It is indicated that UII may act as an autocrine and/or paracrine hormone rather than as a circulating hormone, playing important roles in the development of ventricular hypertrophy induced by chronic hypoxia, and that the pathophysiologi-cal significance of UII in pulmonary and cardiovascular alteration induced by Chronic Hypoxia deserves further investigation.
The results demonstrate that group IIPLA2 gene transcripts were overexpressed in rat liver during the progression of sepsis and that the overexpression was a result of the enhanced synthesis of group II PLA2 mRNA.
The alteration of Na(+)-Ca2+ exchange during different phases of sepsis might be related to the activities of Gq, protein kinase C, and phosphorylation/dephosphorylation.
Because PKC mediated phosphorylation plays an important role in regulating myocardial contractility, an activation in cytosolic PKC may contribute to the development of a hypercardiodynamic state during the early phase of sepsis.
To determine how the heat shock and acute phase responses were reprioritized during stress, expression of beta-fibronogen and HSP 72 was induced simultaneously in the same animal by administration of endotoxin and total body hyperthermia, respectively.
Analyzing the expression of heat shock protein (HSP) 72 in different rat organs after a total body hyperthermia suggests that this disparate expression of HSP 72 is due to intrinsic characteristics of the cell types rather than to physiological or environmental conditions.
The results indicate that beta-ARs in the rat heart were externalized from light vesicles to sarcolemma during early sepsis but were internalized from surface membranes to intracellular sites during late sepsi.
Data show that HO/CO system has an anti-hypertension biological action, suggesting that endogenous CO plays an important role in hypertension pathogenesis.