Nonseptic Causes of Shock

To assess the proinflammatory response, antiinflammatory response, site of mediator production, and route of cytokine diffusion in acute pancreatitis, Dugernier and coworkers obtained simultaneous samples of ascites, thoracic lymph, and blood at the onset of end-organ dysfunction and for the subsequent 6 days in 60 patients. Tumor necrosis factor- ${alpha}$ and interleukin-1ß were found in less than 15% of blood and lymph samples. Secondary proinflammatory and antiinflammatory cytokines were elevated early and throughout the sampling period in all compartments. Cytokine levels decreased from ascites to lymph to blood, suggesting a splanchnic origin. Prolonged diversion of ascites and lymph did not alter cytokine gradients, suggesting transfer of mediators via the splanchnic blood circulation. The authors conclude that the magnitude of the inflammatory response in patients with acute pancreatitis is proportional to pancreatic damage and end-organ dysfunction, that inflammatory mediators are primarily released from the splanchnic area, mediators gain access to the systemic compartment mainly by the portal and suprahepatic circulations, the proinflammatory response is dominant in the pancreas and splanchnic areas, and the antiinflammatory response is dominant in the thoracic duct and systemic circulation. An editorial commentary by Raraty and Neoptolemos accompanies this article.

To determine whether critical oxygen delivery, the point at which oxygen consumption becomes limited by oxygen delivery, is higher when hypoxia is caused by stagnant flow versus anemia, Morita and coworkers induced sepsis in rats by cecal legation and perforation. Rats were randomized to anemic hypoxia (induced by isovolumic hemodilution) or stagnant hypoxia (induced by stepwise inflation of a balloon in the right atrium). The level for critical oxygen delivery did not differ between anemic hypoxia and stagnant hypoxia in the septic animals. The critical hemoglobin concentration for anemic hypoxia was equivalent for septic animals and control animals, indicating that tolerance to acute anemia is not altered by sepsis. The authors conclude that critical oxygen delivery did not differ between anemic and stagnant hypoxia in either septic or control rats.

Citations 1-3 of 3 total displayed.

Compartments That Cause the Real Damage in Severe Acute Pancreatitis

John P. Neoptolemos
Am. J. Respir. Crit. Care Med. 168: 141-142. [Full text]

Compartmentalization of the Inflammatory Response during Acute Pancreatitis: Correlation with Local and Systemic Complications

Thierry L. Dugernier, Pierre-François Laterre, Xavier Wittebole, Jean Roeseler, Dominique Latinne, Marc S. Reynaert, and Jérôme Pugin
Am. J. Respir. Crit. Care Med. 168: 148-157. [Abstract] [Full text]

Critical Oxygen Delivery in Conscious Septic Rats under Stagnant or Anemic Hypoxia

Yoshihisa Morita, Ian Chin-Yee, Pei Yu, William J. Sibbald, and Claudio M. Martin
Am. J. Respir. Crit. Care Med. 167: 868 -872. First published online as doi:10.1164/rccm.200205-490OC [Abstract] [Full text]

Year in Review Home