Myocardial and vascular adrenergic alterations in a rat model of endotoxin shock

Abstract

In ex vivo experiments, 3 hrs after endotoxin injection, vascular responsiveness was sharply decreased. This impaired response was improved in vitro by the inhibition of nitric oxide. The heart response to isoproterenol, nevertheless, was maintained, even though there was an obvious decrease in receptor density and an impaired myocardial accumulation of cAMP. Anti-TNF-alpha antibody partially prevented the alteration of both myocardial pressure response to isoproterenol and biochemical parameters, and was not efficacious in preventing vascular hyporeactivity to vasoconstrictor agents.

Evaluation of plasma catecholamine and serum cortisol concentrations in horses with colic

“…Circulating concentrations of epinephrine and norepinephrine in humans, pigs, and rats with experimentally induced or naturally occurring septic shock or endotoxemia are increased, compared with values in unaffected individuals, and those increases are greater in animals or humans with more severe disease. 8,10,11,20,21 In pigs, increases in plasma epinephrine concentration are strongly associated with increasing severity of septic shock, as indicated by the extent of lactic acidosis and EQUINE deterioration in hemodynamic status. 8 This direct association between the severity of shock (as determined by increases in plasma lactate concentration and heart rate and decreases in blood pH and base excess) and plasma concentration of epinephrine was also evident in the horses in our study.…”

Vasoplegia treatments: the past, the present, and the future

“…NO activates cyclic guanosine monophosphate (cGMP) production as well as calcium-sensitive potassium channels, potassium ATP channels, and myosin light chain phosphatase, all of which contribute to vasodilation [15]. Other mechanisms equally involved in vasodilatation include prostacyclin and cyclooxygenase 2 (COX2) pathways, although with no currently known positive therapeutic consequences [16].…”

Regulation of leukocyte adhesion to heart by the tripeptides feG and feG(NH2)

“…In a variety of species such as the guinea pig (Keller et al 1995;Rubin et al 1994), rabbit (Lew et al 1996), and rat (Boillot et al 1997;Hasan and McDonough 1997;Wu et al 1997;Mathison et al 1999b), sepsis or endotoxemia reduces myocardial contractility. Clinically, septic shock affects the heart; systolic and diastolic myocardial dysfunction is commonly described (Turner et al 1999;Ognibene et al 1988;Ellrodt et al 1985).…”