The response of plasma immunoreactive adrenocorticotropin, beta-endorphin/beta-lipotropin, gamma-lipotropin and cortisol to experimentally induced pain in normal subjects.
The response of plasma immunoreactive adrenocorticotropin, beta-endorphin/beta-lipotropin, gamma-lipotropin and cortisol to experimentally induced pain in normal subjects.
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血浆免疫反应性促肾上腺皮质激素、β-内啡肽/β-促脂激素、γ-促脂激素和皮质醇对正常受试者实验诱发的疼痛的反应。
DOI：
10.1042/cs0630397
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Orth,DN
中科院分区：
文献类型：
--
作者：
Güllner,HG;Nicholson,WE;Wilson,MG;Bartter,FC;Orth,DN
1.本研究检测了10名正常人在缺血性疼痛和持续等长肌肉收缩时血浆免疫反应性γ-促脂素（γLPH）、β-内啡肽/β-促脂素（βEND/βLPH）和促肾上腺皮质激素（ACTH）以及血浆皮质醇的变化.通过将血压计袖带充气至250 mmHg来产生实验性疼痛，该血压计袖带放置在“优势”手臂手肘上方，之后受试者挤压手部测力计，负载至12 kg，以2 s的间隔挤压20次。在疼痛前、疼痛后5分钟和10分钟以及释放袖带后30分钟抽血。在控制阶段，受试者被要求以最大力量的30%单独挤压手柄5分钟，这一过程可以升高血压而不会引起疼痛。1例受试者的基线肽浓度升高（30-71 pmol/l）原因不明。其他9名受试者的基线值为：ACTH，7.3 ± 1.9 pmol/l（平均值±sem）; γLPH，18.6 ± 1.0 pmol/l; βEND/βLPH，10.0 ± 1.1 pmol/l;皮质醇，599 ±55 nmol/l。血浆ACTH与血浆γLPH（r= 0.701;P<0.001）、βEND/βLPH（r = 0.970;P <0.001）和血浆皮质醇（r= 0.758;P<0.05）呈正相关.本研究表明，在正常人中，血浆内啡肽不会随着实验性缺血性疼痛而变化。血浆皮质醇升高而ACTH未伴随升高的现象无法解释，但表明肾上腺皮质水平上的某些其他药物的作用。
1. We examined the effect of ischaemic pain and sustained isometric muscle contraction on plasma immunoreactive γ-lipotropin (γLPH), β-endorphin/β-lipotropin (βEND/βLPH) and corticotropin (ACTH), which are all synthesized from a common precursor (pro-opiocortin), and plasma Cortisol in 10 normal subjects.2. Experimental pain was produced by inflation to 250 mmHg of a sphygmomanometer cuff, placed above the elbow of the ‘dominant’ arm, after which the subject squeezed a hand dynamometer, loaded to 12 kg, 20 times at 2 s intervals. Blood was drawn before, after 5 and 10 min of pain, and 30 min after release of the cuff. In a control session, the subjects were asked to squeeze the handgrip alone for 5 min at 30% of their maximum strength, a procedure which elevates the blood pressure without causing pain.3. One subject had unexplained high (30–71 pmol/l) baseline peptide concentrations. Baseline values for the nine other subjects were: ACTH, 7·3 ± 1·9 pmol/l (mean ±sem); γLPH, 18·6 ± 1·0 pmol/l; βEND/βLPH, 10·0 ±1·1 pmol/l; Cortisol, 599 ±55 nmol/l. Neither procedure significantly increased the plasma concentration of ACTH or any other peptide, whereas plasma Cortisol was significantly increased at both 5 min and 10 min. Plasma ACTH was positively correlated with plasma γLPH (r= 0·701;P< 0·001), βEND/βLPH (r= 0·970;P< 0·001) and plasma Cortisol (r= 0·758;P< 0·05).4. The present study demonstrates that, in normal man, plasma endorphins do not change with experimental ischaemic pain. The rise in plasma Cortisol without concomitant rise in ACTH is not explained, but suggests the action of some other agent at the level of the adrenal cortex.