Bacteremia Due to Gram-Negative Bacilli Other Than the Salmonella

Waisbren, Burton A.

doi:10.1001/archinte.1951.03810100051005

Cited by 182 publications

(32 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sepsis is a severe clinical syndrome with high mortality, resulting in the associated multiple organ dysfunction syndrome (MODS) and septic shock (Vincent, 2008;Boomer et al, 2011). Heart is one of the target organs susceptible to attack by sepsis; its dysfunction during sepsis has been studied for decades, and a number of results have been shown to be associated with myocardial depression in sepsis (Waisbren, 1951;Rivers et al, 2001;Young, 2004;Merx & Weber, 2007). It's reported that the presence of cardiac dysfunction in sepsis is related to a notable increased mortality of 70-90% compared to the mortality of 20% in patients without heart dysfunction (Parrillo et al, 1990;Merx & Weber, 2007).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of curcumin against cardiac dysfunction in sepsis rats

Yang¹,

Wu²,

Shanghai³

et al. 2013

Pharmaceutical Biology

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Protective effect of curcumin against cardiac dysfunction in sepsis rats

Yang¹,

Wu²,

Shanghai³

et al. 2013

Pharmaceutical Biology

View full text Add to dashboard Cite

“…This was observed in the initial phase of hospitalization due to septic shock. In contrast, "cold shock" seemed to be related to low cardiac output and was correlated with the later clinical stages of septic shock before patients succumbed to sepsis (1)(2)(3). Based on these findings, it was concluded that patients during septic shock initially encountered an early hyperdynamic phase from which they either recovered or declined into a hypodynamic phase associated with myocardial depression, heart failure, and death (4).…”

Section: Introductionmentioning

confidence: 99%

Molecular Events in the Cardiomyopathy of Sepsis

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

109

View full text Add to dashboard Cite

Septic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression. SYSTEMIC, SUPRACELLULAR MECHANISMS Decreased Coronary Blood FlowOne of the first suggestions was that reduced coronary perfusion in the septic heart might be responsible for a setting of global cardiac ischemia. This hypothesis was soon abandoned after direct measurements of coronary blood flow were obtained, showing no reduced, but rather increased, coronary blood flow (22,23). In later studies, however, increased levels of plasma troponin were observed and correlated with the severity of myocardial depression during sepsis and septic shock (24). Myocardial necrosis could not be observed in patients who died from septic shock (3,25), however, raising the question whether increases in troponin were due to cytokine-induced, transient increases in cardiomyocyte membrane permeability to troponin. To date, this remains to be determined. Alterations of MicrovasculatureThere is now increasing evidence that sepsis and septic shock leads to changes of the myocardial microvasculature. In a canine model of endotoxemia, maldistribution of heterogeneous coronary blood flow has been reported (26). These findings might be caused by endothelial swelling and nonocclusive intravascular fibrin deposits in the microvasculature (27). In parallel, activated cardiomyocytes from septic mice promoted transendothelial migration and activation of circulating neutrophils into the interstitium (28) where these cells may augment the sepsis-induced intracardial inflammation, and contribute to an increased vascular leakage, which has been described to also impair cardiac function and compliance secondary to myocardial edema (29,30). Yet, studies have failed to confirm cellular hypoxia in a murine sepsis model (31). Cardiosuppressing Circulating Proinflammatory MediatorsAnother hypothesis suggested circulating myocardium-depressing factors as the cause of septic cardiomyopathy (32). Parrillo et al. (33) confirmed the existence of a cardiodepressant substance by incubating isolated rat cardiomyocytes with serum obtained from septic shock patients, leading to decreased amplitude and velocity of cardiomyocyte shortening. Levels of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and the complement anaphylatoxin, C5a, are known to be elevated in the circulation during sepsis an...

show abstract

“…Approximately 30 years ago, early studies of septic shock emphasized two distinct clinical syndromes (3). One type had a bounding pulse ascribed to a high cardiac output; a second syndrome was characterized by "cold, clammy" skin and a faint pulse and this syndrome was postulated to result from a low cardiac output.…”

Section: Introductionmentioning

confidence: 99%

A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.

Parrillo¹,

Burch²,

Shelhamer³

et al. 1985

J. Clin. Invest.

555

180

View full text Add to dashboard Cite

We have previously described a subpopulation of patients with septic shock who had a reversible depression of radionuclidedetermined left ventricular ejection fraction (EF). To investigate the mechanism of this myocardial depression, an in vitro model of mammalian myocardial cell performance was established employing primary spontaneously beating rat myocardial cells. The contraction of a single cardiac cell was quantitated by recording the changes in area occupied by the cell during contraction and relaxation. In 20 septic shock patients during the acute phase, the mean left ventricular EF was decreased (mean = 033, normal mean = 0.50), and serum obtained during this acute phase induced a mean (±standard error of the mean) 33±4% decrease in extent and 25±4% decrease in velocity of myocardial cell shortening during contraction (P < 0.001). In contrast, serum obtained from 11 of these same patients before shock (n = 2) or after recovery (n = 9) of the left ventricular EF (mean = 0.50) showed a return toward normal in extent and velocity of shortening (P < 0.001). Sera from 17 critically ill nonseptic patients, from 10 patients with structural heart disease as a cause for a depressed EF, and from 12 healthy laboratory personnel, induced no significant changes in in vitro myocardial cell performance. In 20 patients during the acute phase of septic shock, the decreased EF in vivo demonstrated a significant correlation (r = +0.52, P < 0.01) with a deerease in the extent of myocardial cell shortening in vitro. The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substance in producing the reversible cardiomyopathy seen during septic shock in humans.

show abstract

Bacteremia Due to Gram-Negative Bacilli Other Than the Salmonella

Cited by 182 publications

References 31 publications

Protective effect of curcumin against cardiac dysfunction in sepsis rats

Protective effect of curcumin against cardiac dysfunction in sepsis rats

Molecular Events in the Cardiomyopathy of Sepsis

A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.

Contact Info

Product

Resources

About