Unsuspected mesenteric hypoperfusion despite apparent hemodynamic recovery in the early phase of septic shock in piglets.

We have developed an animal model of group B beta Streptococcal sepsis especially conducive to observation of hemodynamic sequelae of the early phases of septic shock. In piglets (N = 7), direct continuous measurements were made of aortic pressure (AOP), left atrial pressure (LAP), central venous pressure (CVP), mesenteric artery blood flow (QMES), and pulmonary artery blood flow, equivalent to cardiac output (CO). Systemic vascular resistance (SVR) and regional mesenteric vascular resistance (MVR) were calculated. Sepsis was induced by bolus intravenous administration of live, washed, type 1b group B beta Streptococcus (GBS) at approximately 1 X 10(10) organisms/kg. Early in septic shock, AOP, LAP, CO, and QMES fell to 66%, 20%, 62%, and 34% of pre-GBS levels, respectively, while SVR and MVR rose to 139% and 224% of control. The decrease in QMES and increase in MVR were significantly more extensive than the fall in CO or the rise in SVR, respectively. Subsequently, systemic hemodynamic function improved over time while regional mesenteric circulation did not. AOP and CO recovered to 86% and 88% of pre-GBS levels, respectively, and SVR returned to 105% of baseline. However, QMES remained only 48% of control, and MVR continued at 173% of pre-GBS levels. Mesenteric blood flow could not accurately be inferred from measurements of either AOP or CO during sepsis in these piglets. Relative mesenteric hypoperfusion persisted despite systemic hemodynamic recovery during this GBS sepsis protocol.