Myocardial Depression in Septic Shock: Role of Nitric Oxide and Other Mediators

1995 ◽  
pp. 322-343 ◽  
Author(s):  
A. Kumar ◽  
J. E. Parrillo
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Myocardial Depression

Role of nitric oxide and cGMP in human septic serum-induced depression of cardiac myocyte contractility

1999 ◽  
Vol 276 (1) ◽  
pp. R265-R276 ◽  
Author(s):  
Anand Kumar ◽  
Rupinder Brar ◽  
Peter Wang ◽  
Linda Dee ◽  
Greg Skorupa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Cardiac Myocytes ◽  
Guanylate Cyclase ◽  
Cardiac Myocyte ◽  
Intracellular Cgmp ◽  
Human Septic Shock ◽  
Tnf Α ◽  
Myocyte Contractility

Previous studies have demonstrated the existence of a circulating myocardial depressant substance during human septic shock. We have recently identified this substance as a synergistic combination of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). This study utilized an in vitro cardiac myocyte assay to evaluate the potential mechanistic role of nitric oxide (NO) and cGMP in depression of myocyte contractility induced by TNF-α, IL-1β, TNF-α + IL-1β (at low concentrations), and human septic shock serum (HSS). TNF-α, IL-1β, TNF-α + IL-1β, and each of 5 sera from patients with acute septic shock caused depression of both maximum extent and peak velocity of cardiac myocyte shortening and an increase in intracellular cGMP concentration during 30 min of exposure (minimum P < 0.01). NO synthetase (NOS) and guanylate cyclase inhibitors such as N-methyl-l-arginine (l-NMA) and methylene blue prevented these effects; an excess ofl-arginine withl-NMA restored them (minimum P < 0.01). In contrast,d-arginine failed to reestablish cytokine-induced myocyte depression and cGMP accumulation prevented byl-NMA. Exposure of myocytes to TNF-α, IL-1β, or TNF-α + IL-1β produced a concentration-dependent increase in intracellular cGMP that paralleled the depression of cardiac myocyte contractility (minimum P < 0.001). In addition, TNF-α, IL-1β, TNF-α + IL-1β, or HSS application to cardiac myocytes resulted in increased NO gas generation, which was inhibited byl-NMA (minimum P < 0.01). Furthermore, unstimulated cardiac myocytes were shown to harbor constitutive but not inducible NOS activity. These data suggest that the sequential generation of NO by a constitutive NOS and cGMP by guanylate cyclase represents an important mechanism of cardiac myocyte depression by TNF-α, IL-1β, TNF-α + IL-1β, and the myocardial depressant substance(s) of septic shock.

Effects of Vasopressin in Septic Shock

2008 ◽  
Vol 19 (3) ◽  
pp. 281-287
Author(s):  
Margaret S. Ruggiero
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Septic Shock ◽  
Cardiovascular Effects ◽  
The Body ◽  
Myocardial Depression ◽  
Restore Blood Pressure ◽  
Dose Dependent ◽  
Pituitary Adrenal Axis ◽  
Major Mediator

Septic shock continues to be one of the leading causes of death in the intensive care unit today. The confluence of many factors contributes to the deterioration of patients’ condition in septic shock. Increased levels of nitric oxide, in part, mediate the cardiovascular effects of septic shock. Nitric oxide is major mediator of vasodilation and hypotension as well as myocardial depression. It also contributes to decreased production and release of endogenous vasopressin. Vasopressin effects are actualized by stimulation of V1, V2, and V3 receptors located in various parts of the body. The response is dose dependent. Endogenous vasopressin and angiotensin II act synergistically to preserve and restore blood pressure levels. Decreased circulating vasopressin contributes to adrenal insufficiency via hypothalamic-pituitary-adrenal axis suppression and increased catecholamine resistance to vasopressors. Exogenous vasopressin supplementation in physiologic doses has been shown to improve blood pressure levels and decrease vasopressor needs in patients with septic shock.

Role of nitric oxide in thermoregulation during septic shock: involvement of vasopressin

2003 ◽  
Vol 447 (2) ◽  
pp. 175-180 ◽  
Author(s):  
Alexandre Giusti-Paiva ◽  
Luiz G. S. Branco ◽  
Margareth de Castro ◽  
José Antunes-Rodrigues ◽  
Evelin C. Carnio
Keyword(s):  
Nitric Oxide ◽  
Septic Shock

Role of inducible nitric oxide synthase in the reduced responsiveness of the myocardium to catecholamines in a hyperdynamic, murine model of septic shock*

2006 ◽  
Vol 34 (2) ◽  
pp. 307-313 ◽  
Author(s):  
Eberhard Barth ◽  
Peter Radermacher ◽  
Christoph Thiemermann ◽  
Sandra Weber ◽  
Michael Georgieff ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Murine Model ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide
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