Decreased α-Adrenergic Response in the Intestinal Microcirculation after “Two-Hit” Hemorrhage/Resuscitation and Bacteremia

Chronic Porcine Two-Hit Model with Hemorrhagic Shock and <i>Pseudomonas aeruginosa</i> Sepsis

“…Microvascular changes are one explanation of the 'twohit' theory of multiple organ failure [17][18][19][20]. Gelfand et al [21] support the concept that the hemorraghic shock accounts for the septic complication, since they did not find any significant bacterial translocation within 6 h of hemorrhagic shock in the pig.…”

Downregulation of Hepatic Cytochrome P-450 Isoforms and PPAR-γ: Their Role in Hepatic Injury and Proinflammatory Responses in a Double-Hit Model of Hemorrhage and Sepsis

“…It has been shown that bacterial translocation from the gut to mesenteric lymph nodes induced by hemorrhagic shock, in combination with the immunosuppressive effects of hemorrhage, can amplify the second hit [17]. Moreover, hypoxia after hemorrhage is considered to be a main reason that induces cell-mediated immune dysfunction [20]. The alteration of microvasculature after hemorrhage appears to be responsible for the abnormal response to a second stress [18,20].…”

“…In 1977, Polk and Shields reported that organ failure occurred at a higher rate in patients who developed postoperative intra-abdominal infection [16]. Based on the "two-hit" theory, a number of studies have been performed to investigate pathophysiologic and immunological responses to sepsis after hemorrhagic shock [15,[17][18][19][20][21][22]. It is proposed that the host primed by an initial stress such as hemorrhage shows an abnormal response to a second stress such as infection [19].…”

“…Moreover, hypoxia after hemorrhage is considered to be a main reason that induces cell-mediated immune dysfunction [20]. The alteration of microvasculature after hemorrhage appears to be responsible for the abnormal response to a second stress [18,20].…”

Granulocyte colony-stimulating factor prophylaxis improves survival and inflammation in a two-hit model of hemorrhage and sepsis*

“…Previous investigations have shown that a first insult, such as hemorrhage (H), primes the host for an extended response to a second hit such as infection (10). We used a fixed volume model of around 30% (16 mL/kg) blood loss (11) resulting in hemorrhagic hypotension, from which a normal healthy animal recovers independent of the volume substitution with Ringer's solution (12).…”