Denofre-Carvalho S, Collares E F, Fernandes G A
Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP, Brasil.
Braz J Med Biol Res. 1997 Sep;30(9):1121-7. doi: 10.1590/s0100-879x1997000900011.
The effects of dorsomedial hypothalamic (DMH) nucleus lesion on body weight, plasma glucose levels, and the gastric emptying of a liquid meal were investigated in male Wistar rats (170-250 g). DMH lesions were produced stereotaxically by delivering a 2.0-mA current for 20 s through nichrome electrodes (0.3-mm tip exposure). In a second set of experiments, the DMH and the ventromedial hypothalamic (VMH) nucleus were lesioned with a 1.0-mA current for 10 s (0.1-mm tip exposure). The medial hypothalamus (MH) was also lesioned separately using a nichrome electrode (0.3-mm tip exposure) with a 2.0-mA current for 20 s. Gastric emptying was measured following the orogastric infusion of a liquid test meal consisting of physiological saline (0.9% NaCl, w/v) plus phenol red dye (6 mg/dl) as a marker. Plasma glucose levels were determined after an 18-h fast before the lesion and on the 7th and 15th postoperative day. Body weight was determined before lesioning and before sacrificing the rats. The DMH-lesioned rats showed a significantly faster (P < 0.05) gastric emptying (24.7% gastric retention, N = 11) than control (33.0% gastric retention, N = 8) and sham-lesioned (33.5% gastric retention, N = 12) rats, with a transient hypoglycemia on the 7th postoperative day which returned to normal by the 15th postoperative day. In all cases, weight gain was slower among lesioned rats. Additional experiments using a smaller current to induce lesions confirmed that DMH-lesioned rats had a faster gastric emptying (25.1% gastric retention, N = 7) than control (33.4% gastric retention, N = 17) and VMH-lesioned (34.6% gastric retention, N = 7) rats. MH lesions resulted in an even slower gastric emptying (43.7% gastric retention, N = 7) than in the latter two groups. We conclude that although DMH lesions reduce weight gain, they do not produce consistent changes in plasma glucose levels. These lesions also promote faster gastric emptying of an inert liquid meal, thus suggesting a role for the DMH in the regulation of gastric motility.
在雄性Wistar大鼠（170 - 250克）中，研究了下丘脑背内侧核（DMH）损伤对体重、血浆葡萄糖水平以及流食胃排空的影响。通过镍铬电极（尖端暴露0.3毫米）施加2.0毫安电流20秒，立体定位制造DMH损伤。在第二组实验中，使用1.0毫安电流10秒（尖端暴露0.1毫米）损伤DMH和下丘脑腹内侧核（VMH）。还使用镍铬电极（尖端暴露0.3毫米）施加2.0毫安电流20秒，单独损伤内侧下丘脑（MH）。在经口胃内注入由生理盐水（0.9% NaCl，w/v）加酚红染料（6毫克/分升）作为标记物的流食测试餐之后，测量胃排空情况。在损伤前禁食18小时后以及术后第7天和第15天测定血浆葡萄糖水平。在损伤大鼠和处死大鼠之前测定体重。与对照大鼠（胃潴留33.0%，N = 8）和假损伤大鼠（胃潴留33.5%，N = 12）相比，DMH损伤大鼠的胃排空明显更快（P < 0.05）（胃潴留24.7%，N = 11），术后第7天出现短暂低血糖，术后第15天恢复正常。在所有情况下，损伤大鼠的体重增加都较慢。使用较小电流诱导损伤的额外实验证实，与对照大鼠（胃潴留33.4%，N = 17）和VMH损伤大鼠（胃潴留34.6%，N = 7）相比，DMH损伤大鼠的胃排空更快（胃潴留25.1%，N = 7）。MH损伤导致胃排空比后两组更慢（胃潴留43.7%，N = 7）。我们得出结论，尽管DMH损伤会减少体重增加，但它们不会使血浆葡萄糖水平产生持续变化。这些损伤还促进惰性流食的胃排空更快，因此表明DMH在胃动力调节中起作用。
