Cholecystectomy of a patient with Churg-Strauss syndrome: A case report / 대한마취과학회지

Churg-Strauss syndrome is an allergic granulomatous angitis and the organ most commonly involved in this condition is the lung. However, this syndrome also affects the skin, cardiovascular system, kidney, peripheral nervous system and gastrointestinal system. Cardiac involvement is a rare complication but can lead to rapid-onset heart failure as the result of specific cardiomyopathy. Pericardial effusion may also occur. Acalculous cholecystitis is also a rare complication of Churg-Strauss syndrome. Here, we present a case of a patient with Churg-Strauss syndrome and severe heart failure scheduled for cholecystectomy due to acalculous cholecystitis. The patient had mild asthma symptoms, peripheral neuritis in both legs, and severe heart failure. During the preoperative period, steroids, beta2 agonists, diuretics, and antihypertensive drugs were administered. During anesthesia we attempted to prevent compromising the patient's cardiac and pulmonary functions. The surgery was completed successfully, and the patient was discharged without any complications.

The Antiallodynic Effect and the Change of the alpha2 Adrenergic Receptor Subtype mRNA Expression by Morphine Administration in a Spinal Nerve Ligation Rat Model

BACKGROUND: The neuropathic pain arising from nerve injury is difficult to treat and the therapeutic effects of opioid drugs remain debatable. Agonists acting at the alpha2 adrenergic and opioid receptors have analgesic properties and they act synergistically when co-administered in the spinal cord. The lack of subtype-selective pharmacological agents has previously impeded the synergistic effects that are mediated by the adrenergic receptor subtypes. METHODS: We created neuropathic pain model by ligating the L5 spinal nerve in Sprague-Dawley rats (n = 18). We divided the rats into three groups (n = 6 for each group), and we administered intraperitoneal morphine (1 mg/kg, 3 mg/kg, 5 mg/kg) and then we measured the mechanical allodynia with using von-Frey filaments for 8 hours. We then injected morphine (5 mg/kg) intraperitoneally, twice a day for 2 weeks. We measured the tactile and cold allodynia in the morphine group (n = 9) and the saline group (n = 9). After 2 weeks, we decapitated the rats and harvested the spinal cords at the level of lumbar enlargement. We compared the alpha2 subtype mRNA expression with that of control group (n = 6) by performing real time polymerase chain reaction (RTPCR). RESULTS: Intraperitoneal morphine reduced the neuropathic pain behavior in the dose-dependent manner. Chronic morphine administration showed an antiallodynic effect on the neuropathic pain rat model. The rats did not display tolerance or hyperalgesia. The expression of the mRNAs of the alpha2A, alpha2B, alpha2C subtypes decreased, and morphine attenuated this effect. But we could not get statistically proven results. CONCLUSIONS: Systemic administration of morphine can attenuate allodynia during both the short-term and long-term time course. Morphine has an influence on the expression of alpha2 receptor subtype mRNA. Yet we need more research to determine the precise effect of morphine on the alpha2 subtype gene expression.

Spinal alpha2 Adrenoceptor and Antiallodynic Effect by Clonidine after Chronic Administration of 4-Methylcatechol in Neuropathic Rat Pain Model / 대한통증학회지

BACKGROUND: The adrenergic nervous system in the spinal cord contributes to the development of neuropathic pain after nerve injury. Brain derived neurotrophic factor may facilitate the sympathetic change in the spinal cord and influence the state of neuropathic pain. We probed the effect of chronic repetitive administration of systemic 4-methylcatechol, which is known to be a neurotrophic factor inducer, in a spinal nerve ligation model. METHODS: We made the rat neuropathic pain model by the ligation of the L5 spinal nerve. Intraperitoneal 4-methylcatechol (10microgram/kg) or the same volume of saline wasadministrated twice daily just after the operation for 7 days. The tactile allodynia was measured by using von Frey filaments and its change was followed up from 3 days after SNL. The lumbosacral enlargement of the spinal cord was taken out and the mRNA contents of the alpha(2)-adrenoceptor subtypes were measured by real time polymerase chain reaction and this was then compared with the control groups. The antiallodynic effect of intrathecal clonidine (3, 10, 30 microgram) was evaluated and compared in the 4-methylcatechol treated rats and the control rats. RESULTS: The expression of the alpha(2A) and alpha(2C) adrenoceptor subtypes did not change after 4-methylcatechol treatment. Intrathecal clonidine showed an earlier and better effect at the highest dose (30 microgram intrathecal), but not with any other doses. CONCLUSIONS: Chronic intraperitoneal administration of 4-methylcatechol may improve the effect of intrathecal clonidine, but we could not prove the increase of alpha(2A) and alpha(2C) adrenoceptors in the spinal cord of 4-methylcatechol treated rats.