Eörs Bajusz

Simple Techniques for the Surgical Occlusion of Coronary Vessels in the Rat

From the Institut de Médecine et de Chirurgie expérimentales, Université de Montréal, Montreal, Canada. * The essence of this communication was presented to the International College of Angiology at a Meeting held in Montreal, February 20, 1960. t Fellow of the Gustavus and Louise Pfeiffer Research Foundation.

Induction of bone, cartilage and hemopoietic tissue by subcutaneously implanted tissue diaphragms

Fellow of the Rotary Club (D 191). Experimental coronary occlusion has been studied extensively in large laboratory animals, but these subjects do not lend themselves well to the large-scale testing of surgical procedures and drugs that may be useful in the prophylaxis

Observations on histochemical differential diagnosis between primary and secondary cardiomyopathies: Behavior of monoamine oxidase, phosphorylase, and glycogen in heart muscle☆

SummaryThe subcutaneous implantation of appropriate tissue diaphragms (short, broad glass cylinders) rather regularly induces the formation of bones provided with marrow cavities and junction cartilage plates, in the rat.Bone formation, unlike the development of hemopoietic tissue, can be prevented, under these circumstances, by topical blockade of the phagocyte system with carbon particles.The role of nonspecific topical stress factors, in the induction of such highly specific structural transformations, has been discussed.

Sensitization by dihydrotachysterol (DHT) and calcium acetate for the induction of cardiac lesions by various agents.

Abstract Comparative histochemical and morphologic studies were performed during the development of three primary (nonocclusive, or metabolic) and three secondary (occlusive, or anoxic) necrotizing cardiomyopathies, in the rat. The primary types of lesion were induced by the injection of plasmocid, the administration of dihydrotachysterol, and the feeding of a potassium-deficient diet. On the other hand, the secondary types of cardiac damage were elicited by ligature of a coronary artery as well as by two synthetic amines, methoxamine and metaraminol, which possess sustained pressor and vasoconstrictor properties. It was observed that myocardial monoamine oxidase, phosphorylase, and the stainable, labile fraction of glycogen behave differently during the development of primary and secondary cardiomyopathies, and it is suggested that the histochemical techniques for these three substances are applicable for purposes of morphologic differential diagnosis, since the changes are not only quantitatively but also qualitatively distinguishable and provide a basis for etiological considerations.

Action of Parathyroidectomy and Dihydrotachysterol on Myocardial Calcification Due to Coronary Vein Obstruction.

Abstract Calcium acetate can replace sodium phosphate as a sensitizing agent that permits the production of severe cardiovascular and renal lesions with otherwise ineffective doses of dihydrotachysterol (DHT). Still, the effect of the two electrolytes is not the same. Under the influence of DHT, sodium phosphate induces comparatively little cardiac and vascular calcification, much suppurating myocarditis, and a type of nephrocalcinosis that is primarily characterized by the formation of calcium casts within the tubular lumina at the corticomedullary junction line. On the other hand, under the same conditions, calcium acetate induces only mild myocarditic changes, much calcium deposition in the cardiovascular system, and a type of nephrocalcinosis that is almost exclusively limited to the stroma of the renal cortex. In rats simultaneously treated with comparatively small doses of DHT plus calcium acetate the resulting cardiovascular lesions can be considerably aggravated by a variety of stressor agents (cold baths, restraint, motor denervation). Furthermore, although noradrenalin does not normally produce any cardiovascular calcification in the rat, it is higly effective in this respect when the animal is pretreated with comparatively small doses of DHT plus calcium acetate. Finally, the oral administration of corn oil or glucose likewise aggravates the cardiovascular effects of DHT plus calcium acetate intoxication; these dietary supplements also act upon the course of the DHT plus calcium acetate syndrome in the same manner as they were previously shown to act upon the cardiopathy induced by corticoids plus sodium salts.

Stress and cardiac infarcts. Effect of sodium deficiency upon necrotizing cardiopathies produced by various agents.

Summary Experiments in the rat indicate that ligature of the 2 main coronary veins induces inflammatory and degenerative changes in the subepicardial muscle layers followed by massive calcification. This type of myocardial calcification, unlike the onset of necrosis, is greatly enhanced by parathyroidectomy. The aggravating action of parathyroid deficiency is, however, counteracted by simultaneous removal of the thyroids. On the other hand, administration of dihydrotachysterol (DHT) actually prevents the myocardial calcification in intact, thyroidectomized, or parathyroidectomized rats. DHT merely influences the extent of calcification, not the cardiac necrosis itself. The changes recorded in serum calcium and inorganic phosphorus levels do not help explain the above findings.

Erzeugung und Verhütung von Herznekrosen bei der dehydrotachysterinsensibilisierten Ratte

moneys might help to elucidate some fundamental problems of cardiac physiology and pathology.’ We noted that among all the 49 steroids tested, only some corticoids (deoxycorticosterone, cortisone, cortisol and halogenated corticoids) proved to sensitize the heart for the production of the ESCN. Furthermore, only certain sodium salts could produce an ESCN, following treatment with corticoids. The formation of the large, necrotic foci is usually preceded by a singular &dquo;fuchsinophilic degeneration&dquo; of the muscle fibers. It was also observed that in animals conditioned

Role of sodium in production of myocardial necroses by stress.

Nach kurzdauernder Vorbehandlung mit Dehydrotachysterin (DHT) entsteht bei der Batte eine geringgradige Arteriosklerose vom Typus Mönckeberg. Eine derartige Vorbehandlung verursacht keine wesentlichen Veränderungen im Myokard. Wenn man jedoch nach dieser DHT-Vorbehandlung die Tiere einer sonst wenig wirksamen Behandlung mit Vasopressin, Noradrenalin, Kälte oder Papain aussetzt, so entstehen schwere Myokardnekrosen. Diese auf arteriosklerotischer Basis, durch verschiedene Agentien hervorrufbaren Herznekrosen können ihrerseits durch prophylaktische Behandlung mit Kaliumchlorid, Magnesiumchlorid oder Aderlaß fast vollkommen verhfitewerden. Following pretreatment with dihydrotachysterol (DHT), there develops in rats a slight arteriosclerosis of the Mönckeberg type. This pretreatment in itself causes no significant changes in the myocardium. However, if, following such pretreatment, the rats are exposed to otherwise ineffective or only slightly effective treatment with vasopressin, noradrenaline, cold, or papain, then severe myocardial necroses ensue. The necroses that are thus normally elicited in the arteriosclerotic heart can be prevented by KCl, MgCl2, or hemorrhage.Nach kurzdauernder Vorbehandlung mit Dehydrotachysterin (DHT) entsteht bei der Batte eine geringgradige Arteriosklerose vom Typus Monckeberg. Eine derartige Vorbehandlung verursacht keine wesentlichen Veranderungen im Myokard. Wenn man jedoch nach dieser DHT-Vorbehandlung die Tiere einer sonst wenig wirksamen Behandlung mit Vasopressin, Noradrenalin, Kalte oder Papain aussetzt, so entstehen schwere Myokardnekrosen.

Influence of variations in dietary intake of chlorides upon diverse necrotizing cardiopathies

Summary Certain Na-salts (chloride, acetate, citrate and lactate) are well tolerated even by rats simultaneously treated with 2α-methyl-9α-chlorocortisol (Me-Cl-COL) or a severe stressor, such as forced restraint. However, these same salts produce massive and sometimes fatal myocardial necroses, in rats exposed to the stress of forced restraint after conditioning with Me-Cl-COL. It appears that during stress the metabolism of certain otherwise innocuous Na-salts and/or steroids is so altered that they acquire severe cardio-toxic properties.

Sensitization by dihydrotachysterol (DHT) for induction of cardiac lesions by various agents

Experiments on rats were performed to examine the effect of variations in dietary intake of chlorides upon diverse experimental cardiac lesions, which differ widely from each other in both their causative agents and their histologic characteristics. It was found that chloride-deficiency significantly enhances the susceptibility of the heart to the production of necrosis, inflammation, and/or calcification by plasmocid, papain, dihydrotachysterol, Ca-acetate + dihydrotachysterol, Na2HPO4 + fluorocortisol, Na-acetate + fluorocortisol, as well as by the stressor effect of forced restraint or quadriplegia after conditioning with fluorocortisol. On the other hand, a dietary excess of chlorides proved to be effective in protecting the myocardium against all the cardiotoxic agents enumerated above. The observation that a number of diverse cardiopathies are uniformly aggravated by a low-chloride diet, and prevented by a dietary excess of chlorides, suggests that chlorides may play an important role in the pathogenesis of various necrotizing cardiopathies. The spotty myolysis normally due to the administration of noradrenalin or vasopressin remained uninfluenced by variations in the dietary intake of chlorides; hence, it was concluded that this type of cardiac lesion differs basically in its mechanism from all the other forms studied.