Thromb Haemost 1984; 51(03): 362-365
DOI: 10.1055/s-0038-1661102
Original Article
Schattauer GmbH Stuttgart

Blood Changes and Enhanced Thromboxane and 6-Keto Prostaglandin F Production in Experimental Acute Plasmodium Bergei Infection in Hamsters

E M Essien
*   The Department of Haematology, University of Ibadan, Nigeria
,
J Arnout
The Center for Thrombosis and Vascular Research, Department of Medical Research, University of Leuven, Belgium
,
H Deckmyn
The Center for Thrombosis and Vascular Research, Department of Medical Research, University of Leuven, Belgium
,
J Vermylen
The Center for Thrombosis and Vascular Research, Department of Medical Research, University of Leuven, Belgium
,
M Verstraete
The Center for Thrombosis and Vascular Research, Department of Medical Research, University of Leuven, Belgium
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 12. Dezember 1982

Accepted 05. April 1984

Publikationsdatum:
19. Juli 2018 (online)

Summary

Golden hamsters inoculated intraperitoneally with Plasmodium bergei infected mouse blood regularly developed P. bergei parasitaemia. This was associated with progressive thrombocytopenia and leucocytosis as the degree of parasitaemia increased with time. When infected whole blood was stimulated with collagen, significantly enhanced thromboxane B2 (TXB2) production per platelet was seen. 6-keto prostaglandin (PG) F formation in the same system increased from the sixth infection day onwards and correlated with the relative leukocytosis. The production of 6-keto PGF by aorta rings was significantly higher during the 4-7th days postinoculation. The increase in thromboxane production however was much more important than that of 6-keto PGF and it therefore is concluded that P. bergei parasitaemia in hamsters tilts the haemostatic balance towards the platelet hyperaggregability that has also been described in P. falciparum infection in man.

 
  • References

  • 1 Knüttgen H. Knochenmarksbefunde bei malaria tertiana. Z Tropenmed Parasitol 1949; 1: 178-194
  • 2 Hill GJ, Knight V, Jeffery GM. Thrombocytopenia in vivax malaria. Lancet 1964; 1: 240-241
  • 3 Skudowitz RB, Katz J, Lurie A, Levin J, Metz J. Mechanisms of thrombocytopenia in malignant tertian malaria. Br Med J 1973; 2: 515-517
  • 4 Essien EM, Oruamabo RS. Depression of platelet count during acute falciparum malaria infection. Niger J Paediatr 1976; 3: 69-70
  • 5 Essien EM, Adekunle CO, Ebhota MI, Oruamabo RS. Effect of acute plasmodium falciparum infection on platelet count in man. Niger J Med Sei 1979; 1: 59-63
  • 6 Horstman RD, Dietrich M, Bienzle U, Rasche H. Malaria-induced thrombocytopenia. Blut 1981; 42: 157-164
  • 7 Borochovitz D, Crosley AL, Metz J. Disseminated intravascular coagulation with fatal haemorrhage in cerebral malaria. Br Med J 1970; 2: 710-712
  • 8 Srichaikul T, Puwasatien P, Karnjanajetanee J, Bokish VA. Complement changes and disseminated intravascular coagulation in plasmodium falciparum malaria. Lancet 1975; 1: 770-772
  • 9 Fajardo LF, Tallent C. Malaria parasites within human platelets. J Am Med Assoc 1974; 229: 1205-1207
  • 10 Kelton JG, Keystone J, Moore J, Denomme G, Tozman E, Glynn M, Neame PB, Gauldie J, Jensen J. Immune-mediated thrombocytopenia of malaria. J Clin Invest 1983; 71: 832-836
  • 11 Essien EM, Ebhota MI. Platelet hypersensitivity in acute malaria plasmodium falciparum infection in man. Thromb Haemostas 1981; 46: 547-549
  • 12 Ludlam CA, Moore S, Bolton AE, Pepper DS, Cash JD. The release of a human platelet-specific protein measured by a radioimmunoassay. Thromb Res 1975; 6: 543-548
  • 13 Kaplan BS, Fong JS. Platelet aggregation in haemolytic uraemic syndrome. Lancet 1980; 1: 46
  • 14 Hamberg M, Svensson J, Samuelsson B. Novel transformations of prostaglandin endoperoxides: formation of thromboxanes. Adv Prostaglandin Thromboxane Res 1976; 1: 19-27
  • 15 Moncada S, Vane JR. Pharmacology and endogenous roles of prostaglandin endoperoxides, thromboxane A2 and prostacyclin. Pharmacol Rev 1979; 30: 293-329
  • 16 Defreyn G, Deckmyn H, Vermylen J. A thromboxane synthetase inhibitor reorients endoperoxide metabolism in whole blood towards prostacyclin and prostaglandin E2 . Thromb Res 1982; 26: 389-400
  • 17 Carreras LO, Chamone DA F, Klerckx P, Vermylen J. Decreased vascular prostacyclin (PGI2) in diabetic rats. Stimulation of PGI2 release in normal and diabetic rats by the antithrombotic compound Bay g 6575 Thromb Res 1980; 19: 663-670
  • 18 Cox FE. Concomitant infections. In: Rodent Malaria. Killic-Kendrick R, Peters W. (eds) pp 309-343 Academic Press; London: 1978
  • 19 Goldstein IM, Malmsten CL, Kindahl H, Kaplan HB, Rädmark O, Samuelsson B, Weissmann G. Thromboxane generation by human peripheral blood polymorphonuclear leukocytes. J Exp Med 1978; 148: 787-792
  • 20 Gordon D, Nouri AM I, Thomas RU. Selective inhibition of thromboxane synthesis in human blood mononuclear cells and the effects on mitogen-stimulated lymphocyte proliferation. Br J Pharmacol 1981; 74: 469-475
  • 21 Salmon JA. Inhibition of arachidonic acid metabolism. In: Cardiovascular Pharmacology of the Prostaglandins. Herman AG, Vanhoutte PM, Denolin H, Goossens A. (eds) pp 7-22 Raven Press; New York: 1982
  • 22 Parry MJ, Randall MJ, Tyler HM, Myhre E, Dale J, Thaulow E. Selective inhibition of thromboxane synthetase by dazoxiben increases prostacyclin production by leukocytes in angina patients and healthy volunteers. Lancet 1982; 1: 164
  • 23 Weston MJ, Jackman N, Rudge C, Bowles J, Brady C, Bielawska C, O’Grady J. Prostacyclin in falciparum malaria. Lancet 1982; 2: 609