The effects of prostaglandins E2 and F2 alpha on renal lesions induced by an anti-rat serum were investigated in rats. It was found that these prostaglandins, administered concomitantly with the antiserum, were able to prevent or remarkably attenuate these lesions. A very interesting finding is that, after prostaglandin administration, no or insignificant morphological alterations of the kidney occurred, in spite of the fact that its mononuclear cell infiltration was somewhat persistent. Hence, in addition to the known effects of these prostaglandins on the immune response components, the blockade of cellular receptors for immunoglobulins is to be considered as a main mechanism in explaining their preventive action in allergic nephritis.

Optic and electron microscopical investigations as well as histochemical investigations were performed in rats which have intraperitoneally received an anti-rat serum together with either PGE2 or PGF2 alpha, in order to study the effect of these prostaglandins on antibody-induced myocardial lesions. PGE2 and, especially, PGF2 alpha were found to considerably prevent the myocardium against these lesions (mononuclear cell infiltration, interstitial and intracellular hyperhydration, disintegration of myofibrils, vacuolization of sarcoplasmic reticulum, mitochondrial swelling and degradation, lysosomal activation and disruption of myocardial sarcolemmas and blood capillary membranes). Their protective actions were revealed in animals killed 24 h and 6 days after the administration of anti-rat immunoglobulins.

Since there are controversial data and opinions on the use of lactate as a viability test for preserved hearts, investigations were carried out of the variations of lactate and pyruvate amounts in the perfusion fluid during hypothermic preservation of canine hearts by means of a perfusion fluid containing amino acids in "cytoplasmic" concentrations. These variations were interpreted in connection with the changes in the coronary perfusion flow during storage and the functional performances of the preserved hearts during long periods of subsequent ex vivo functional testing. Likewise, investigations of the ability of the myocardial mitochondria to oxidize in vitro lactate and pyruvate at low temperature levels were performed in order to explain the nature of the impairment in using these metabolic substrates during preservation and of the functional cardiac disturbances after resuscitation. The investigations have led to the conclusion that lactate should not be used as the sole index of heart storage efficiency and that it gains in significance only when a high myocardial lactate production is associated with a progressively increasing resistance in the coronary vasculature during preservation. The possible metabolic significance of the results obtained in these investigations are amply discussed.

In the present paper, the involvement of the renal kallikrein-kinin system in the pathogenic mechanism of essential hypertension is discussed in the larger framework of the complex hormonal actions of prostaglandins (PGs), catecholamines, renin and angiotensins in the long-term control of arterial blood pressure and sodium metabolism. An attempt is also made to emphasize the role of the cerebral renin-angiotensin system in this pathogenic mechanism. To better understand the problems raised in this paper, the concomitant consultation of two previously published papers [88], [89] is recommended.

AbstractThe problem of the existence of a prostaglandin (PG) receptor is still controversial, but it seems to be clear that the main action of the PGs concerns the interface of the cellular membrane (which has a predominantly lipid character) and the extracellular liquid (which mainly consists of water). Also especially in the case of the exogenous PGs, the transport of these substances in the organism in influenced by the hydrophilic‐hydrophobic properties of the reactive molecules. These properties can be estimated by MO studies using a solvation model and a semiempirical method of calculation. This paper is concerned with the molecules of PGA1 and PGE1. MO studies were performed for these molecules with the CNDO/SW method in order to calculate ionization potentials, dipole moments, and molecular polarizabilities. With these computed molecular properties, the electrostatic and van der Waals interactions with water and octanol molecules are evaluated and compared within the framework of the original model. This study allows the differentiation of the hydrophilic–hydrophobic character of the PGs investigated and the comparison of the results with experimental data.

Beside exerting an impressive variety of physiological and pharmacological actions on different systems of the organism, prostaglandins (PGs) may also be main factors in the pathogenesis of essential hypertension. Their role in this process is mostly explained by their multivalent interference with the tissue hormones which regulate the vascular tone and the water-sodium balance. In this paper a discussion regarding the results of a widespread research and the growing literature dealing with this interference is made on the basis of a personal point of view. The present paper is a continuation of a previous one on this topic.

Investigations regarding the main biochemical systems of the erythrocyte membrane were performed on rat erythrocyte ghosts after treating the animals with PGA1, PGE1 and PGF2alpha. These investigations have shown that the prostaglandins which were found to induce changes in the erythrocyte flexibility (PGE1 and PGF2ALPHA) also induce significant changes in the concentrations of lipid peroxides, SH groups, proteins and nicotinamide adenine nucleotides, as well as in the activity of some electron transportors belonging to the nicotinamide proteins, in the erythrocyte membrane.

Myocardial adenine nucleotides (nicotinamide adenine nucleotides included), glutathione, catecholamines (DOPA, dopamine, noradrenaline, adrenaline) and some enzymes in correlation were investigated in dogs with cardiac failure induced by bilateral iliac arteriovenous fistulas, and unilateral (left) heart vagotomy was also studied for its influence on the changes in the myocardial amounts of these compounds occuring in this pathological circumstance. The cardiac failure in arteriovenous fistula was characterized by the following myocardial metabolic aspects: (I) no change in the amount of proteins (although an important cardiac hypertrophy was present); (II) decreases in the amounts of adenine nucleotides (especially ADP and ATP), without significant variations in the adenosine concentration, accompanied by increases in the concentrations of nicotinamide adenine nucleotides (in both their oxidized and reduced forms) in the heart mitochondria; (III) no change in the amounts of oxidized and reduced glutathione and in the activity of NADH2-dependent glutathione reductase; (IV) a very significant increase in the activity of MAO without significant influences on the levels of the studied catecholamines. The partial vagal denervation of the heart was found to attenuate substantially the changes in the amounts of adenine nucleotides and nicotinamide adenine nucleotides in the myocardial mitochondria and to facilitate the action of MAO on noradrenaline leading to a significant decrease in its myocardial level.

anastomosis 94 Creatine phosphate 322 Cyanide intoxication 382

In this paper, an attempt was made to describe the alterations of the myocardial energy metabolism following moderate stenoses of aorta or pulmonary artery. Biochemical investigations regarding the main high energy phosphates and a large series of dehydrogenases in the myocardium of the overloaded ventricles have revealed the following facts: (1) the myocardial CP-CPK system appears to be more labile than the myocardial AMP-ATP system in response to a ventricular overload; (2) the changes in the amounts of myocardial high energy phosphates seem to be more important in the right chronic cardiac overload than in the left one; (3) before the overloaded ventricle becomes insufficient, the myocardial dehydrogenase system elicits no alteration, suggesting that the oxidative phosphorylation is not affected; (4) there is a closer relationship between the coronary flow and pressure and the myocardial energy metabolism than that existing between this metabolism and the tension of the myocardial fibres following a persistent increase in the systemic arterial resistance.

The total amounts of cyclic AMP (cAMP), prostaglandin E1 (PGE1) and prostaglandin F2alpha (PGF2alpha) in cerebra have been measured in rats, at constant intervals, up to 18 days after whole body exposure to either a unique moderate dose (500 rads) or a unique lethal dose (750 rads) of cobalt-60 gamma-radiation. The experimental findings indicate that this radiation (i) results in an abrupt short-lasting increase in the amount of cerebral cAMP after a 500 rad-irradiation and a progressive long-lasting increase in its amount after a 750 rad-irradiation, and (ii) induces no change in the normally, existing correlation between cerebral PGE1 and cAMP, but affects deeply the normally existing correlation between cerebral PGF2alpha and cAMP. These biochemical alterations generally parallel the evolution of the radiation-induced brain edema.

In this study both prostaglandin A1 (PGA1) and prostaglandin F2alpha (PGF2alpha) have been shown to be effective long-lasting stimulators of the cyclic AMP (cAMP) synthesis in the liver, intestinal mucosa and brain, whereas prostaglandin E1 (PGE1) was found to have a similar effect on the cerebral cAMP synthesis and a dissimilar effect (decrease) on the hepatic one. A lack of sensitivity of the intestinal mucosa cAMP to PGE1 was also observed.