[Effect of thymic peptides on the functional activity of phagocytic cells of donor peripheral blood]. / Vliianie timicheskikh peptidov na funktsional'nuiu aktivnost' fagotsitarnykh kletok perifericheskoi krovi donorov.

The direct action of synthetic peptide preparations, analogous to thymic hormones, on the functions of phagocytic cells was studied. The preparations Thymogen, Neogen and Thymodepressin in a dose of 10 mM produced a stimulating effect on the ingestive activity of the neutrophil, but not monocytic, population. All three preparations also enhanced the formation of oxygen metabolites registered in the luminol-dependent chemiluminescent analysis. The characteristics of spontaneous chemiluminescence (CL) reflecting the basal level of the synthesis of the active forms of oxygen and CL induced by opsomized zymosan significantly increased also in those cases when the preparations were used in a dose of 10 mM. The level of the synthesis of hydrogen peroxide in individual cells could be appraised by the intensity of the luminescence of dichlorofluorescein diacetate (DCF-DA), evaluated with the use of flow cytometry. All preparations produced a stimulating effect on the formation of hydrogen peroxide in monocytes. The reaction of neutrophils was even more active: Neogen (10 mM) produced the twofold change in the intensity of the luminescence of DCF-DA) in neutrophils, Thymogen and Thynodepressin increased the average intensity of the luminescence of DCF-DA by 80% and 60%, respectively.

Endotoxin-induced myocardial dysfunction: is there a role for nitric oxide?

Nitric oxide has been implicated in the regulation of cardiac contractile function as well as the depressed myocardial contractility associated with sepsis and endotoxemia. We examined the effects of nitric oxide synthase (NOS) inhibitors and a nitric oxide generator on contractile responses of left atrial preparations and ventricular myocytes isolated from endotoxemic guinea pigs, which exhibit depressed myocardial contractile function. The NOS inhibitor L-NAME had no effect on contractile tension developed by control atria or atria isolated from guinea pigs 4 or 16 h after an intraperitoneal injection of endotoxin. Similarly, contraction of ventricular myocytes isolated from control or endotoxemic guinea pigs (4 h after endotoxin injection) was unchanged by exposure to several NOS inhibitors. In addition, neither Ca(2+)-dependent nor Ca(2+)-independent ventricular NOS activity was affected by endotoxemia. These data suggest that nitric oxide alone is not responsible for the cardiac contractile dysfunction of endotoxemic guinea pigs.