Windberger U, Urbanek P, Vierhapper H, Wieselthaler G, Dolezel S, Nowotny P, Trubel W, Dostal M, Vasku J, Losert U
Center for Biomedical Research, University of Vienna, Austria.
Artif Organs. 1992 Aug;16(4):392-7. doi: 10.1111/j.1525-1594.1992.tb00538.x.
Venous hypertension after total artificial heart (TAH) replacement, a common problem in humans as well as experimental animals, is thought to be related to reduced release of atrial natriuretic factor (ANF) due to atrial damage. To verify this hypothesis, we stimulated the release of ANF in 6 calves before (-7 days) and after TAH replacement (+25, +50, +80, and +100 days) by the rapid (+ = 10 min) infusion of 2 L of Ringer's solution. In normal calves (-7 days) this procedure induced a rise in plasma concentration of ANF from 18.5 +/- 12 to 31.6 +/- 12 pmol/L (p < 0.05). After TAH the ANF release continuously decreased (analysis of variance, p < 0.02). Thus, ANF increased by 9.8 +/- 9.3, 6.8 +/- 17.5, 0.4 +/- 5.2, and 0.5 +/- 3.2 pmol/L at days 25, 50, 80, and 100, respectively. The central venous pressure increased by 3.4 +/- 1.5 mm Hg (before TAH) and by 6 +/- 2.9 mm Hg (after TAH) during this procedure. A decrease in plasma concentrations of aldosterone, most likely due to extracellular volume expansion and a decrease in total protein plasma concentrations and in hematocrit due to the dilution of blood, was seen in each experiment. Necropsy demonstrated massive atrial dilatation and myocardial dystrophy with atrial fibrosis. ANF granules were present to a small extent in every calf. We conclude that rapid intravenous infusion is an adequate stimulus to release ANF in normal calves. After TAH implantation the release of ANF by high venous pressure declines although ANF granules are still present in the damaged atrial stumps. Therefore, the loss of stimulated ANF could contribute to the observed increase in venous pressure in TAH calves although other pathophysiologic mechanisms cannot be excluded.
全人工心脏(TAH)置换术后的静脉高压,在人类以及实验动物中都是一个常见问题,被认为与心房受损导致心房利钠因子(ANF)释放减少有关。为验证这一假设,我们在6头小牛TAH置换前(-7天)和置换后(+25、+50、+80和+100天)通过快速(10分钟)输注2升林格氏液来刺激ANF的释放。在正常小牛(-7天)中,该操作使血浆ANF浓度从18.5±12升高至31.6±12 pmol/L(p<0.05)。TAH置换后,ANF释放持续减少(方差分析,p<0.02)。因此,在第25、50、80和100天时,ANF分别升高了9.8±9.3、6.8±17.5、0.4±5.2和0.5±3.2 pmol/L。在此过程中,中心静脉压在TAH置换前升高了3.4±1.5 mmHg,在TAH置换后升高了6±2.9 mmHg。每次实验均可见醛固酮血浆浓度降低,这很可能是由于细胞外液量增加以及由于血液稀释导致血浆总蛋白浓度和血细胞比容降低所致。尸检显示有大量心房扩张以及伴有心房纤维化的心肌营养不良。每头小牛均有少量ANF颗粒存在。我们得出结论,快速静脉输注是刺激正常小牛释放ANF的适当刺激。TAH植入后,尽管受损心房残端仍存在ANF颗粒,但高静脉压引起的ANF释放减少。因此,尽管不能排除其他病理生理机制,但刺激后ANF的丧失可能导致TAH小牛中观察到的静脉压升高。