Author(s): Di Giantomasso D, May CN, Bellomo R
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Abstract OBJECTIVES: To develop a nonlethal model of hyperdynamic sepsis, and to measure vital organ blood flows in this setting. DESIGN: Randomized crossover animal study. SETTING: Animal laboratory of university-affiliated physiology institute. SUBJECTS: Seven Merino cross sheep. INTERVENTIONS: Surgical implantation of transit-time flow probes around sagittal sinus and circumflex coronary, superior mesenteric, and left renal arteries, and of an electromagnetic flow probe around the ascending aorta. After recovery, randomization to either 6 h of observation under normal conditions (control) or 6 h of observation after the induction of hyperdynamic nonlethal sepsis (sepsis), with each animal crossing over to the other treatment after a 2-week interval. MEASUREMENTS AND MAIN RESULTS: Injection of Escherichia coli induced nonlethal hyperdynamic sepsis within 5 to 6 h with hypotension (mean arterial pressure [+/- SD], 85 +/- 7 mm Hg vs 69 +/- 8 mm Hg), increased cardiac output (4.0 +/- 0.9 L/min vs 7.2 +/- 1.2 L/min), tachycardia (60 +/- 10 beats/min vs 160 +/- 15 beats/min), fever, oliguria, and tachypnea. Compared to control animals, hyperdynamic sepsis increased renal (330 +/- 101 mL/min vs 214 +/- 75 mL/min), mesenteric (773 +/- 370 mL/min vs 516 +/- 221 mL/min), and coronary (54 +/- 24 mL/min vs 23 +/- 10 mL/min) blood flow (p < 0.05). There was no significant change in sagittal sinus flow. Despite increased coronary flow, myocardial contractility decreased (800 +/- 150 L/min/s vs 990 +/- 150 L/min/s). Despite increased mesenteric and renal blood flow, there was hyperlactatemia (0.5 +/- 0.1 mmol/L vs 1.9 +/- 0.3 mmol/L); despite increased renal blood flow, all experimental animals acquired oliguria (160 +/- 75.3 mL/2 h vs 50.2 +/- 13.1 mL/2 h) and increased serum creatinine levels (0.07 +/- 0.02 mmol/L vs 0.11 +/- 0.02 mmol/L). CONCLUSIONS: Injection of E coli induced hyperdynamic nonlethal sepsis. During such hyperdynamic sepsis, blood flow to heart, gut, and kidney was markedly increased; however, organ dysfunction developed. We speculate that global ischemia may not be the principal mechanism of vital organ dysfunction in hyperdynamic sepsis.
This article was published in Chest
and referenced in Journal of Clinical Toxicology