Septic shock and cardiac effects?

Why would septic shock lead to a decreased systemic vascular resistance?

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Answers:

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http://en.wikipedia.org/wiki/Tumor_necro…

And:

http://en.wikipedia.org/wiki/Histamine

?

Wouldn't Mast Cells Release Histamine too?

http://www.jimmunol.org/cgi/content/abst…

As if you Need More:

http://www.jimmunol.org/cgi/content/abst…

EDIT: Looks Like I Have Cause and Effect Reversed.


EDIT: http://en.wikipedia.org/wiki/Mast_cell

More:

http://www.scitopics.com/Mast_Cells_in_I…

Even More:

http://www.geocities.com/thjuland/mast-t…

And:

Critical protective role of mast cell in a model of acute septic peritonitis.

Echtenacher B, M"annel DN, Hültner L.

Institut für Pathologie/Tumorimmunologie, Universit"at Regensburg, Germany.

Mast cells play a detrimental role in IgE-dependent allergic reaction. In contrast, a protective function for mast cells has be proposed on the basis of some worm infection models. No reports exist on the in vivo significance of these cells contained by bacterial infections. Here we use congenitally mast-cell-deficient W/Wv mice and normal +/+ littermates to analyse the role of mast cells within a model of acute septic peritonitis (caecum ligation and puncture (CLP)). Following CLP, W/Wv mice showed a significantly increased mortality compared to +/+ mice. The selective reconstitution of W/Wv mice with cultured +/+ mast cells substantially protected them from the fatal effects of CLP, whereas an anti-tumor-necrosis-factor (TNF) antibody injected immediately after CLP completely suppressed this protection. Our results reveal a previously unrecognized protective role of mast cells and mast-cell-derived TNF surrounded by acute bacterial peritonitis.

PMID: 8609992 [PubMed - indexed for MEDLINE]

And:

Protective roles of mast cells against enterobacterial infection are mediated by Toll-like receptor 4.
Supajatura V, Ushio H, Nakao A, Okumura K, Ra C, Ogawa H.

Department of Dermatology, Juntendo University School of Medicine, Tokyo, Japan.

Toll-like receptors (TLRs) are mammalian homologues of the Drosophila Toll receptors and are thought to own roles in innate recognition of bacteria. We demonstrated that TLR 2, 4, 6, and 8 but not TLR5 be expressed on mouse bone marrow-derived mast cells (BMMCs). Using BMMCs from the genetically TLR4-mutated strain C3H/HeJ, we demonstrated that functional TLR4 was required for a full responsiveness of BMMCs to produce inflammatory cytokines (IL-1beta, TNF-alpha, IL-6, and IL-13) by LPS stimulation. TLR4-mediated stimulation of flagstaff cells by LPS was followed by activation of NF-kappaB but not by stress-activated protein kinase/c-Jun NH2-terminal kinase signaling. In addition, contained by the cecal ligation and puncture-induced acute septic peritonitis model, we demonstrated that genetically mast cell-deficient W/W(v) mice that were reconstituted with TLR4-mutated BMMCs have significantly higher mortality than W/W(v) mice reconstituted with TLR4-intact BMMCs. Higher mortality of TLR4-mutated BMMC-reconstituted W/W(v) mice was capably correlated with defective neutrophil recruitment and production of proinflammatory cytokines in the peritoneal cavity. Taken together, these observations provide definitive evidence that flagstaff cells play important roles in exerting the innate imperviousness by releasing inflammatory cytokines and recruitment of neutrophils after recognition of enterobacteria through TLR4 on mast cell.

PMID: 11490012 [PubMed - indexed for MEDLINE]

And:

Toll-like receptor 4-mediated activation of murine mast cells.
McCurdy JD, Lin TJ, Marshall JS.

Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.

Toll-like receptors (TLRs) are a family of model recognition receptors that are critical for cellular responses to a variety of bacterial, viral, and fungal products. Mast cells are major to host survival in a number of models of bacterial infection and might act as sentinel cell in host defense. We therefore examined the expression of TLRs and associated molecules by murine bone marrow-derived mast cell (BMMCs). BMMCs and the murine mast cell line MC/9 expressed mRNA for TLR2, TLR4, and TLR6 but not TLR5 and for both adapter molecule MD-2 and signaling molecule MyD88 but lacked surface CD14. After activation next to the TLR2- and TLR4-dependent stimuli Staphylococcus aureus-derived peptidoglycan and Escherichia coli-derived lipopolysaccharide (LPS), respectively, mast cells produced significant levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha). To determine whether flagstaff cells require TLR4 for cellular responses to LPS, mast cells be derived from the bone marrow cells of C3H/HeJ and C57Bl/10ScNCr mice containing a point mutation and a null mutation, respectively, in TLR4. Using these models, we demonstrated that the BMMC IL-6 and TNF-alpha responses to LPS were completely dependent on functional TLR4 near no significant LPS response observed in its absence. These findings have exalted implications for the mechanism of mast cell responses to pathogens and their products and suggest that different TLR4-expressing cell might have different thresholds for activation with LPS.

PMID: 11739561 [PubMed - indexed for MEDLINE]

I'm Sorry, Kinda Neat, I Need to Get a Life.

EDIT: Sorry, Couldn't Help Myself:

http://en.wikipedia.org/wiki/Toll-like_r…

EDIT: the Above Looks to Explain Why this Happens, Additionally:

http://en.wikipedia.org/wiki/Anaphylacti…
From Above: "The systemic release of TNF-α causes vasodilatation, which lead to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually to shock."
And:

http://en.wikipedia.org/wiki/Septic_shoc…

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In response to toxins released by the bacteria, cytokines of the immune system are released and this causes systemic vasodilation, which decrease systemic vascular resistance.
As the effects of the toxins progress, metabolic changes occur that lead to discharge of fluid out of blood vessels and into tissues, and to weakening of the force of heart contractions. These contribute to further decreasing SVR. Source(s): RN

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Check out Tumor Necrosis Factor. It plays a significant role in the pathophysiology of sepsis. Source(s): Pharmacist

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