title: Effects of ATP-magnesium chloride on the cardiopulmonary manifestations of group B streptococcal sepsis in the piglet.
abstract: Low dose ATP-MgCl2 is reported to cause selective pulmonary vasodilation during hypoxic and thromboxane mimetic-induced constriction. In addition, it has been shown to increase cardiac output and improve cellular function during circulatory shock. Based on these properties we hypothesized that ATP-MgCl2 might ameliorate the cardiopulmonary manifestations of sepsis secondary to group B streptococci (GBS). We studied 14 anesthetized, mechanically ventilated piglets who received a continuous infusion of GBS (7.5 x 10(7) colony-forming units/kg/min) and were randomly assigned to a treatment group that received a continuous infusion of ATP-MgCl2 at 0.6 mumol/kg/min or a control group that received normal saline as placebo. Comparison of the hemodynamic measurements, pulmonary mechanics, and arterial blood gases over the first 120 min of ATP-MgCl2 infusions with those of the control group revealed the following: GBS infusion caused significant increases in mean pulmonary artery pressure, pulmonary vascular resistance (PVR), mean systemic arterial blood pressure, systemic vascular pressure (SVR), and PVR/SVR ratio with decreases in cardiac output and stroke volume. ATP-MgCl2 caused significant reduction in mean pulmonary artery pressure (p < 0.001), PVR (p < 0.0001), mean systemic arterial blood pressure (p < 0.003), SVR (p < 0.01), and PVR/SVR ratio (p < 0.03) with improvement in cardiac output (p < 0.001) and stroke volume (p < 0.01). The partial pressure of arterial O2 (p < 0.04), and pH (p < 0.001) were higher and the partial pressure of arterial CO2 (p < 0.02) lower in ATP-MgCl2-treated animals. Also dynamic lung compliance was higher (p < 0.001) and pulmonary airway resistance lower (p < 0.001) in treated animals. Median survival in control animals was 153 min, whereas all treated animals survived to 240 min (p < 0.001). These data demonstrate that ATP-MgCl2 ameliorates the deleterious cardiopulmonary manifestations of GBS sepsis and results in improved survival in a young animal model.
authors.affiliation: Department of Pediatrics, University of Miami School of Medicine, Florida 33101, USA.
authors.forename: A
authors.initials: A
authors.lastname: Ali
authors.forename: R N
authors.initials: RN
authors.lastname: Goldberg
authors.forename: C
authors.initials: C
authors.lastname: Suguihara
authors.forename: J
authors.initials: J
authors.lastname: Huang
authors.forename: O
authors.initials: O
authors.lastname: Martinez
authors.forename: W
authors.initials: W
authors.lastname: Feuer
authors.forename: E
authors.initials: E
authors.lastname: Bancalari
mesh_terms: D000255:Adenosine Triphosphate / Q000627:therapeutic use*; D000818:Animals; D001785:Blood Gas Monitoring, Transcutaneous; D001794:Blood Pressure; D002302:Cardiac Output; D008170:Lung Compliance; D015636:Magnesium Chloride / Q000627:therapeutic use*; D011651:Pulmonary Artery; D018805:Sepsis / Q000188:drug therapy* / Q000503:physiopathology; D013290:Streptococcal Infections / Q000188:drug therapy* / Q000503:physiopathology; D013292:Streptococcus agalactiae; D013552:Swine; D014655:Vascular Resistance
chemical_list: D015636:Magnesium Chloride; D000255:Adenosine Triphosphate