• The Korean Journal of Pharmacology
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• v.18 no.1
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• pp.11-16
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• 1982

This study was carried out in order to clarify whether the cardiovascular effect of prostaglandin(PG) $F_{2{\alpha}}$ might be centrally mediated. In unrestrained conscious rat, $PGF_{2{\alpha}}$ was administered into the lateral ventricle. The mechanism of action was also studied by observing the interaction with several adrenergic antagonists injected subcutaneously, Indomethacin was administered into lateral ventricle to investigate the role of endogenous $PGF_{2{\alpha}}$ on the central regulation of cardiovascular system. The results were as follows: 1) The intraventricular injection of $PGF_{2{\alpha}}$ produced an increase in blood pressure and heart rate. 2) The pretreatment with phenoxybenzamine (2 mg/g, s.c.) inhited pressor, but not heart rate responses to the intraventricular injection of $PGF_{2{\alpha}}$ $(2{\mu}g/kg)$. 3) The pretreatment with propranolol (1 mg/kg, s.c.) inhibited tachycardia, but not pressor responses to the intraventricular injection of $PGF_{2{\alpha}}(2{\mu}g/kg)$. 4) The intraventricular injection of indomethacin $(40{\mu}g/kg)$ could not induce significant changes in blood preesure and heart rate. 5) The result indicates that intraventricular injection of $PGF_{2{\alpha}}$ produces pressor and tachycardia responses in the unanesthetized rat, and it is mediated primarily by centrally increased sympathetic outflow. But the endogenous $PGF_{2{\alpha}}$ synthetized in the brain seems to play minor role in the direct regulation of cardiovascular system.

• Archives of Plastic Surgery
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• v.34 no.4
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• pp.531-534
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• 2007

Purpose: Plastic surgeons are responsible for the management of spinal cord injury patients with upper and lower extremity reconstruction, pressure sore, and wounds. Derailment of autonomic nervous systems caused by injury to the spinal cord may result in fatal autonomic dysreflexia. Autonomic dysreflexia is a syndrome of massive imbalance of reflex sympathetic discharge occurring in patients with spinal cord lesion above the splanchnic outflow(T6). It is characterized by a sudden onset and severe increase in blood pressure and is potentially life threatening. The other classic symptoms are headache, chest pain, sweating, and bradycardia. In order to lower the blood pressure, it is important to remove the noxious stimulus for autonomic dysreflexia. If such symptoms last for more than 15 minutes despite conservative interventions, antihypertension drugs are recommended. Methods: In this case study, we report an autonomic dysreflexia case that developed in a 45 year-old tetraplegia patient with sacral pressure sore. When he got bladder irrigation, his blood pressure went up very high and his mentality became stuporous. He was sent to ICU for his blood pressure and mental care. ICU care made his vital sign stabilized and his mentality alert. Results: After the patient underwent proper treatment like inotropic agent, he was transferred to the general ward and his pressure sore on sacral area was coveraged with gluteus maximus myocutaneous advancement flap. Conclusion: If treatment is not effective, the patients have to undergo sudden, severe hypertension, which can cause stroke or death. To provide safe and effective care, plastic surgeons should be able to recognize and treat autonomic dysreflexia.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.171-179
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• 1992

Effects of a $M_1$ receptor antagonist, pirenzepine, a $M_2$ receptor antagonist, AF-DX116, and a nicotinic receptor antagonist, mecamylamine on the pressor responses to preganglionic sympathetic nerve stimulation (PNS) and McN-A-343 and DMPP in spinal (pithed) rabbits were investigated, in order to elucidate a functional role of $M_1$, $M_2$ and nicotinic receptors in ganglionic transmission. Pirenzepine and AF-DX116 selectively inhibited the McN-A-343-induced pressor response in chlorisondamine-treated rabbit and the BCh-induced bradycardia, respectively. Electrical stimulations of preganglionic sympathetic outflow at T8 level produced increases in blood pressure. Pirenzepine $(3\;{\mu}g/kg)$ significantly inhibited the PNS-induced pressor response and the degree of inhibition was not changed by increasing the doses to $100\;{\mu}g/kg$. AF-DX116 $(100\;{\mu}g/kg)$ had no effect on the PNS-induced pressor response. Mecamylamine inhibited the PNS-induced pressor response in a dose-dependent manner. The inhibitory action of mecamylamine was significantly augmented by combined-treatment with pirenzepine $(30\;{\mu}g/kg)$ but AF-DX116 $(100\;{\mu}g/kg)$ did not affect the inhibitory action of mecamylamine. McN-A-343 and DMPP elicited pressor response in the spinal rabbit. Pirenzepine and AF-DX116 dose-dependently inhibited the McN-A-343-induced pressor response but they did not affect DMPP-induced pressor response. Mecamylamine inhibited both pressor responses induced by McN-A-343 and DMPP. These results suggest that not only nicotinic receptors but also $M_1$ receptors play a facilitatory role in ganglionic transmission but $M_2$ receptors do not contribute the transmission in spinal (pithed) rabbits.

• The Korean Journal of Pain
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• v.6 no.2
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• pp.231-236
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• 1993

Clonidine, a centrally-acting antihypertensive agent known to reduce central sympathetic outflow and modulate presynaptic transmitter's release, has shown to suppress central noradrenergic hyperactivity induced by immobilization stress in animals, by decreasing the MAC of halothane and the dose of narcotics required to prevent reflex cardiovascular response to noxious stimuli, and to have potent analgesic properties in humans. These characteristics suggest that clonidine might be a useful adjunct to the anesthetic management of patients with preexisting hypertension. Accordingly, we determined the clinical efficacy and safety on analgesia, sedation and hemodynamic stability in the perioperative period. Thirty patients(ASA physical status II-III) with a history of arterial hypertension, scheduled for elective orthopedic surgery were randomly assigned to two groups. We applied CPA-clonidine patch($6.9\;mg/cm^2$, 0.2 mg delivered daily) or placebo patch to each groups, 48 hours prior to induction of anesthesia. Antihypertensive medication was continued until the morning of the scheduled surgery. All patients received premedication of atropine and lorazepam, and induced anesthesia with thiopental and succinylcholine, and maintained with enflurane and 50% nitrous oxide, while sustaining the BP and pulse rate at acceptable range. For the relief of pain postoperatively, diclofenac and fentanyl were administered intramuscularly on demand. The results were as follows: 1) The change of hemodynamic responses in clonidine group was less compared to the placebo group. 2) Intraoperative anesthetic requirement for enflurane in clonidine group were significantly lower than placebo group. 3) Postoperative analgetic requirement in clonidine group were significantly lower than placebo group. In clonidine group, 5 cases out of 15 cases were required no analgetics, and the incidence of administration of additional fentanyl was decreased to 5 cases, comparing with 10 cases in placebo group.