Search

Although phenol has long been used clinically as a neurolytic agent or as a preservative for injections, little information is available regarding its direct vascular action. We therefore studied the effects of phenol (0.1 μM-2mM) on isolated rabbit small mesenteric arteries, using isometric tension recording methods. All experiments were performed on endothelium-denuded strips. Phenol (≥10 μM) generated transsient contractions in a concentration-dependent manner in both normal Krebs and Ca(2+)-free solutions with EC50 values (concentrations that produced 50% of the maximal response) of 39.8 μM and 99.7 μM, respectively. Depletion of intracellular Ca(2+) stores by A23187 or ryanodine completely elimited the phenol-induced contractions. When caffeine (10 mM) and noradrenaline (NA, 10μM) were consecutively applied in Ca(2+)-free solution with an interval of 7 min (sufficient to prevent caffeine-induced inhibition of Ca(2+) sensitivity), caffeine eliminated the contractions induced by subsequent application of NA. In similar experiments where phenol (1 mM) and NA (10 μM) were consecutively applied in Ca(2+)-free solution, phenol significantly inhibited contractions induced by subsequent application of NA. Phenol (0.1 mM, ∼EC65), applied in the presence of either 128 mM K(+) or NA (10 μM), produced transient vasoconstrictions superimposed on both high K(+)-and NA-induced contractions, but had a lesser effect on maintenance of these contractions. The vascular responses to high K(+), NA, and caffeine after washout of phenol were not significantly different from those before application of phenol (up to 2 mM). The results suggest that phenol stimulates Ca(2+) release from intracellular Ca(2+) stores, which are sensitive to both caffine and NA in this resistance artery. The effect does not appear to reflect a toxic effect on vascular smooth muscle. It seems unlikely that phenol causes adverse hemodynamic changes because of the observed direct vascular action.

Protamine has been suggested to relax vascular smooth muscle by reducing the intracellular Ca2+ concentration ([Ca2+]i). However, there has been no direct evidence that protamine reduces the [Ca2+]i of vascular smooth muscle. We therefore studied the effects of protamine on changes in [Ca2+]i and tension induced by norepinephrine (NE) and high K+ in endothelium-denuded strips from rabbit small mesenteric artery, using fura-2-fluorometry and isometric tension recording methods. Both NE (1 μM) and high K+ (40 mM) produced a transient phasic increase, followed by a tonic increase in [Ca2+]i and tension. Protamine concentration (15–500 μg·ml−1)-dependently inhibited (P

Key words: Bell's palsy, brainstem glioma, magnetic reso- nance imaging Introduction Facial palsy of the peripheral type is generally seen in the pain clinic and is often treated with a stellate gang- lion block. The most common cause of peripheral facial nerve palsy is Bell's palsy, although its etiology remains controversial. The diagnosis of Bell's palsy is usually made by exclusion of other conditions such as herpes zoster oticus (Ramsay Hunt syndrome), trauma (including skull base fracture and surgery), otitis media, and neoplasm [1]. Isolated peripheral facial nerve palsy of neoplastic origin is uncommon. We herein describe a case of peripheral facial nerve palsy which was initially diag- nosed as Bell's palsy but was later found to be caused by an intrinsic brain stem tumor. Case report A 9-year-old boy presented to the Pediatric Depart- ment of our University Hospital in August 1990 with left facial weakness. His mother noticed the hyperemic conjunctiva and lacrimation of his left eye at the end of June. Consultation with the ophthalmologist revealed no abnormality in his left eye and the hyperemia im- proved with conservative therapy. In July, facial asym- metry became obvious. He was diagnosed as having Bell's palsy by a pediatrician in August and was referred to. our pain clinic. Address correspondence to: K. Kodama Received for publication on May 31, 1993; accepted on January 6, 1994 Upon examination, the patient had a left facial nerve palsy of the peripheral type (score of the facial paresis was 24/40), however, no other neurological deficits were seen. An audiogram failed to reveal a hearing abnormality. Although repeated stellate ganglion block was given, his facial palsy progressed slowly over a 2- month period, suggesting an etiology other than Bell's palsy. Magnetic resonance imaging (MRI) in September demonstrated a tumor in the left pons and brachium pontis extending into the left cerebellopontine angle (Fig. 1). The lesion was seen as a hypointense and hyperintense area on T1- and T2-weighted images, re- spectively. He was admitted to the Neurosurgical De- partment on September 29. The positive neurological findings on admission were Bruns' nystagmus, absence of left corneal reflex, decreased gag reflex, and mild trunkal ataxia, in addition to left facial nerve palsy. He underwent a wide suboccipital decompressive craniec- tomy, and biopsy of the tumor indicated low-grade glioma. In spite of postoperative radiation (60 Gy) and chemotherapy including Ranimustine and tumor necro- sis factor, he died due to tumor progression 17 months from the time of his initial symptom. Discussion Eighty percent of peripheral facial nerve palsy cases represent idiopathic or Bell's palsy, of which approxi- mately 20% can be demonstrated to have a specific etiology [2]. Peripheral facial nerve palsy with neoplas- tic origin is uncommon, and is estimated to be the cause in approximately 5% of all cases [3]. The diagnosis of Bell's palsy is unjustified unless an accurate history is taken along with a careful examina- tion of the ear and central nervous system (CNS). The differential diagnosis of neoplastic facial palsy is vast

175 arterial and 122 urinary samples from 20 patients admitted in ICU for organ system failure (OSF) were analysed. Besides arterial blood gases and lactate, electrolyte concentrations, pH, rH2 and specific resistance (R) in blood and urine were measured. Redox potential (E) and base excess were calculated from these data. Patients were defined as having MOSF if their organ systems met failure criteria during their ICU stay. Data were classified with corresponding number of OSF developed in the patients when samples were obtained. Acid-base balance or base excess alone could not be used to predict the severity of illness as assessed by increasing number of organ system failures. Significant elevations in blood lactate concentrations were observed only in patients with four, five or six OSF. A lack of correlation between blood lactate and severity of OSF indicates that blood lactate is not valid as a guide to ultimate outcome of the patients. Arterial redox potentials progressively decreased with increasing number of OSF, therefore, it can be stated that the serial measurements of arterial redox potential are useful in assessing the patient's status or predicting their ultimate outcome.