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Thromb Haemost 1979; 41(03): 553-566
DOI: 10.1055/s-0038-1646808
Original Articles
Schattauer GmbH Stuttgart

Thrombosis: A Study of Coagulation Parameters and Mechanisms during Allograft Rejection

Stanley R Mandel
The Departments of Surgery, Radiology and Pathology and the Dental Research Center University of North Carolina at Chapel Hill, N. C. 27514, U.S.A.
,
Richard Shermer
The Departments of Surgery, Radiology and Pathology and the Dental Research Center University of North Carolina at Chapel Hill, N. C. 27514, U.S.A.
,
Richard Clark
The Departments of Surgery, Radiology and Pathology and the Dental Research Center University of North Carolina at Chapel Hill, N. C. 27514, U.S.A.
,
Edward V Staab
The Departments of Surgery, Radiology and Pathology and the Dental Research Center University of North Carolina at Chapel Hill, N. C. 27514, U.S.A.
,
William P Webster
The Departments of Surgery, Radiology and Pathology and the Dental Research Center University of North Carolina at Chapel Hill, N. C. 27514, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 24 February 1978

Accepted 03 May 1978

Publication Date:
24 July 2018 (online)

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Summary

Thrombosis of the microvasculature has been recognized as the end product of organ rejection, but the exact biological pathway through which this occurs has not been clarified. Normal, factor VII deficient and heterozygous hemophilic (factor VIII) dogs were grouped to study the intrinsic and extrinsic clotting and platelet mechanisms during unmodified renal allograft rejection. The observed alterations of the hemostatic mechanisms are related to the changes observed in the microvasculature. Six groups of donor-recipient animals were studied: Group I - autografts (control); Group II - normal to normal allografts with bilateral nephrectomy; Group III - heterozygotes for factor VIII deficiency; Group IV - normal to normal allografts with unilateral nephrectomy; Group V - normal to factor VII deficiency without nephrectomy; and Group VI - normal to normal allografts with unilateral nephrectomy and dipyridamole. Each engrafted animal was followed pre- and posttransplantation for change in the blood clotting factors, fibrin split products, platelets, white blood cells, renal function and microvasculature. The animals with factor VII deficiency rejected in a similar fashion as the control animals. The group with impaired factor VIII synthesis and platelet function had longer survival times. These data suggest that the intrinsic clotting pathway and platelets are the primary mechanism through which thrombosis occurs secondary to immune injury.