ABSTRACT
In vitro growth kinetics of two Trypanosoma cruzi (Kinetoplastida: Trypanosomatidae) clones in myocardial cells from rodents of different susceptibility. Two Trypanosoma cruzi isolates, TCR-4 from Costa Rica and UES-1 from El Salvador, were studied in vitro to compare their infectivity or resistance and intracellular replication in myocardial cells in three strains of mice and rats: NGP white mice, C3 H mice and Sprague Dowley rats. Myocardial cells were cultured on coverslips at 37 degrees C in a humid 10% CO2 atmosphere and then infected at a ratio of one tripomastigote per cell. Samples were studied after 24, 72, 96 and 120 h of infection to determine parasite infection capacity and intracellular multiplication. Both parasites had the highest infection capacity in C3 H mice, followed by NGP mice cells with a very low infection rate. Lastly, almost no Trypanosoma cruzi multiplication was observed in Sprague Dowley rats, suggesting a strong natural resistance in this animal to both strains of the parasite. The UES-1 isolate presented higher multiplication and greater invasion than the TCR-4 strain, showing greater virulence of UES-1 in heart cells, at least in vitro.
Subject(s)
Animals , Mice , Rats , Myocytes, Cardiac/parasitology , Trypanosoma cruzi/growth & development , Kinetics , Costa Rica , Clone Cells/parasitology , Cells, Cultured , El Salvador , Time Factors , Rats, Sprague-Dawley , Trypanosoma cruzi/genetics , Trypanosoma cruzi/pathogenicity , VirulenceABSTRACT
In order to explore the mechanism of cardiac damage by PTH, the release of PGI2 from heart cells was measured. The results showed that bPTH ( 1-34) increased the release of 6-keto-PGFla from heart cells in a dose dependent manner. Calcium inophone A23187 also increased the 6-keto-PGF1? release, while EDTA and verapamil reduced it. These suggest that the PGI2 synthesis in heart cells was affected by intra and extracellular calcium. The significance of bPTH( 1-34) induced increase of PGI2 synthesis might be associated with interference of energy metabolism, and then, cell damage.
ABSTRACT
In order to obtain some evidences of the role of parathyroid hormone (PTH) in regulating calcium metabolism, and explore the mechanisms by which PTH regulates calcium in the heart, 45Ca was used to study the influence of bovine PTH1-34 fragment (bPTH1-34) on calcium transsacolemma. The results indicate that bPTH1-34(l?I0-7mol ? L-1) increases beating rate of heart cells under normal state and it markedly increases the rapid (5 min) and the slow (120 min) phases of 45Ca influx in heartcells (under normal, KC1 10-5 mol?L-1 high K+depolarised, NA 10-7mol?L-1receptors activated states), but it could also reduce 45Ca efflux from the cultured heart cells. It suggests that the mechanisms caused by bPTH1-34 which enhances the cytosolic calcium concentration and myocardial beating rate may be related with cAMP level elevated in heart cells.
ABSTRACT
At the concentrations of 10-8mol/L, 5.5?l0-8mol/L, 10-7mol/L morphine produced a dose-dependent increase of beating rate in cultured rat heart cells with 9%,32%and 81% respectively. The increase was antagonized by opiate antagonist naloxone ( 10-5mol/L ) , but not affected by propranolol ( 10-5mol/L ) which could cancel the positive chronotropy of isoprenaline ( 10-9mol/L ) on the beating cells. The results support the concept that morphine may be a direct effect on myocadium, perhaps through opiate receptors.