Renal modulation of electrically stimulated adrenal medullary secretion.

Renal modulation of electrically stimulated adrenal medullary secretion.
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电刺激肾上腺髓质分泌的肾脏调节。

DOI:
10.1016/0022-4804(84)90082-9
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发表时间:
1984
期刊:
The Journal of surgical research
影响因子:
--
通讯作者:
Harrison,TS
Harrison,TS
中科院分区:
--
文献类型:
--
作者:
Badder,EM;Duarte,B;Seaton,JF;Harrison,TS

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在急性肾病犬中,反射性肾上腺髓质分泌(AMS)降低可能与血浆血管紧张素水平低有关。局部(肾上腺髓质)或中枢神经系统机制负责。左内脏神经切断后评估急性双侧肾切除术对 AMS 的局部影响。两组,每组 5 只健康、禁食的杂种狗(16-20 kg),准备进行剖腹术(戊巴比妥钠静脉注射麻醉、98% O2/2% CO2、Harvard 容量呼吸机),测量血压并在股动脉切开术和左肾上腺-股静脉 T 形硅橡胶分流术中取样导管。第2组狗接受了急性双侧肾切除术。对急剧分开的远端左内脏神经进行电刺激(Grass、双极神经刺激器、10V、1毫秒延迟、10Hz、10毫秒方波)。维持肝素抗凝并监测动脉pH值。在 10 分钟交替电刺激和神经休息后,同时测定肾上腺静脉、主动脉血样和肾上腺血流量 (F)。计算肾上腺素 (E) 和去甲肾上腺素 (NE) 的 AMS [肾上腺静脉减去主动脉的 E 和 NE 血浆浓度(单同位素放射酶技术)差异乘以 F]。对结果进行分组、方差分析并进行比较(Wilcoxon 未配对秩和、Student'stest、Fischer 表、ANOVA)。主动脉 E、NE 浓度低证实缺乏全身肾上腺素能刺激。无肾组中 NE:E 的 AMS 比值较低。在第一个刺激间隔时,肾完整犬的 NE:E 为 0.28 ± 0.14 (1 SD),而无肾犬为 0.11 ± 0.04,P < 0.05。休息时,第 1 组狗的 NE:E 为 0.33 ± 0.12,第 2 组狗为 0.17 ± 0.02,P < 0.02。无肾组的血浆 NE 也较低(289 mg/L ± 126 (1 SD) 对比 612 ± 189,P= 0.033,静息)。这项研究表明,急性肾切除术后无肾病犬的血浆 NE 受到抑制,NE 的 AMS 相对受到抑制,但在电刺激分开的内脏神经期间 E 的分泌得以维持。这些结果表明,血管紧张素局部调节儿茶酚胺的 AMS 相对比例,并且与 CNS 水平上更重要的 AII 交感神经活动调节一致。
In acutely anephric dogs, depressed reflex adrenal medullary secretion (AMS) may be related to low plasma angiotensin. Either local (adrenal medulla) or central nervous system mechanisms are responsible. Local influences of acute bilateral nephrectomy on AMS were evaluated after left splanchnic nerve section. Two groups of five healthy, fasted mongrel dogs (16–20 kg) were prepared (Na pentobarbital iv anesthesia, 98% O2/2% CO2, Harvard volume ventilator) at celiotomy with blood pressure and sampling catheters per femoral arteriotomies and left adrenal-femoral venous T-shaped Silastic shunt. Group 2 dogs had acute bilateral nephrectomy. The acutely divided distal left splanchnic nerve was arranged for electrical stimulation (Grass, bipolar nerve stimulator, 10 V, 1-msec delay, 10 Hz, 10-msec square wave). Heparin anticoagulation was maintained and arterial pH monitored. Simultaneous adrenal vein, aortic blood sampling, and adrenal blood flow (F) determinations followed 10-min periods of alternating electrical stimulation and nerve rest. AMS for epinephrine (E) and norepinephrine (NE) was calculated [E and NE plasma concentration (single isotope radioenzymatic technique) differences of adrenal vein minus aorta multiplied by F]. Results were grouped, analyzed for variance, and compared (Wilcoxon unpaired rank sum, Student'sttest, Fischer's tables, ANOVA). Low aortic E, NE concentrations confirmed absent systemic adrenergic stimulation. The AMS ratio of NE:E was low in the anephric group. At the first stimulation interval NE:E was 0.28 ± 0.14 (1 SD) in renal intact dogs vs 0.11 ± 0.04 in anephric dogs,P< 0.05. At rest NE:E was 0.33 ± 0.12 in group 1 vs 0.17 ± 0.02 in group 2 dogs,P< 0.02. Plasma NE was also low in the anephric group (289 mg/liter ± 126 (1 SD) vs 612 ± 189,P= 0.033, resting). This study indicates suppressed plasma NE and relative suppression of AMS of NE in anephric dogs after acute nephrectomy but maintenance of E secretion during electrical stimulation of the divided splanchnic nerve. These results suggest that angiotensin modulates locally the relative proportions of AMS of catecholamines and are consistent with more important AII modulation of sympathetic activity at the CNS level.
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