Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats.
Effects of antihypertensive drugs on ultrasound production and cardiovascular responses in 15-day-old rats.
复制标题
抗高血压药物对 15 日龄大鼠超声产生和心血管反应的影响。
DOI:
10.1016/s0166-4328(01)00369-2
复制
发表时间:
2002
影响因子:
2.7
通讯作者:
Lewis,SeanJ
中科院分区:
文献类型:
--
作者:
Blumberg,MarkS;Sokoloff,Greta;Kirby,RobertF;Knoot,TriciaG;Lewis,SeanJ
When exposed to extreme cold or injected with the α2-adrenoceptor agonist, clonidine, infant rats emit ultrasonic vocalizations (USVs). Based upon the cardiovascular changes that accompany these two manipulations, especially decreased venous return, it was hypothesized that USVs are the acoustic by-product of the abdominal compression reaction (ACR), a maneuver that increases venous return. If this hypothesis is correct, then other anithypertensive drugs that decrease venous return should evoke USVs. In Experiment 1, sodium nitroprusside (SNP, 400 μg/kg), a direct-acting dilator of arteries and veins, was administered to 15-day-old rats under thermoneutral conditions while cardiac rate and ultrasound production were monitored. In Experiment 2, femoral artery pressure was monitored after SNP administration. Infants responded to SNP administration with decreased arterial pressure and tachycardia and, in addition, significantly increased ultrasound production. In Experiment 3, chlorisondamine (5 mg/kg), a ganglionic blocker that causes vasodilation and bradycardia, and hydralazine (20 mg/kg), a selective dilator of arteries, was administered to 15-day-olds. As predicted, chlorisondamine evoked ultrasound production and hydralazine did not. These results introduce SNP and chlorisondamine as only the second and third known agents capable of independently evoking USVs in thermoneutral conditions, and provide further support for the notion that ultrasound production is triggered by decreased venous return.