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Biomedical subjects

A Genovese

Publications and source records attributed to A Genovese.

At least 91 records · Page 5Linked to original sources

Effects of antiplatelet and calcium antagonist drugs on infarct size in rats.

The authors performed the experimental model of infarct-like myocardial lesions in rats treated with large doses of ISP. Myocardial necrosis was assessed on the basis of serum enzyme changes as well as of gross and microscopic findings. The infarct size was measured by a direct enzymatic method assaying creatine kinase (CK) depletion in infarcted myocardium. Pretreatment of the infarcted rats with antiplatelet (Lysin Acetyl Salicylate) or calcium antagonist drugs (Verapamil or Nifedipine) allowed the reduction of the necrotic area. Since a smaller size of infarct was achieved through different types of interventions it should be suggested that ISP-myocardial damage is due to several effects of the drug involving metabolic, vascular and/or coagulative patterns.

Acute Disease↗

[The role of the platelets in myocardial infarction induced by isoproterenol in the rat (author's transl)].

The AA. suggest that the myocardial infarction induced by isoproterenol in the rat may be determined by phenomenons of intracoronaric platelets aggregation. The effects on the degree and extension of the infarctual necrotic area have been evaluated in a drug with remarkable platelets antiaggregation activity (ASL). The following parameters are considered: wet and dry weight of the organ, and tissutal CPK levels.

Animals↗

Kinetics of erythroid and myeloid stem cells in post-hypoxia polycythaemia.

The number of erythroid burst-(BFU-E) and colony-forming units (CFU-E), as well as of myeloid-macrophage colony-forming units (CFU-C), has been evaluated in tibial marrow and spleen of ex-hypoxic polycythaemic mice, at sequential time intervals after the end of hypoxia. In both marrow and spleen, the kinetics of the CFU-E pool is characterized by a sharp fall from above normal to lower than normal values. BFU-E and CFU-C however rise from below normal to higher than normal levels. These results have been correlated with both the erythropoietin (Ep) and the erythropoietic activity curves. It is apparent that Ep levels largely control both the differentiation and the amplification of the CFU-E pool and it is suggested that Ep may act as a 'survival factor' at the CFU-E level and/or increase the flow of cells from BFU-E to CFU-E. The difference in response between CFU-E and BFU-E favours a clearcut distinction between these populations, whereas the similarity between the BFU-E and CFU-C response suggest a close relationship between these two cell populations. It is also of interest that the murine spleen functions as a large reservoir of erythroid microenvironment for hypoxia-induced stress erythropoiesis.

Animals↗

Hepatic erythropoietin: enhanced production in anephric rats with hyperplasia of Kupffer cells.

Erythropoietin (Ep) levels were assayed in serum of adult male rats subjected sequentially to (1) administration of colloidal carbon, Zymosan or their vehicles (2) sham operation or bilateral nephrectomy with and without subtotal hepatictomy, and (3) hypoxia (0.45-0.40 atmospheres of air for 6 h starting 1 h after the operation). In anephric rats these agents induced a significant potentiation of hypoxic Ep activity. Since they did not apparently modify the kinetics of exogenous Ep, it is postulated that this phenomenon is mediated by enhanced extrarenal Ep production. Both colloidal carbon and Zymosan induced hyperplasia of the reticuloendothelial system (RES). Moreover, subtotal hepatectomy almost abolished the Ep response to hypoxia evoked by Zymosan. The correlation between hyperplasia of hepatic RES and enhanced Ep production in anephric rats primed with these agents suggests that Kupffer cells constitute a major source for extrarenal Ep. Additionally, it is of interest that colloidal carbon and Zymosan did not significantly modify the renal production of Ep.

Animals↗

Erythropoietin production in the rat: additive role of kidney and liver.

Erythropoietin (Ep) levels were evaluated in serum of neonate, weanling, or adult rats subjected to 1) sham operation, nephrectomy, and/or subtotal hepatectomy and 2) a standard bout of hypoxia (0.45 atm air/6 h, starting 1 h after the operation). Ep activity was quantitated by means of strictly controlled assays in exhypoxic polycythemic mice. The sum of Ep titers in the serum of nephrectomized or hepatectomized rats was compared to Ep levels in sham-operated animals of corresponding age levels, with the exception of 1-wk-old rats: it is relevance that no significant difference is apparent between these Ep production curves. Thus, evidence is presented indicating for the first time that Ep derives from two functionally distinct and additive sources, i.e., the kidney and the liver. Liver Ep, although prevalent in neonatal animals, is obscured in the weanling adult rat by both gradual initiation of massive renal Ep production and progressive decrease of hepatic Ep activity.

Age Factors↗

Increased erythropoietin production in anephric rats with hyperplasia of the reticuloendothelial system induced by colloidal carbon or zymosan.

Adult rats were subjected sequentially to (1) administration of colloidal carbon, zymosan, or gadolinium; (2) subtotal hepatectomy, bilateral nephrectomy, or sham operation; and (3) a 6-hr bout of hypoxia, starting 1 hr or 24 hr after the operation. Control animals received the respective vehicles. The erythropoietin (Ep) activity was assayed in exhypoxic polycythemic mice on the basis of 48-hr per cent RBC(-59) Fe incorporation values. Ep levels in serum of anephric rats primed with either colloidal carbon or zymosan were considerably more elevated than in control animals. This potentiating effect was observed in rats subjected to hypoxia starting either 1 or 24 hr after nephrectomy. On the other hand, gadolinium did not enhance the extrarenal Ep response to hypoxia. It is emphasized that both colloidal carbon and zymosan induced marked hyperplasia of the hepatic and splenic reticuloendothelial system (RES), while gadolinium did not induce this effect. A strict correlation was thus established between potentiation of extrarenal Ep production and hyperplasia of the RES. It is therefore tentatively concluded that the RES is a source of extrarenal Ep. Additionally, since the liver plays a prominent role in extrarenal Ep production, Kupffer cells may represent a major source for Ep in the anephric rat. Finally, it is of interest that both colloidal carbon and zymosan did not potentiate the Ep response to hypoxia in sham-operated or subtotally hepatectomized rats.

Animals↗

[Demonstration of 2 experimental models of pure chronic erythroblastopenia].

Two experimental models for pure red cell aplasia (PRCA) were established. In the first one, administration of PRCA serum IgG in normal mice induced a sustained inhibitory effect on erythropoiesis, a progressive decline of the hematocrit values and an inverse rise of erythropoietin (Ep) levels in serum. Thus, the physiopathological pattern of PRCA type I (or A) was established, In the second model a rabbit producing anti-Ep crossreacting with endogenous Ep was subjected to a booster injection of Ep. The rise of the immune response was associated with decrease of Gct values and disappearance of erythroid precursors from marrow smears, and its subsequent decline with reticulocytosis and regression of the anemia, thus reproducing the physiopathological pattern of PRCA type II (or B).

Anemia, Aplastic↗

Pure red cell aplasia: studies on an IgG serum inhibitor neutralizing erythropoietin.

A new type of IgG serum inhibitor in adult pure red cell aplasia (PRCA) has been investigated. This inhibitor is directed against circulating erythropoietin (Ep) (PRCA type B), rather than the erythroid marrow (PRCA type A). Thus, the IgG inhibitor, after interaction with Ep in solution, is precipitated together with Ep by addition of goat anti-human gamma-globulins. Pre-therapy PRCA serum, although apparently devoid of Ep, shows considerable Ep activity following acidification and boiling. The inhibitor is absent from post-therapy serum, while Ep levels are elevated. An experimental model for PRCA type B has been established in normal mice after prolonged administration of pre-remission serum IgG.

Aged↗