妊娠中毒症 : 妊娠中毒症の病態;母体血流動態の視点から(その他)
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Eclampsia and preeclampsia are major cause of maternal and neonatal deaths in many countries. Despite the ubiquity of the disease and its public health impact, neither its pathophysiology nor maternal circulatory changes have been clearly established. While some vasoconstrictors including endothelin-1, noradrenalin and angiotensin II increase and vasodilators including nitric oxid, adrenomedulin and prostacyclin decrease in maternal plasma or placenta of preeclampsia. The unbalance of these vasoactive agents may result in maternal systemic vasoconstriction and hypertension. However, no investigator has found a key agent by which the pathogenesis of preeclampsia is explained. Recently, more principle hypotheses have been documented on the anatomical basis. Preeclampsia has been reported only in human and panda. In these animals, enlarged uterus during pregnancy may oppress abdominal artery/vein or sympathetic nervous nodes, resulting in systemic vasoconstriction and endothelial damage. The long-term epidural anesthesia is reported to be available for the treatment of preeclampsia via the inhibition of sympathetic stimulation. Vasospasm of hepatic artery has been documented in HELLP syndrome. Systemic vasoconstriction and endothelial damage leads to the increase of blood pressure. It was reported that 17% of maternal deaths in the United States were due to eclampsia. However, maternal cerebral circulatory change in preeclampsia and eclampsia has not been established. There are two different hypotheses for the pathogenesis of eclampsia ; one involves cerebral hyperperfusion due to breakdown of the cerebral circulatory autoreguration, and the other, cerebral ischemia caused by cerebral arterial vasospasm. We examined Doppler values in several cerebral arteries in preeclampsia to clarify cerebral circulatory change. We demonstrated the increased intracranial blood flow volume without cerebral vasospasm just after eclamptic attack by xenon-CT and MR angiography. Ultrasonographic assessment of maternal middle cerebral artery, ophthalmic artery, internal carotid artery and vertebral artery allow us to know the circulatory change invasively. We established a new blood flow volume index as follows ; flow volume index (FVI) = mean velocity χ πrd2/4 (d : luminal diameter). The sum of FVI of the bilateral internal carotid arteries and vertebral arteries (IC-FVI) increased in severe preeclampsia. In preeclamptic woman with postpartum photophobia, IC-FVI increased at the onset of photophobia and blood pressure elevation. These findings strongly suggested the breakdown of cerebral blood flow autoreguration and consequent reversible hypertensive encephalopathy in eclampsia. Further circulatory assessments is necessary for the establishment of pathogenesis of preeclampsia and eclampsia.
- 社団法人日本産科婦人科学会の論文
- 2003-08-01
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