• The Korean Journal of Pharmacology
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• v.28 no.1
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• pp.61-74
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• 1992

Influence of the blockade of the three major pressor systems-sympathetic nervous system (SNS), renin-angiotensin system (RAS) and vasopressin system-on the pressor responsiveness to norepinephrine (NE), angiotensin II (AII), and vasopressin (VP) as well as on basal blood pressure (BP) levels was investigated in urethane-anesthetized rabbits. To block the SNS and RAS, chlorisondamine (CS) and pirenzepine (PZ), sympathetic ganglionic blockers, and enalapril (ENAL), an inhibitor of angiotensin converting enzyme, respectively were used. And for suppressing the VP system bremazocine (BREM), a kappa opiate receptor agonist shown to suppress plasma levels of VP, was employed. Each of CS (0.4 mg/kg), ENAL (2 mg/kg), and BREM (0.25 mg/kg) produced almost same levels of steady hypotensive state. The hypotensive effect of BREM was significantly attenuated by desmopressin, a synthetic VP-like analogue, suggesting the hypotension being at least in part due to suppression of plasma levels of VP. CS, ENAL and BREM elicited further fall of the BP which had been lowered by ENAL or BREM, CS or BREM, and CS or ENAL, respectively. The hypotension produced by both CS and PZ together with either of ENAL or BREM was more marked than that produced by the three drugs other than CS. CS potentiated the pressor response not only to NE but to AII and VP. The pressor effect of AII was increased by ENAL and BREM, too. The pressor response to VP was also enhanced by BREM. Blockade of ${\alpha}-adrenergic$ receptors with phentolamine or phenoxybenzamine potentiated the pressor response to AII and that to VP. The results on basal BP levels indicate that the three major pressor systems are all participating in control of BP, but SNS has the greatest potential for supporting BP. The finding that blockade of one of the pressor systems induced enhanced pressor responsiveness to the pressor hormone of that particular system as well as to the pressor hormone(s) of the other systems(s) provides evidence for important interactions among the three major pressor systems.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.123-131
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• 1987

The possible inolvement of central opiate system in the control of cardiovascular function and in the antihypertensive action of clonidine has been examined in unanesthetized rats with shamoperated or 2-kidney, 1-clip (2K1C) renal hypertension. In both groups of rats, intraventricular clonidine $(3-30\;{\mu}g/kg)$ produced hypotension and bradycardia. Hypotensive action of clonidine was more potent in the hypertensive rats than in the normotensive sham-operated rats. Yohimbine $(30\;{\mu}g/kg,\;i.v.t.)$ inhibited the hypotension and bradycardia produced by clonidine. Naloxone ($50\;{\mu}g/kg$, i.v.t.) inhibited the action of clonidine in 2K1C hypertensive rats but not influenced in the sham-operated rats. Intraventricular morphine $(10-100\;{\mu}g/kg)$ also reduced rats. Intraventricular morphine $(10-100\;{\mu}g/kg)$ also reduced blood pressure and heart rate in both groups of rats. But these effects were not affected by yohimbine, but antagonized by naloxone ($50\;{\mu}g/kg$, i.v.t.). Chronic treatment of 2K1C rats with clonidine ($3{\times}20\;{\mu}g/kg$, p.o.,) for 14 days from 1 day after 2K1C operation) suppressed the development of hypertension and maintained the blood pressure in normal level and this errect of clonidine was abolished by naloxone (2 mg/kg, i. p.). In the 2K1C hypertensive rats, immunoreactive ${\beta}-endorphin$ content was significantly decreased, but maximum binding (Bmax) of $(^3H)-naloxone$ was significantly increased in brain of 2K1C hypertensive rats. However, Kd value was not changed. These results suggest that the opioidergic component might be involved in the antihypertensive action of clonidine only in hypertensive and that central opiate system might play important roles in pathophysiology of development and maintenance of hypertension.

• Korean Journal of Acupuncture
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• v.26 no.4
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• pp.195-209
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• 2009

Objectives : Transient inflammation has been demonstrated to alter visceral sensory function in animal models and acute mucosal inflammation may precede the manifestation of visceral hyperalgesia. Thus in this study we compared effects of herbal acupuncture of Nidus Vespae (NV) applied to the different acupoints in the acute colitis induced by trinitrobenzenesulphonic acid (TNBS) intracolonic injection in rats. Methods : In Male Sprague-Dawley rats, weighing 250 ~ 400 g, TNBS (5 mg/kg) was infused intrarectally through a silicon rubber catheter into the anus under isoflurane anaesthesia. Under general anesthesia, acupoints of LI4 (Hapkok), SI25 (Cheonchu), ST36 (Joksamni), BL25 (Daejangsu) were intramuscularly injected by NV. Expressions of cFos protein in the periaqueductal gray (PAG), locus coeruleus (LC), nucleus of solitary tract (Sol), and the 6th lumbar spinal cord (L6 s.c.) were observed at 24 hrs after TNBS induced colitis by immunohistochemistry. Results : The expression of c-Fos protein in L6 s.c., Sol, LC and PAG increased 24 hrs after TNBS injection into colorectum as compared to normal group. NV herbal acupuncture also inhibited the expression of c-Fos protein in Sol but not L6 s.c., LC, and PAG. NV to ST36 inhibited significantly the c-Fos expression in Sol and PAG. NV to ST25 inhibited the c-Fos protein expression all over the observation area. NV to BL25 showed the inhibitory effects in the areas except LC. Whether or not a role of endogenous opioids, intrathecal injection of naltrexone (30 ug / 30 ul) was applied before the 2nd herbal acupuncture treatment 24 hrs after TNBS-induced colitis in rat. Naltrexone reversed the inhibition of c-Fos protein expression in the spinal cord and brainstem under different conditions such as type of herbal acupuncture compound and choice of acupoint. Conclusions : In summary, these data show that herbal acupuncture of NV inhibits signal pathways such as spinal cord and brain stem ascending hypersensitivity of colorectum after TNBS induced colitis. This effect may be mediated by acupoints through the endogenous opioid system involving the pain modulation.

• Journal of Hospice and Palliative Care
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• v.14 no.4
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• pp.197-203
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• 2011

Purpose: Pain is the most common and influential symptom in cancer patients. Few studies concerning pain intensity in the terminally ill cancer patients have been done. This study aimed to identify factors related with more than moderate pain. Methods: This study used secondary data of 162 terminal cancer inpatients at the palliative ward of six training hospitals in Korea. Physician-assessed pain assessment was by 10 point numeric rating scale. Substantial pain was defined more than moderate intensity by the Korean National Guideline for cancer pain. The Korean version of the MD Anderson Symptom Inventory was self-administered to assess symptoms. Survival prediction was estimated by the attending physicians at the time of admission. Results: Less than six weeks of predicted survival and more than numeric rating of six for worst drowsiness in the previous 24 h were significantly related to substantial pain (P=0.012 and P=0.046, respectively). The dose of opioid analgesics was positively related to substantial pain (P=0.004). Conclusion: Factors positively related to substantial pain were less than six weeks of predicted survival and considerable drowsiness. Careful monitoring and active preparation for pain are required in terminal cancer patients having those factors.