The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Septic Shock in Humans: Advances in the Understanding of Pathogenesis, Cardiovascular Dysfunction, and Therapy
Abstract
Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
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Cites
Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia
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Detection of circulating tumor necrosis factor after endotoxin administration
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Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway
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Pathogenetic Mechanisms of Septic Shock
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Self-citationVasopressin Deficiency Contributes to the Vasodilation of Septic Shock
Landry, D. W., Levin, H. R., Gallant, E. M., Ashton, R. C., Seo, S., D'Alessandro, D., Oz, M. C., & Oliver, J. A. (1997) · Circulation · doi:10.1161/01.cir.95.5.1122 · Cited by 990
Treating Patients with Severe Sepsis
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Statin treatment after onset of sepsis in a murine model improves survival.
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Martich, G. D., Boujoukos, A. J., & Suffredini, A. F. (1993) · Immunobiology · doi:10.1016/s0171-2985(11)80353-0 · Cited by 275
Self-citationApolipoprotein E Protects Against Bacterial Lipopolysaccharide-induced Lethality
Van Oosten, M., Rensen, P. C. N., Van Amersfoort, E. S., Van Eck, M., Van Dam, A.-M., Brevé, J. J. P., Vogel, T., Panet, A., Van Berkel, T. J. C., & Kuiper, J. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m009915200 · Cited by 186
Is nitric oxide overproduction the target of choice for the management of septic shock?
Feihl, F., Waeber, B., & Liaudet, L. (2001) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(01)00155-3 · Cited by 151
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Genetic polymorphisms in sepsis
Dahmer, M. K., Randolph, A., Vitali, S., & Quasney, M. W. (2005) · Pediatric Critical Care Medicine · doi:10.1097/01.pcc.0000161970.44470.c7 · Cited by 101
Lien, J.-C., Lee, F.-Y., Huang, L.-J., Pan, S.-L., Guh, J.-H., Teng, C.-M., & Kuo, S.-C. (2002) · Journal of Medicinal Chemistry · doi:10.1021/jm020070b · Cited by 26
Metadata
- Authors
- Parrillo, J. E., Parker, M. M., Natanson, C., Suffredini, A. F., Danner, R. L., Cunnion, R. E., & Ognibene, F. P.
- Venue
- Annals of Internal Medicine
- Publisher
- American College of Physicians
- Published
- 1990-08-01
- Volume
- 113
- Issue
- 3
- Pages
- 227-242
- ISSN
- 0003-4819 (ISSN-L)
- 1539-3704
- OpenAlex
- W2045010042
- Cited by
- 1,179
- References
- 2
- FWCI
- 34.98
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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