Tobian L
J Hypertens Suppl. 1986 Oct;4(4):S67-76.
Male stroke prone spontaneously hypertensive rats (SHRSP) were fed 4% NaCl diet containing either 0.75% normal potassium or 2.11% high-potassium, starting at 6 weeks of age. After 8 months on these diets, 40 out of 58 SHRSP on 0.75% potassium had died (69% mortality) versus two dead out of 95 on 2.11% potassium (2% mortality), a 97% reduction in mortality, P less than 0.000 01. After 20 weeks on the diet, the daytime and night-time blood pressures (BPs) of each rat were measured intra-arterially under light ether. Using these accurate BPs, we selected two groups precisely matched for BP. One matched SHRSP group (BP 182) ate the 0.75% potassium diet and 30 out of 47 rats died (64% mortality). The other matched SHRSP group (BP 182) ate the 2.11% potassium diet and two out of 35 died (6% mortality) a 91% reduction of mortality, P less than 0.0001. Seemingly, the striking reduction in mortality rate with the 2.11% high-potassium diet does not depend on a lowering of BP. High-potassium diets do not change muscle, aorta or body sodium or potassium. Dry weight of mesenteric arterioles was reduced 29% on the 2.11% potassium diet versus the 0.75% potassium diet [5.43 mg versus 7.66 mg] (P less than 0.0001) indicating a greatly reduced hypertensive hypertrophy, even though BP was equal in the two groups being compared. Aortic wall wet weight was reduced 25.5% in 36 rats on a 2.11% potassium diet versus 26 rats on a 0.75% potassium diet (36.7 mg versus 49.2 mg) P less than 0.001, even though BP was equal in the two groups being compared. In nine surviving SHRSP rats on 0.75% potassium, 13 of 36 brain hemisphere slides (four slides per rat) showed infarcts (36%). In 11 surviving SHRSP rats on 2.11% potassium, one of 44 brain slides showed infarcts (2%, a 95% reduction) P less than 0.0001. In other SHRSP rats on a 0.75% diet for 8 weeks, 18 of 25 rats (72%) had spots of brain haemorrhages whereas only two of 36 rats (5.5%) on 2.11% potassium had similar haemorrhages - a 92% reduction (P less than 0.000 01). High-potassium diets allow cerebral arteries to carry very high BPs without sustaining damage to the artery wall, thereby drastically reducing brain haemorrhages and infarcts and lowering the death rate. Moreover, hypertension does not invariably lead to artery hypertrophy, since a high-potassium diet can prevent most of it.
雄性易患中风的自发性高血压大鼠（SHRSP）从6周龄开始喂食含0.75%正常钾或2.11%高钾的4%氯化钠饮食。在这些饮食喂养8个月后，58只食用0.75%钾饮食的SHRSP中有40只死亡（死亡率69%），而95只食用2.11%钾饮食的大鼠中只有2只死亡（死亡率2%），死亡率降低了97%，P小于0.00001。饮食20周后，在轻度乙醚麻醉下通过动脉内测量每只大鼠的白天和夜间血压（BP）。利用这些精确的血压值，我们精确挑选出两组血压匹配的大鼠。一组匹配的SHRSP组（血压182）食用0.75%钾饮食，47只大鼠中有30只死亡（死亡率64%）。另一组匹配的SHRSP组（血压182）食用2.11%钾饮食，35只中有2只死亡（死亡率6%），死亡率降低了91%，P小于0.0001。显然，2.11%高钾饮食导致的死亡率显著降低并不依赖于血压降低。高钾饮食不会改变肌肉、主动脉或体内的钠或钾含量。与0.75%钾饮食相比，2.11%钾饮食使肠系膜小动脉干重降低了29%[5.43毫克对7.66毫克]（P小于0.0001），这表明即使在比较的两组大鼠血压相等的情况下，高血压性肥厚也大大减轻。与26只食用0.75%钾饮食的大鼠相比，36只食用2.11%钾饮食的大鼠主动脉壁湿重降低了25.5%（36.7毫克对49.2毫克），P小于0.001，尽管两组大鼠血压相等。在9只存活的食用0.75%钾饮食的SHRSP大鼠中，36个脑半球切片（每只大鼠4个切片）中有13个显示梗死（36%）。在11只存活的食用2.11%钾饮食的SHRSP大鼠中，44个脑切片中有1个显示梗死（2%，降低了95%），P小于0.0001。在其他食用0.75%饮食8周的SHRSP大鼠中，25只大鼠中有18只（72%）有脑溢血点，而食用2.11%钾饮食的36只大鼠中只有2只（5.5%）有类似的出血——降低了92%（P小于0.00001）。高钾饮食使脑动脉能够承受非常高的血压而不会对动脉壁造成损伤，从而大幅减少脑溢血和梗死，并降低死亡率。此外，高血压并不总是导致动脉肥厚，因为高钾饮食可以预防大部分这种情况。
