Peuler J D, Schelper R L
Department of Medicine, University of Iowa, Iowa City.
Stroke. 1992 Apr;23(4):532-8. doi: 10.1161/01.str.23.4.532.
Repeated demonstration of an antihypertensive effect of high oral calcium in stroke-prone spontaneously hypertensive rats led us to determine whether it also protects such rats from premature mortality and stroke-related lesions.
Female stroke-prone rats (11-13 per diet) were fed high- and low-calcium (2.0% and 0.4%, respectively) diets with both high and low salt (7.0% and 0.3%, respectively) content from age 4 weeks until spontaneous death. In addition to life span, other variables measured included blood pressures, plasma chemistries, and histological characterization of stroke-related lesions.
Life span was increased from 51 +/- 4 to 68 +/- 1 weeks (p less than 0.05) by high versus low oral calcium in rats fed high-salt diets; it was further increased to greater than or equal to 82 weeks (p less than 0.05) in rats fed low-salt (+/- added calcium) diets. As seen previously, high oral calcium attenuated salt-induced hypertension but did not affect blood pressure in rats fed low-salt diets. High versus low oral calcium exerted contrasting effects (p less than 0.05) on brain lesions (hemorrhages and infarctions) in rats fed high-salt diets, decreasing lesion size (242 +/- 21 versus 712 +/- 276 microns per rat [diameters seen in histological sections]) but increasing lesion number (8.9 +/- 2.4 versus 3.4 +/- 2.2 per rat); it exerted little influence on the few brain lesions that appeared in rats fed low-salt diets.
High oral calcium may protect stroke-prone hypertensive rats from early salt-induced mortality at least partially by decreasing severity (size) of stroke-related lesions, an effect which may relate to decreased blood pressure. However, this protection may be limited by increased number (incidence) of such lesions, an effect which suggests that high oral calcium may increase the number of brain vessels susceptible to stroke-related injury independent of change in blood pressure.
多次证明高剂量口服钙对易卒中自发性高血压大鼠具有降压作用,这促使我们确定其是否还能保护此类大鼠免于过早死亡和与卒中相关的损伤。
雌性易卒中大鼠(每种饮食11 - 13只)从4周龄开始直至自然死亡,分别给予高钙和低钙(分别为2.0%和0.4%)饮食,同时设置高盐和低盐(分别为7.0%和0.3%)含量。除寿命外,测量的其他变量包括血压、血浆化学成分以及与卒中相关损伤的组织学特征。
在高盐饮食的大鼠中,高剂量口服钙与低剂量口服钙相比,寿命从51±4周增加到68±1周(p<0.05);在低盐(±添加钙)饮食的大鼠中,寿命进一步延长至≥82周(p<0.05)。如先前所见,高剂量口服钙可减轻盐诱导的高血压,但对低盐饮食大鼠的血压无影响。高剂量口服钙与低剂量口服钙对高盐饮食大鼠的脑损伤(出血和梗死)产生相反作用(p<0.05),减少损伤大小(每只大鼠[组织学切片中所见直径]为242±21对712±276微米)但增加损伤数量(每只大鼠8.9±2.4对3.4±2.2);对低盐饮食大鼠出现的少数脑损伤影响很小。
高剂量口服钙可能至少部分通过降低与卒中相关损伤的严重程度(大小)来保护易卒中高血压大鼠免于早期盐诱导的死亡,这种作用可能与血压降低有关。然而,这种保护作用可能会受到此类损伤数量(发生率)增加的限制,这表明高剂量口服钙可能会增加易受卒中相关损伤的脑血管数量,而与血压变化无关。