Abstract

Although the blood histamine concentration during normal pregnancy is within the normal range, the serum histaminolytic power is greatly increased (1-3). This remarkable increase in serum histaminolytic power is much more characteristic of pregnancy in man than in any other animals (4). The increase in serum histaminase activity starts as a rule during the second or third month, reaching a maximum in the fifth to the seventh month at which level it remains with modest variations until full term. It then rapidly returns within 3 or 4 days postpartum to the negligible values as found in normal nonpregnant women (2). The placenta is very rich in histaminase activity (5) and is the principal source of increased serum enzyme activity (6). Pathological changes in the placenta can, therefore, be expected to produce alterations in the normal pattern or sequence of changes in the serum histaminolytic power during pregnancy. Lindberg (6) recently showed that an intravenous infusion of histamine resulted in a lower concentration of histamine in blood when a woman was pregnant, and that administration of aminoguanidine, an inhibitor of histaminase, to pregnant women raised the concentration of histamine in blood (7). It has been suggested that deviations from the normal pattern of increase in serum histaminase activity are indicative of an abnormal pregnancy (1), and variable changes in the enzyme activity in cases of pre-eclampsia have been reported (8). Studies on urinary excretion of histamine in cases of pre-eclampsia (9) suggest that there is increased concentration of histamine in circulation under this condition. Until recently, it has been thought that serum histaminase estimations might possibly serve to indicate indirectly the histamine content of blood, and that the high histaminolytic power of blood could thus be satisfactorily correlated with the common clinical observation of remission of allergic manifestations during pregnancy. Hopes were entertained of throwing light on the significance of tissue and blood histamine via studies of this factor, in the same way that studies of acetylcholinesterase have yielded valuable information on the functions of acetylcholine in the body. The reported similarities between lesions produced by experimental poisoning with histamine in pregnant animals and the clinico-pathological features of pre-eclampsia and eclampsia, and the partly difect and partly indirect evidences that have accumulated pointing toward an excess of circulating histamine in pre-eclampsia and eclampsia together with the establishment of the fact that histamine produces definite hypertensive effects under certain conditions have stimulated our interest in the study of the problem of histamine metabolism in normal and toxaemic pregnancy, and have led to the hypothesis that histamine plays a decisive role in the aetiology of preeclampsia and eclampsia, which has, hitherto, eluded discovery despite extensive research in the past six decades. It seemed desirable from the foregone facts to investigate into the possible variations from normal of the serum histaminase and whole blood histamine contents in pre-eclampsia and eclampsia, and also to make an attempt to find out the correlation, if any, between the enzyme activity and blood histarnine concentration and the severity of the condition.

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