Changes in myocardial blood flow rates during hyperdynamic sepsis with induced changes in arterial perfusing pressures and metabolic need.
OBJECTIVE
To determine whether hyperdynamic sepsis is associated with dysregulation in the control of myocardial blood flow rates unrelated to hypotension or the use of anesthetic agents.


METHODS
Prospective, nonrandomized, controlled trial.


METHODS
Experimental laboratory.


METHODS
Fifteen mature male sheep (34 to 61 kg).


METHODS
Data were recorded in study subjects before and after the induction of sepsis following cecal ligation and perforation. Data were then recorded during: a) an infusion of prostaglandin E1 (PGE1), which decreased mean arterial perfusing pressure; and b) an infusion of zymosan-activated plasma, which increased mean pulmonary arterial pressures.


RESULTS
Myocardial blood flow rates were measured by the radiolabeled microsphere technique and cardiac index was measured by the thermodilution technique. Cardiac index (change delta) postcecal ligation and perforation minus baseline (+2.3 +/- 1.0 L/min/m2; p < .01) was increased in the septic study. Blood flow rate to the left ventricle was simultaneously increased, and was not further affected when the PGE1 infusion decreased the mean arterial perfusing pressures (-19 +/- 4%). During the infusion of zymosan-activated plasma, mean pulmonary arterial pressures increased (50 +/- 30%) and right ventricular blood flow was increased (zymosan minus postcecal ligation and perforation study: delta 17.8 +/- 50 mL/100 g/min; p < .01).


CONCLUSIONS
In this model of hyperdynamic sepsis, increases in blood flow to both the left and right ventricles were positively coupled to changes in respective ventricular work. From the interventional PGE1 and zymosan-activated plasma infusion studies, we found no evidence to support previous suggestions that the regulation of myocardial blood flow rates according to changes in perfusing pressure and/or metabolic oxygen need is significantly altered during hyperdynamic sepsis.
Raper
R F
RF
A.C. Burton Vascular Biology Laboratory, Victoria Hospital Research Institute, London, ON, Canada.
Sibbald
W J
WJ
Hobson
J
J
Neal
A
A
Cheung
H
H
D000527:Alprostadil / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001783:Blood Flow Velocity; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000187:drug effects; D007262:Infusions, Intravenous; D007553:Isotope Labeling; D008297:Male; D008863:Microspheres; D017202:Myocardial Ischemia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D010101:Oxygen Consumption; D010949:Plasma; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology; D012756:Sheep; D013815:Thermodilution; D016276:Ventricular Function; D015054:Zymosan
D015054:Zymosan; D000527:Alprostadil