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Plasma, dextran, and other preparations, although effective as plasma expanders, cannot carry oxygen and therefore are not as useful as whole blood for management of acute hemorrhage. Blood, on the other hand, has a limited storage time and must be typed and cross-matched prior to use. Hemoglobin in solution has several unique properties which could be desirable for treating hemorrhagic shock. In addition to its osmotic activity (tool wt 68,000), hemoglobin can transport and exchange oxygen and has the advantage of not requiring typing or cross-matching (1). Despite its potential, the use of hemoglobin solutions has not progressed past the animal experimentation stage because of reports of renal damage and methemoglobin formation following its administration (2--4).Recent studies strongly suggest that disseminated intravascular coagulation may play an important role in the pathogenesis of renal damage seen in shock, intravascular hemolysis, and other situations (5-8). It has also been dearly demonstrated that hemolyzed erythrocytes can initiate blood coagulation (9, 10) and that this coagulant activity is confined to erythrocyte stroma (11). With these observations in mind, it may be postulated that renal damage, following administration of hemoglobin solution, could be due to coagulant activity of red cell stromal contaminants. A stromalfree hemoglobin solution would therefore not have deleterious effects on renal function.It is the purpose of this report to describe a method for preparation ot large quantities of a hemoglobin solution which is rdativdy free of stromal particles or lipid and has no demonstrable coagulant activity. We also wish to report results of acute and chronic experiments which show distribution, excretion, oxygen-carrying capacity, and effect on renal function of this solution when it is administered to healthy mongrel dogs. Methods and MaterialsPreparation of Hemoglobin Sobut/on.--Erythroeytes were separated from outdated, human whole blood and washed three times with 1.6% saline. The washed cells were lysed by adding

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Summary Infusion of autologous haemolysed erythrocytes (haemolysate) into dogs produces hypercoagulability frequently followed by actual intravascular coagulation as evidenced by depressed Factor V and Factor VIII activity, fall in fibrinogen and demonstrable pulmonary artery thrombi. Depression of the reticulo‐endothelial system by carbon or splenectomy produces accentuation of this phenomena. It is postulated that haemolysis can be an important contributing factor in the pathogenesis of ‘the syndromes of disseminated intravascular coagulation’. It is also suggested that the thrombotic phenomena associated with the generalized Shwartzman phenomenon, thrombotic thrombocytopenic purpura, the haemolytic uraemic syndrome, paroxysmal nocturnal haemoglobinuria, and incompatible blood transfusion reaction, may be related to intravascular haemolysis.

Two tests were used to differentiate abnormalities in release of platelet factor 3 (PF3) from quantitative deficiencies of this factor in normal subjects and in patients with renal failure. The first test was an assay which determined availability of PF3 (PF3-A time) and involved the use of a mixture of patient's plateletrich plasma (PRP) and normal platelet-poor plasma (PPP) in a fixed ratio (1: 8). The second test was similar but used "frozen and thawed" platelets to obtain a quantitative estimate of PF3 (PF3-F time). An abnormal PF3-A time was found in approximately three-quarters of 55 patients with renal insufficiency; 43 of these had chronic and 12 had acute renal failure. This abnormality was present both in patients with and without hemorrhagic manifestations, although it was slightly more common in bleeders. The PF3-F test was abnormal in approximately one-third of the bleeding patients and one-quarter of the nonbleeders. The PF3-A time returned to normal or was significantly shortened 24-48 hr after peritoneal or hemodialysis. Studies on patients who were not dialyzed showed no statistically significant correlations between the PF3-A time and either the serum urea nitrogen, creatinine, calcium, or phosphorus. Furthermore, the PF3-A time was not affected by guanidinosuccinic or guanidinoacetic acids. We therefore conclude that the demonstrable platelet abnormality in patients with uremia is produced by an unknown dialyzable material.Dr. Hrodek's present address is 2nd Pediatric

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