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THE concept that the deleterious effects of maternal hypertension on the foetus are due to changes in the maternal vessels supplying the placenta has always been attractive. Its attractiveness was enhanced when Young described areas of infarction in the placentae of eclamptic women, and when Browne and Veal1 (1953) demonstrated that the blood flow in the maternal intervillous space was markedly reduced in the presence of maternal hypertension, whatever its cause. This observation was confirmed by Dixon, Browne and Davey (1963) and in a less direct fashion by Morris, Osborn and Wright (1955).The examination of the spiral arteries in pregnancy associated with hypertension has not been easy because of two factors. The first was the difficulty of obtaining suitable material and the second the occurrence in the same spiral arteries of extensive morphological changes due to pregnancy itself. We have discussed both these problems in the previous paper in this issue (Brosens, Robertson and Dixon, 1967).As early as 1903 Seitz presented a remarkable study of two uteri obtained with the placentae in situ from patients who had died from eclampsia. In the vessels directly underlying an infarcted area of the placenta he observed an arterial lesion consisting of a " small cell " infiltration around the vessel, a concentric narrowing of the lumen, thrombosis of the lumen by a uniform, homogeneous sometimes fibrillar substance, and in the wall of the artery cells that he thought were similar to decidual cells. Unfortunately the lack of photomicrographs makes it impossible to decide the exact nature of the lesion Seitz was describing, but it seems highly probable that he was seeing a pathological response to hypertension superimposed on the physiological response of the vessels to pregnancy. Williams (1915) examined the uteri obtained by Caesarean hysterectomy from two patients with abruptio placentae, one of whom had associated pre-eclampsia.

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