Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ANAESTHETICS, ENDOCRINE SYSTEM, AND STRESS: The effects of anaesthetics on the nervous system are invariably associated with endocrine reactions, which are of great importance for the general characterization of anaesthetics or anaesthetic regimens. In this context, the endocrine stress response is mainly represented by adrenaline (A), noradrenaline (NA), antidiuretic hormone/vasopressin (ADH), adrenocorticotropic hormone (ACTH), and cortisol. PHARMACOLOGICAL PROFILE AND ANAESTHETIC ACTION OF KETAMINE: The pharmacological profile of ketamine is characterized by the term "dissociative anaesthesia." At the present time, the anaesthetic action of ketamine cannot be explained by a single mechanism. Its overall action might be due to different central and peripheral factors, and stereospecific effects are obvious. ENDOCRINE RESPONSES TO RACEMIC KETAMINE AND S(+)-KETAMINE: In contrast to stereospecific differences in the anaesthetic action of racemic ketamine and S-(+)-ketamine, the endocrine reactions to the S-(+) isomer and the racemic mixture are very similar. When S(+)-ketamine is used as the sole anaesthetic, significant activation of the sympathoadrenergic system with increases in plasma levels of A and NA can be observed. This effect is mitigated by midazolam. In combination with propofol, sympathoadrenergic responsiveness is preserved without overwhelming effects. In contrast to monoanaesthesia with S(+)-ketamine, during combination with midazolam and propofol significant increases in plasma ADH levels are observed, which might be due to suppressed sympathoadrenergic reactivity. In addition, surgical stress activates the pituitary-adrenocortical system with increases in ACTH and cortisol. Effects of midazolam and propofol on this effect are similar. SYNOPSIS AND CLINICAL ASPECTS: S-(+)-ketamine as a monoanaesthetic has significant sympathomimetic properties, which are beneficial during induction of patients in shock and patients with asthma. The combination of S-(+)-ketamine and midazolam has weaker sympathomimetic and general endocrine-stimulating properties, and can be used for analgosedation in patients with cardiovascular instability and exogenous catecholamine requirements. In combination with propofol, the sympathomimetic and general endocrine-stimulating effects of S-(+)-ketamine are less pronounced because of contrasting properties of both drugs. This combination might be useful in patients with endocrine deficits and for analgosedation, when rapid recovery is necessary and negative circulatory effects should be avoided.
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PMID:[Endocrine reactions following S-(+)-ketamine]. 916 76

To investigate the effects of carteolol, which is a nonselective beta-adrenergic agent with intrinsic sympathomimetic activity, on silent myocardial ischemia, exercise-induced myocardial ischemia, indexes of heart rate variability, and pain-modulating system, 20 patients (mean 60 +/- 9 years) with chronic stable angina underwent exercise treadmill testing and 24-hour ambulatory electrocardiographic monitoring during 2 weeks of carteolol administration (15 mg/day) in a double-blind, placebo-controlled design. Plasma levels of beta-endorphin and bradykinin and electrical pain stimulation to the skin were measured at rest and peak exercise. Indexes of heart rate variability of both time-domain and frequency-domain analysis were derived from 24-hour ambulatory electrocardiographic monitoring. Carteolol decreased maximal heart rate responses to daily activities during ambulatory monitoring and significantly reduced the median frequency and duration of silent myocardial ischemic episodes (from 1.0 to 0.0 events/24 hr and from 16 to 0 min/24 hr, respectively). Carteolol significantly decreased the rate-pressure product at rest and during exercise with improving maximal ST segment depression, suggesting amelioration of exercise-induced myocardial ischemia. Carteolol did not significantly affect plasma levels of beta-endorphin and bradykinin or pain threshold. It significantly decreased some indexes (standard deviation of all normal sinus R-R intervals in the entire 24-hour recording and standard deviation of the mean of all 5-minute segments of normal R-R intervals of a 24-hour recording) of heart rate variability. These results suggest that carteolol may reduce total myocardial ischemic burden by the reduction of cardiac oxygen demand during daily activities and exercise stress, while not affecting plasma levels of beta-endorphin, bradykinin, and pain threshold. Because carteolol tended to decrease indexes of heart rate variability, significant caution might be necessary in prescribing the beta-blocking agents with intrinsic sympathomimetic activity like carteolol to patients with potential serious arrhythmia.
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PMID:Effect of carteolol on silent myocardial ischemia, variability in heart rate, and the pain-modulating system. 939 8