Myocardial dysfunction in group B streptococcal shock

• Published in: Pediatric research Vol. 19; no. 6; pp. 511 - 513
• Main Authors: PEEVY, K. J, CHARTRAND, S. A, WISEMAN, H. J, BOERTH, R. C, OLSON, R. D
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.06.1985
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Cardiomyopathies - etiology; Cardiomyopathies - physiopathology; Disease Models, Animal; Emergency and intensive care: infection, septic shock; Hemodynamics; Intensive care medicine; Medical sciences; Prostaglandins - physiology; Rabbits; Shock, Septic - etiology; Shock, Septic - physiopathology; Streptococcal Infections - complications; Streptococcal Infections - physiopathology; Streptococcus agalactiae; Shock; Streptococcaceae; Bacteria; Cardiac performance; Experimental disease; Streptococcus B
• ISSN: 0031-3998; 1530-0447; 1530-0447
• DOI: 10.1203/00006450-198506000-00001

A rabbit model of group B Streptococcal (GBS) shock was used to determine if myocardial dysfunction contributes to GBS shock and, if so, to ascertain if prostaglandins modulate this dysfunction. The infusion of heat-killed GBS (group I) produced a dramatic decrease in the first derivative of left ventricular pressure with respect to time (LVdP/dt) from baseline values (p less than 0.05). LVdP/dt remained stable in rabbits pretreated with indomethacin (group II) and in saline-infused control rabbits (group III), and was significantly different at 30 min from LVdP/dt in group I (p less than 0.05). Values for group I mean arterial pressure, cardiac output, pulmonary vascular resistance, and heart rate and for pH and pO2 after GBS infusion were all significantly different from baseline values and from postinfusion values for groups II and III (p less than 0.05). Systemic vascular resistance and left ventricular end diastolic pressure did not change significantly in any group at any time interval. These results indicate a primary role for myocardial dysfunction in the pathogenesis of GBS shock, and suggest strongly that prostaglandins modulate GBS-induced myocardial dysfunction.