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The effect of alcohol on variant angina was studied in six patients who had a history of chest pain occurring with alcohol ingestion. On alcohol testing, Holter ECG monitoring was performed and a 12-lead ECG was recorded at the time of chest pain. In five, chest pain with ST elevation occurred 5.5 to 17.5 h after the ingestion of alcohol (100 to 150 ml as ethanol). These showed recurrent ST elevation on Holter ECG, most episodes being asymptomatic. Results of provocation testing were reproducible in all four patients in whom tests were repeated and ST elevation occurred in the same leads. No complications were observed. The Holter ECG revealed a higher heart rate after alcohol ingestion. The plasma level of alcohol was zero when angina occurred and plasma epinephrine, norepinephrine and serotonin were unchanged following alcohol ingestion. Alcohol ingestion may be a useful method of provoking variant angina, particularly in those who have a history of angina related to alcohol ingestion.

The effects of ethanol on Cl- uptake were studied using a cell-free subcellular preparation from brain that contains a gamma-aminobutyric acid (GABA)/barbiturate receptor-sensitive Cl- transport system. In isolated vesicles prepared from rat cerebral cortex, ethanol, at concentrations that are present during acute intoxication (20-50 mM), stimulated 36Cl- uptake in a concentration-dependent and biphasic manner. The ethanol-stimulated uptake of 36Cl- was markedly inhibited by the GABA antagonists picrotoxin and bicuculline but not by a variety of other neurotransmitter receptor antagonists. The effects of ethanol in stimulating 36Cl- uptake in isolated brain vesicles were qualitatively and quantitatively similar to that of pentobarbital. Ethanol also markedly potentiated both muscimol- and pentobarbital-stimulated 36Cl- uptake at concentrations below those that directly stimulate 36Cl- uptake. Under our incubation conditions, ethanol did not release GABA, suggesting that it interacts with the postsynaptic GABA/barbiturate receptor complex. The ability of ethanol to stimulate GABA/barbiturate receptor-mediated Cl- transport may explain many of its pharmacological properties and provides a mechanism for the common psychopharmacological actions of ethanol, barbiturates, and benzodiazepines.

The effect of high acetaldehyde (ACe) on acetylcholine (ACh) release was studied in vivo in the medial frontal cortex (mfc) of freely moving rats using brain microdialysis coupled with high performance liquid chromatography and an electrochemical detector. Ethanol (EtOH) and ACe concentrations were quantified simultaneously in the mfc of awake rats by in vivo microdialysis followed by head-space gas chromatography. Rats were treated intraperitoneally with saline, EtOH (1 and 2 g/kg) or cyanamide (CY, 50 mg/kg, a potent aldehyde dehydrogenase inhibitor) plus EtOH (1 and 2 g/kg). No significant effect on ACh levels was observed in saline groups, as compared to baseline value. The basal level of ACh in the dialysate was about 0.30 +/- 0.04 pmol/20 microl, and this value was reduced significantly in the EtOH (1 and 2 g/kg) and CY + EtOH (1 and 2 g/kg) groups for 240 min after EtOH administration. The time courses of ACh release continued to decrease significantly after EtOH administration in the CY + EtOH (1 and 2 g/kg) groups compared to the values in the saline and EtOH (1 and 2 g/kg) groups. A significant decrease in ACh release was observed from 140 to 240 min after EtOH dosing in the EtOH (1 and 2 g/kg) groups, as compared to saline groups. EtOH and ACe concentrations in the mfc were first determined at 15 min after a dose of EtOH, reached a peak at 30 min and then gradually decreased in the CY + EtOH (1 and 2 g/kg) groups. The present study suggests that both EtOH and ACe concentration in the brain can decrease in vivo ACh release in the mfc of free-moving rats, and the ACe-induced decrease in ACh levels was significantly higher than EtOH.

ABSTRACT We tested whether Sake Lees (SL) had inhibitory effects on hyperalgesia in the hindpaw under psychophysical stress conditions. Male rats were subjected to repeated forced swim stress treatments (FST) from Day −3 to Day −1. Intraperiotoneal administration of SL which contained low concentration of ethanol (SLX) was conducted after each FST. On Day 0, formalin-evoked licking behaviors and Fos responses in the lumbar spinal cord (DH) and several areas within the rostral ventromedial medulla (RVM) were quantified as nociceptive responses. FST-induced hyperalgesia in the hindpaw was prevented by repeated SL and SLX treatments. Fos expression was significantly increased in DH and some areas within the RVM under FST, which was prevented by repeated SL or SLX. These findings indicated that daily administration of SL had the potential to alleviate stress-induced hyperalgesia.

Background:Salsolinol, a neuropharmacologically active compound, is formed by the condensation of acetaldehyde (AcH) with dopamine (DA) in the brain. The aim of our study was to examine the effect of a high concentration of AcH on salsolinol formation and to compare the release of DA, serotonin (5‐HT), and salsolinol in the striatum and nucleus accumbens (NAc) in free‐moving rats.Methods:After the insertion of a microdialysis probe, male Wistar rats (250–300 g) were treated with cyanamide (CY, a potent aldehyde dehydrogenase inhibitor) + ethanol (EtOH), CY + 4‐methylpyrazole (4‐MP, a strong alcohol dehydrogenase inhibitor) + EtOH, 4‐MP + EtOH, CY, and 4‐MP. Simultaneous quantitation of DA, 5‐HT, and salsolinol in dialysates was performed by using in vivo microdialysis coupled with high‐performance liquid chromatography with an electrochemical detector and blood EtOH and AcH by using a head‐space gas chromatographic method.Results:Salsolinol was detected only in the CY + EtOH groups in both the striatum and NAc, and we also detected a high AcH concentration in the blood in those groups. A correlation was found between the dialysate levels of salsolinol and blood concentrations of AcH. The striatal levels of DA and 5‐HT were approximately two times higher, whereas salsolinol levels were approximately three times higher compared with the usual level in the NAc. No significant difference of DA and 5‐HT levels in the dialysates was observed in either the control or the other study groups.Conclusion:Our observation suggested that the brain salsolinol formation may depend on the concentrations of DA and AcH in freely moving rats, and there is no effect of a high concentration of AcH on DA and 5‐HT levels in the striatum and NAc.

The amygdaloid complex (AMY) is implicated in emotional and motivational aspects of behavior, including the formation of positive reinforcement association. AMY may also associated with brain rewarding circuitry. In the present study, the effect of ethanol (EtOH) on the release of dopamine (DA) and serotonin (5-HT) was studied in the central amygdaloid nucleus (CeAMY), and projecting excitatory afferents to the ventral tegmental area (VTA), of freely moving Wistar rats by brain microdialysis. Within 20 min of i.p. injection of EtOH (2 g/kg), the levels of DA and 5-HT in the CeAMY dialysate increased over the baseline value by 270 and 160% (N = 6-7), respectively. Addition of EtOH (25, 50 and 100 mM) to the microdialysis perfusion medium for 1 h caused a 115-150% dose-related increase in the extracellular level of DA in the CeAMY. 100 mM EtOH-induced CeAMY DA release continued to increase for 1 h after the perfusion medium was returned to normal perfusion medium. In contrast, the CeAMY 5-HT level was increased only by the addition of 100 mM EtOH for 1 h to 130% for 80 min. The stimulation of the CeAMY by EtOH through the microdialysis membrane showed delayed responses of DA and 5-HT compared with the i.p. injection of EtOH. Overall, the present findings are not sufficient to conclude whether EtOH acts directly or indirectly on the major monoamine nerve cells in the CeAMY, but the degree of acute EtOH action affected the differences in time at the peak response on EtOH-induced DA and 5-HT releases in the CeAMY via VTA.

Sedentary/inactive lifestyle leads middle-aged and older adults to metabolic syndrome and frailty. Capsinoids from nonpungent chili pepper cultivar have been reported to reduce body fat mass, promote metabolism, and improve unidentified complaints of chills. Additionally, they have an anti-inflammation effect; therefore, we hypothesized that continuous oral ingestion of capsinoids alleviates age-related inflammation in the brain and improves the physical activity (PA) in middle-aged and older adults. In our double-blind human study, 69 participants (17 male, 52 female; mean age: 74.1 ± 7.7 years; range: 52–87 years) were administered either 9 mg of capsinoids which were extracted from pepper fruit variety CH-19 Sweet (Capsicum anuum L.) (CP group), or a placebo (PL group) daily over a 3 month period. In an animal study, PA and inflammation-related mRNA expression in the brain were examined in 5-week (young) and 53-week (old) aged mice fed a diet with or without 0.3% dihydrocapsiate, a type of capsinoids, for 12 weeks. In a human study, capsinoids intake did not increase the amount of light-to-moderate PA less than 6.0 metabolic equivalents (METs) (CP: 103.0 ± 28.2 at baseline to 108.2 ± 28.3 at 12 weeks; PL: 104.6 ± 19.8 at baseline to 115.2 ± 23.6 at 12 weeks, METs × hour/week); however, in participants exhibiting an inactive lifestyle, it showed significant increase (CP: 84.5 ± 17.2 at baseline to 99.2 ± 24.9 at 12 weeks; PL: 99.7 ± 23.3 at baseline to 103.8 ± 21.9 at 12 weeks). The energy expenditure in physical activity also improved in the inactive CP group (CP: 481.2 ± 96.3 at baseline to 562.5 ± 145.5 at 12 weeks; PL: 536.8 ± 112.2 at baseline to 598.6 ± 127.6 at 12 weeks; kcal/day). In all participants, CP showed reduced waist circumference, percent body fat, and visceral fat volume; in addition, chills were eased in subjects aged 80 years and older. The older mice fed capsinoids showed increased locomotion activity, decreased inflammation, and oxidative stress in the brain. The results suggest that the continuous oral ingestion of capsinoids gains PA through anti-inflammation effect in the brain as well as reduces fat accumulation and chills in inactive and older humans.

AbstractOromandibular dystonia is a focal dystonia involving the masticatory and tongue muscles, causing difficulties in speech or mastication. We treated 13 patients with this condition by injecting diluted lidocaine and alcohol intramuscularly. This method is aimed at reducing muscle spindle afferent activity. The symptoms had been resistant to other therapies such as pharmacotherapy or dental treatment. All patients showed clinical improvement after this therapy with reduced EMG activities in the affected muscles, whereas control injection of normal saline gave no changes in EMG activities. The overall subjective improvement was 57.7 ± 25.1% (mean ± standard deviation) in a self‐rating scale. The mean response of the jaw elevator muscles (70 ± 13.1%) was significantly higher (p < 0.02, t test) than that of the depressor muscles (38 ± 28.4%). Despite the precise mechanism being unknown, this difference might be related to the smaller number of muscle spindles in the depressor than the elevator muscles. This therapy is useful for the treatment of drug‐resistant oromandibular dystonia.