Rundgren M, Fyhrquist F
Acta Physiol Scand. 1978 Aug;103(4):463-71. doi: 10.1111/j.1748-1716.1978.tb06241.x.
Cerebral lesions involving most of the anterior wall of the ventricle, and the medial part of the septal region, induced a permanent loss of thirst in two goats. The ventral part of the lamina terminalis remained intact in one of the animals. Pronounced dehydration (10--13% loss of b.wt.) developed during periods (3--7 days) when water supplementation was omitted. Determinations of plasma arginine vasopressin in one of the animals revealed that the dehydration did not cause any significant increase in the secretion of antidiuretic hormone. However, the water deficit induced a considerable rise in plasma renin activity and tachycardia. If anything, the caroitid blood pressure became slightly elevated towards the end of 7 d dehydration periods. The lesions obviously inactivated a cerebral sensory mechanism controlling water balance. It may have been due mainly to destruction of juxtaventricular receptors in the anterior hypothalamic region, but perhaps also to a disruption of afferents from such receptors located posterior to this cerebral level.
涉及脑室前壁大部分和隔区内侧部分的脑损伤,导致两只山羊永久性口渴丧失。其中一只动物终板的腹侧部分保持完整。在不补充水分的时期(3 - 7天)内,出现了明显的脱水(体重减轻10 - 13%)。对其中一只动物的血浆精氨酸加压素测定显示,脱水并未导致抗利尿激素分泌显著增加。然而,缺水导致血浆肾素活性显著升高和心动过速。在7天脱水期接近尾声时,颈动脉血压甚至略有升高。这些损伤明显使控制水平衡的脑感觉机制失活。这可能主要是由于下丘脑前部区域室旁受体的破坏,但也可能是由于该脑水平后方此类受体传入纤维的中断。