a shift on the ascending limb of the Starling curve. CONCLUSION: In a selected population, this rehabilitation program is effective for hemodynamic improvement that can be partially explained by metabolic and biochemical changes already reported from this Center.

Adult↗
PubMed1985

Enhanced incidence of isoproterenol-induced ventricular fibrillation in the magnesium-deficient rat.

The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations.

Animals↗
PubMed1982

[Open study of bromapezan in ambulatory and psychiatric hospital patients (author's transl)].

Psychiatrists working in hospital and in private practice took part in co-operative trial aimed at evaluating the effectiveness and safety of bromazepam. The study was of the open type and involved 10 hospital patients and 20 ambulatory patients. The same protocole was followed for each patient. Twenty-five patients (including 5 in hospital) had anxiety neurosis; the remaining 5 had anxiety following weaning from alcohol. The anxiolytic effects of the drug, determined by means of Hamilton's anxiety scale and overall clinical judgement, were generally found to be satisfactory. The effective doses ranged from 1 to 3 tablets per day in ambulatory patients and from 3 to 5 tablets per day in hospital patients. The main side-effects were related to unwanted sedation; they only occurred with the higher doses and rarely interfered with the beneficial effects of bromazepam.

Adult↗
PubMed1982

Enhanced arrhythmogenic activity of beta-adrenoceptor stimulants in desoxycorticosterone-pretreated rats.

The arrhythmogenic activity of four beta-adrenoceptor stimulants, metaproterenol, salbutamol, isoetharine, and dobutamine, was determined in adult, Wistar rats pretreated for 3-4 weeks with desoxycorticosterone (DOCA) and 1% saline as drinking fluid. Doses (SC) of these stimulants which were well tolerated in untreated animals elicited severe ventricular dysrhythmias, often leading to death in ventricular fibrillation. The LD50 in mg/kg was as follows: metaproterenol, 0.28; salbutamol, 0.60; isoetharine, 2.3; and dobutamine, 4.8. The relative potency of metaproterenol, salbutamol, and isoetharine correlates well with their ability to stimulate beta 1-adrenoceptors. It is suggested that DOCA-saline pretreatment in rats may be used as a model for the rapid screening of drugs affecting beta-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1981

Epinephrine induced myocardial necrosis: effects of aminophylline and adrenergic blockade.

The pathogenesis of myocardial necrosis produced in the albino rat by a single large dose of the potent alpha and beta adrenergic agonist epinephrine was investigated. In confirmation and extension of earlier observations with the alpha adrenergic antagonist tolazoline, it was found that alpha adrenergic blockade with phenoxybenzamine or beta adrenergic blockade with propranolol only partially attenuated the cardiotoxic effect of epinephrine while complete prevention of myocardial injury was achieved with the combined use of the two antagonists. In the presence of alpha adrenergic blockade alone, phosphodiesterase inhibition (aminophylline) caused a dramatic increase of epinephrine cardiotoxicity, demonstrating the importance of unopposed beta adrenergic activation. These results are consistent with the assumption that, in the rat, a cardiotoxic dose of epinephrine produces powerful alpha adrenergic activation which overshadows the effects of the beta adrenergic component of this catecholamine. It is concluded that in epinephrine induced myocardial necrosis, excessive alpha-adrenergic receptor activation in the cardiovascular system is clearly dominant in the initial phases. However, the contribution of the beta-adrenergic component of this catecholamine is of considerable importance for the eventual full development of the injury.

Aminophylline↗
PubMed1980

Role of alpha- and beta-adrenergic activation in ventricular fibrillation death of corticoid-pretreated rats.

Death in ventricular fibrillation was induced consistently in desoxycorticosterone acetate-pretreated rats by the beta-adrenergic agonist isoproterenol but not by norepinephrine or epinephrine, both of which possess alpha- as well as beta-adrenergic activity. Aminophylline, which enhances beta-adrenergic activity, and phenoxybenzamine, an alpha-receptor blocking agent, were used to study the roles of alpha- and beta-adrenergic stimulation in the production of ventricular fibrillation. With the addition of aminophylline, both norepinephrine and epinephrine produced death in ventricular fibrillation, and the existing cardiotoxicity of isoproterenol was potentiated. Similarly, in the presence of phenoxylbenzamine, doses of norepinephrine and epinephrine that had been well tolerated became lethal. Internventions that favor beta-adrenergic preponderance, either by enhancing beta-effects or by blocking protective alpha-adrenergic activation, apparently increase the arrhythmogenic propensity of norepinephrine and epinephrine in steroid-pretreated rats. The similarity of some forms of stress to the experimental protocol of chronic steroid treatment followed by acute catecholamine exposure is discussed.

Adrenergic alpha-Agonists↗
PubMed1978

Hemodynamic alterations in isoproterenol-induced cardiac arrhythmias in corticoid-treated rats.

Hemodynamic alterations were studied to determine their role in isoproterenol-induced cardiac arrhythmias in the desoxycorticosterone acetate--saline-treat rat. Since epinephrine, a catecholamine possessing an alpha-adrenergic receptor agonist component, was considerably less potent as an arrhythmogenic agent, an elevation in blood pressure was thought to be protective against arrhythmias. Both albuterol, a beta2-adrenergic agonist, alone and epinephrine administered following tolazoline, an alpha-adrenergic blocking agent, decreased blood pressure to that of isoproterenol but failed to elicit significant arrhythmias. Phenylephrine administered prior to isoproterenol resulted in significant arrhythmias despite the maintenance of mean blood pressure at normal levels. The study shows that blood pressure alterations are not important in the etiology of isoproterenol-induced arrhythmias in the corticoid-pretreated rat.

Adrenal Cortex Hormones↗
PubMed1978

Potentiation of isoproterenol cardiotoxicity by corticoids.

In order to determine whether glucocorticoids share the ability of mineralocorticoids in sensitizing the myocardium to the arrhythmogenic property of isoproterenol, albino rats were implanted subcutaneously with prednisone or desoxycorticosterone acetate (DCA). Water was compared with 1% saline as drinking fluid in order to assess the role of a high sodium intake in the development of myocardial sensitization. At predetermined intervals during corticoid exposure, unanesthetized animals were challenged with a single subcutaneous dose of isoproterenol. In DCA-saline pretreated rats the LD50 of isoproterenol was determined to be 14.5 ug/kg. At a dose of 150 ug/kg isoproterenol, ventricular fibrillation was elicited in all DCA-saline pretreated animals, but in only 50% of rats implanted with predisone, receiving saline as drinking fluid. Substitution of water for saline did not prevent the development of myocardial sensitization. It is concluded that predisone pretreatment also sensitizes the rat myocardium to isoproterenol though to a lesser extent than DCA and that high sodium intake is not an absolute requirement for the development of this phenomenon by either corticoid.

Animals↗