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化合物48/80诱导的大鼠低血容量症中的镇痛作用及血浆β-内啡肽样免疫活性

Analgesia and plasma beta-endorphin-like immunoactivity in compound 48/80-induced hypovolemia of the rats.

作者信息

Izumi H, Hayashi S, Karita K

机构信息

Department of Physiology, Tohoku University School of Dentistry, Sendai, Japan.

出版信息

Life Sci. 1988;42(16):1529-35. doi: 10.1016/0024-3205(88)90010-0.

DOI:10.1016/0024-3205(88)90010-0
PMID:2965294
Abstract

The effects of subcutaneous (s.c.) administration of compound 48/80 (a well known histamine liberator) on latency to thermoalgesic stimulus, hematocrit (Hct) and plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in male rats. The s.c. administration of compound 48/80 in doses ranging from 0.5 to 5.0 mg/kg into the rats produced significant analgesia in the hot plate test and increased Hct in a dose-dependent manner. Concomitant variation was observed between the analgesia and the increase of Hct. This analgesic effect, but not the increase of Hct, was diminished by pretreatment with the opiate receptor antagonist, naloxone (5 mg/kg, s.c.). A significant increase of plasma beta-END-LI was observed by s.c. injection of compound 48/80. Together with a previous finding that compound 48/80 induced-hypovolemia increases the renin release from kidney and then causes water intake in the rats, it is suggested that s.c. administration of compound 48/80 induced analgesia mediated through stimulation of an opioid system, may be closely related to stimulation of the renin-angiotensin system.

摘要

在雄性大鼠中,研究了皮下注射化合物48/80(一种著名的组胺释放剂)对热痛觉刺激潜伏期、血细胞比容(Hct)以及β-内啡肽样免疫反应性(β-END-LI)血浆水平的影响。给大鼠皮下注射剂量范围为0.5至5.0毫克/千克的化合物48/80,在热板试验中产生了显著的镇痛作用,并以剂量依赖的方式增加了Hct。在镇痛作用和Hct增加之间观察到了伴随变化。用阿片受体拮抗剂纳洛酮(5毫克/千克,皮下注射)预处理可减弱这种镇痛作用,但不会减弱Hct的增加。皮下注射化合物48/80后,观察到血浆β-END-LI显著增加。结合之前的一项发现,即化合物48/80诱导的血容量减少会增加大鼠肾脏中的肾素释放,进而导致大鼠饮水,提示皮下注射化合物48/80诱导的通过刺激阿片系统介导的镇痛作用,可能与肾素-血管紧张素系统的刺激密切相关。

相似文献

1
Analgesia and plasma beta-endorphin-like immunoactivity in compound 48/80-induced hypovolemia of the rats.化合物48/80诱导的大鼠低血容量症中的镇痛作用及血浆β-内啡肽样免疫活性
Life Sci. 1988;42(16):1529-35. doi: 10.1016/0024-3205(88)90010-0.
2
The role of renin-angiotensin system in compound 48/80-induced analgesia in rats.肾素-血管紧张素系统在化合物48/80诱导的大鼠镇痛中的作用。
Gen Pharmacol. 1989;20(4):475-8. doi: 10.1016/0306-3623(89)90198-5.
3
Participation of opioid peptide (beta-endorphin) and norepinephrine in the control of compound 48/80-induced hypovolemic thirst in the rats.阿片肽(β-内啡肽)和去甲肾上腺素参与对大鼠中化合物48/80诱导的低血容量性口渴的控制。
Gen Pharmacol. 1991;22(5):825-9. doi: 10.1016/0306-3623(91)90214-q.
4
Increase of plasma renin activity after subcutaneous application of compound 48/80 in the rat.大鼠皮下注射复合48/80后血浆肾素活性的增加。
Eur J Pharmacol. 1985 Feb 26;109(2):249-56. doi: 10.1016/0014-2999(85)90426-1.
5
Different effects of compound 48/80 and histamine on plasma renin activity.化合物48/80和组胺对血浆肾素活性的不同影响。
Eur J Pharmacol. 1983 Jul 22;91(2-3):295-9. doi: 10.1016/0014-2999(83)90482-x.
6
The role of the renin-angiotensin system in compound 48/80-induced thirst in rats.肾素-血管紧张素系统在化合物48/80诱导的大鼠口渴中的作用。
Eur J Pharmacol. 1986 Nov 4;130(3):279-86. doi: 10.1016/0014-2999(86)90279-7.
7
Sexual behavior induces naloxone-reversible hypoalgesia in male rats.性行为可诱导雄性大鼠产生纳洛酮可逆性痛觉减退。
Neurosci Lett. 1987 Oct 16;81(1-2):151-4. doi: 10.1016/0304-3940(87)90356-9.
8
Plasma beta-endorphin and cortisol levels in morphine-tolerant rats and in naloxone-induced withdrawal.吗啡耐受大鼠及纳洛酮诱发戒断时血浆β-内啡肽和皮质醇水平
Eur J Pharmacol. 1990 Jun 21;182(1):117-23. doi: 10.1016/0014-2999(90)90499-v.
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Evidence for the involvement of cerebral renin-angiotensin system (RAS) in stress analgesia.脑肾素-血管紧张素系统(RAS)参与应激镇痛的证据。
Pain. 1986 Nov;27(2):237-245. doi: 10.1016/0304-3959(86)90214-9.
10
Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma.麻醉剂对大鼠血浆中β-内啡肽免疫反应性释放的影响。
Life Sci. 1991;48(14):1371-7. doi: 10.1016/0024-3205(91)90433-c.