Both the selectively bred alcohol-preferring (P) and high alcoholdrinking (HAD) rats exhibit alcohol preference, and develop tolerance to alcohol more quickly than their counterparts, the alcoholnonpreferring (NP) and low alcohol-drinking (LAD) rats, respectively. It has been shown that the P rats retain developed tolerance longer than do NP rats, and alcohol drinking increases concurrently with the development of tolerance. Although alcohol preference and tolerance are fundamental elements of alcoholism, the exact mechanisms underlying these two phenotypes in P and HAD rats are not well understood. Recent studies have suggested that arginine vasopressin (AVP) may be involved in modulation of alcohol tolerance. Accordingly, this study was designed to examine whether the AVP mRNA level in the hypothalamus differs in rats that have been selectively bred for alcohol preference and nonpreference. A =S-AVP antisense oligodeoxynucleotide probe was used for in situ hybridization to localize AVP mRNA in the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON), two major sitesfor AVP synthesis in the hypothalamus. Quantitative autoradiography demonstrated that P rats had higher levels of AVP mRNA in the W N than NP rats. Similarly, higher levels of AVP mRNA were also found in the PVN of HAD rats, compared with LAD rats. The AVP mRNA levels in the SON were similar in the alcohol-preferring and alcohol-nonpreferring rat lines. Basal plasma AVP levels were higher in NP rats than in P rats as determined by radioimmunoassay, whereas plasma AVP levels were not significantly different between HAD and LAD rats. The results suggest that increased AVP gene expression in the PVN may contribute to alcohol preference and the development of alcohol tolerance.A portant phenotypes associated with alc~holism.'~~ Rats with high alcohol preference differ from those with low alcohol preference, not only in voluntary oral alcohol intake, but also in the development and retention of alcohol t o l e r a n~e . ' .~,~~~ Although recent studies have indicated
CGS-21680 elicits coronary vasodilation comparable to that of adenosine and produces profound heterogeneity of MBF and of (201)Tl and (99m)Tc-sestamibi myocardial uptake, rendering it a promising agent for pharmacological myocardial perfusion imaging.
7. Byerly MJ, Greer RA, Evans DL. Behavioral stimulation associated with risperidone initiation. Am J Psychiatry 1995;152:1096-7. 8. Tomlinson WC. Risperidone and mania. Am J Psychiatry 1996;153:132-3. 9. Schnierow BJ, Graeber DA. Manic symptoms associated with initiation of risperidone. Am J Psychiatry 1996;153:1235-6. 10. Goodnick PJ. Risperidone treatment of refractory acute mania. J Clin Psychiatry 1995;56:431-2.Acute liver damage possibly related to sertraline and venlafaxine ingestion TO THE EDITOR: We report a case of a patient with depression taking an overdose of ≥20 tablets of sertraline and 11 tablets of cephalexin that led to transient hepatitis and complications that developed with further treatment with antidepressants.Case Report. A 27-year-old divorced white man attempted suicide by taking an overdose of sertraline and cephalexin. He had no prior history of alcohol or substance abuse. The patient was generally a healthy man with no preexisting medical conditions except depression. On admission, the patient's laboratory test results showed elevated values for aspartate aminotransferase (AST) 124 U/L (normal range 13-39) and total bilirubin 2.1 mg/dL (0.4-1.5), suggesting that the patient had sustained some liver damage. He had negative test results for hepatitis A, B, and C. The patient's prothrombin time was 11.9 sec (1-13.1) and partial thromboplastin time was 28.6 sec (22-32). A complete blood count with differentials was within normal limits and there was no elevation of eosinophils. His general toxicology screen was negative. The patient's ceruloplasmin concentrations were within normal limits. Two days after admission, he started taking venlafaxine 25 mg/d po when his total bilirubin had decreased to 0.7 mg/dL but his AST was 604 U/L and his alanine aminotransferase (ALT) was 1247 U/L (10-43).The patient initially seemed to be tolerating the medications, as his liver function test abnormalities were decreasing. Over seven days the patient's dosage of venlafaxine was increased gradually to 25 mg po tid. Five days later he began developing abdominal pain in the right upper quadrant and vomited bile six times. Venlafaxine was discontinued and the gastrointestinal service was consulted. The patient's laboratory test results showed total bilirubin 1.6 mg/dL, AST 446 U/L, and ALT 814 U/L. He then underwent esophagogastroduodenal endoscopy and an abdominal ultrasound. The patient was reported to have gastritis, esophagitis, and hepatomegaly with no signs of gallstones, dilated biliary ducts, or obstructions. After discontinuing antidepressants for five days, his liver function test abnormalities had decreased. Specifically, total bilirubin had decreased to 1.3 mg/dL, AST to 36 U/L, and ALT to 230 U/L.The patient was then restarted on sertraline 50 mg/d po. He again began to experience abdominal pain three days later. The patient's laboratory test results showed total bilirubin 2.1 mg/dL, AST 44 U/L, and ALT 180 U/L. The patient was then transferred to a medical ward, where his medications were disco...
Both the selectively bred alcohol-preferring (P) and high alcohol-drinking (HAD) rats exhibit alcohol preference, and develop tolerance to alcohol more quickly than their counterparts, the alcohol-nonpreferring (NP) and low alcohol-drinking (LAD) rats, respectively. It has been shown that the P rats retain developed tolerance longer than do NP rats, and alcohol drinking increases concurrently with the development of tolerance. Although alcohol preference and tolerance are fundamental elements of alcoholism, the exact mechanisms underlying these two phenotypes in P and HAD rats are not well understood. Recent studies have suggested that arginine vasopressin (AVP) may be involved in modulation of alcohol tolerance. Accordingly, this study was designed to examine whether the AVP mRNA level in the hypothalamus differs in rats that have been selectively bred for alcohol preference and nonpreference. A 35S-AVP antisense oligodeoxynucleotide probe was used for in situ hybridization to localize AVP mRNA in the paraventricular hypothalamic nucleus (PVN) and supraoptic nucleus (SON), two major sites for AVP synthesis in the hypothalamus. Quantitative autoradiography demonstrated that P rats had higher levels of AVP mRNA in the PVN than NP rats. Similarly, higher levels of AVP mRNA were also found in the PVN of HAD rats, compared with LAD rats. The AVP mRNA levels in the SON were similar in the alcohol-preferring and alcohol-nonpreferring rat lines. Basal plasma AVP levels were higher in NP rats than in P rats as determined by radioimmunoassay, whereas plasma AVP levels were not significantly different between HAD and LAD rats. The results suggest that increased AVP gene expression in the PVN may contribute to alcohol preference and the development of alcohol tolerance.
In patients hospitalized with unstable angina with no new ischemic electrocardiographic changes and negative cardiac enzymes, quantitative stress MPI provides powerful prognostic information that can be used in the risk stratification of these patients.
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