Vital organ blood flow during hyperdynamic sepsis.
OBJECTIVE
To develop a nonlethal model of hyperdynamic sepsis, and to measure vital organ blood flows in this setting.


METHODS
Randomized crossover animal study.


METHODS
Animal laboratory of university-affiliated physiology institute.


METHODS
Seven Merino cross sheep.


METHODS
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.


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.
Di Giantomasso
David
D
Howard Florey Institute, Parkville, Melbourne, Australia.
May
Clive N
CN
Bellomo
Rinaldo
R
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000098:blood supply*; D003326:Coronary Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D004927:Escherichia coli Infections / Q000503:physiopathology*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D018056:Hemorheology; D007422:Intestines / Q000098:blood supply*; D007668:Kidney / Q000098:blood supply*; D009102:Multiple Organ Failure / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012756:Sheep; D012772:Shock, Septic / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology