Left ventricular end-diastolic pressure-volume relationship in septic rats with open thorax.
To estimate changes in compliance, we evaluated the effects of sepsis on the end-diastolic pressure-volume relationship (EDPVR) in the left ventricle of rats that had undergone an open thorax procedure. Sepsis was induced in male Wistar Hannover rats (n = 7; 240 to 270 g) by intraperitoneal administration of a slurry of cecal contents; control rats (n = 7) were given 5% dextrose only. On the third day after induction of sepsis, left ventricular (LV) pressure and LV dimensions were recorded simultaneously in animals of both groups. Using a micromanometer and ultrasonic crystals, measurements were obtained at baseline and during the increase of afterload. Blood samples were taken for determination of complete blood count, white blood cell differential count, and lactate concentration, and for bacteriologic examination. Septic rats lost weight, and developed changes in body temperature, ascites, and abscesses in the abdominal and thoracic cavities, gram-negative bacteremia, and increase in heart rate. On the third day after induction of sepsis, LV EDPVR decreased, compared with that in the control rats (regression coefficients: control group, 8.41 to 23.95; sepsis group, 3.94 to 7.92). Myocardial compliance in the left ventricle increased on the third day of sepsis in the open-thorax rat model, as evidenced by the downward shift of LV EDPVR in rats with sepsis, compared with controls.
Cesar
Simona
S
University of Ljubljana, School of Medicine, Institute of Physiology, Zaloska 4, 1105 Ljubljana, Slovenia.
Potocnik
Nejka
N
Stare
Vito
V
D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D006339:Heart Rate; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications / Q000503:physiopathology*; D013908:Thoracotomy; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology*