Streptococcus sanguis-induced platelet clotting in rabbits and hemodynamic and cardiopulmonary consequences.
By mimicking hemostatic structural domains of collagen, Streptococcus sanguis (aggregation-positive phenotype; Agg+) induces platelets to aggregate in vitro. To test the hypothesis that aggregation occurs in vivo, S. sanguis (Agg+ or Agg- suspension) was infused intravenously into rabbits. The extent of hemodynamic and cardiopulmonary changes and the fate of circulating platelets were Agg+ strain dose dependent. Within 45 to 50 s of the start of infusion, 40 x 10(8) CFU of the Agg+ strain caused increased blood pressure. Thirty seconds after infusion, other changes occurred. Intermittent electrocardiographic abnormalities (13 of 15 rabbits), ST-segment depression (10 of 15 rabbits), and preventricular contractions (7 of 15 rabbits) manifested at 3 to 7 min, with frequencies dose dependent. Respiratory rate and cardiac contractility increased during this phase. Blood catecholamine concentration, thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and ventricular axis deviation also showed dose dependency. Rabbits were unaffected by inoculation of an Agg- strain. Therefore, Agg+ S. sanguis induced platelet aggregation in vitro. Platelet clots caused hemodynamic changes, acute pulmonary hypertension, and cardiac abnormalities, including ischemia.
Meyer
M W
MW
School of Dentistry, University of Minnesota, Minneapolis, Minnesota, USA.
Gong
K
K
Herzberg
M C
MC
D000818:Animals; D016470:Bacteremia / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics; D007262:Infusions, Intravenous; D008297:Male; D009200:Myocardial Contraction; D010974:Platelet Aggregation; D011817:Rabbits; D012119:Respiration; D013290:Streptococcal Infections / Q000503:physiopathology*; D013298:Streptococcus sanguis / Q000472:pathogenicity*