Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the influence of acute normovolemic hemodilution (ANH) on endocrine parameters in orthopedic surgery patients, 20 patients scheduled for total prosthetic replacement of the hip under epidural anesthesia with bupivacaine 0.5% were randomly allocated to the following groups: ANH group, (about 7.5 ml/kg body weight within 30 min) during substitution with 6% HES 200/0.5; Control group (without hemodilution). During a period before the onset of anesthesia and on the 1st day after the operation, MAP, HR, plasma concentrations of adrenaline and noradrenaline (by HPLC/ECD), and of ADH, ACTH and cortisol (by RIA) were determined at 8 points, as were glucose, lactate and free glycerol. Biometric data were comparable between the groups. MAP was significantly higher in the ANH group, and the intraoperative decrease was less pronounced. Adrenaline, ACTH, and cortisol revealed no specific influence of ANH and remained within the normal range in both groups. Noradrenaline was above the normal range in both groups and increased slightly (about 20%) during ANH. ADH was significantly higher in the control group. No specific influence of ANH was found with respect to glucose, lactate and free glycerol. In conclusion, ANH had no negative effects on the endocrine stress response during orthopedic surgery under epidural anesthesia. Sympatho-adrenergic reactions were only moderate and tolerable, even for patients with compensated cardiovascular disorders. Slight increases in endocrine parameters in the perioperative period documented adequate stress protection with epidural anesthesia.
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PMID:[Endocrine reactions during acute normovolemic hemodilution]. 216 33

The influence of nimodipine on plasma-catecholamines, ADH, ACTH and cortisol during standardized, modified neurolept-anaesthesia was investigated in 20 patients for major abdominal and thoracic surgery. The application of nimodipine led to an intra- and postoperative increase in both adrenaline and noradrenaline. No influence could be demonstrated on ADH, ACTH or cortisol. Group-levels of MAP were lower in the nimodipine-group. No statistical differences became obvious for HR, glucose, lactate and free glycerol. The increases in adrenaline and noradrenaline can be attributed to a cardiocirculatory rebound-phenomenon due to the vasodilative properties of the substance. Under the conditions of adequate fentanylanalgesia, no influence of nimodipine on ADH, ACTH or cortisol was found.
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PMID:[Effect of nimodipine on plasma catecholamines and perioperative endocrine stress parameters]. 284

Adrenocorticotropin (ACTH), cortisol, and vasopressin responses to clamped decreases in blood pressure (MAP) and to ovine corticotropin-releasing factor (CRF) infusion (20 ng X kg-1 X min-1) in intact and neurohypophysectomized (NHX) conscious dogs were examined. Mean arterial blood pressure was decreased 28 mmHg by a controlled infusion of sodium nitroprusside. Hypotension induced large increases in ACTH (peak 164 +/- 25 pg/ml), cortisol (peak 12.5 +/- 2.5 micrograms/dl), and vasopressin (peak 221 +/- 64 pg/ml) in intact (n = 7) dogs. NHX (n = 7) significantly attenuated these responses to hypotension. CRF infusion induced increases in ACTH similar in intact (n = 4) and NHX (n = 4) dogs. However, cortisol responses were significantly attenuated by NHX. Interestingly, CRF infusion induced small but significant increases in vasopressin from 3.0 +/- 1.1 to 8.1 +/- 2.0 pg/ml. We conclude that NHX attenuates ACTH and vasopressin responses to hypotension and cortisol responses to CRF-induced increases in ACTH. CRF seems to stimulate vasopressin release.
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PMID:Control of ACTH and vasopressin in neurohypophysectomized conscious dogs. 299 97

For anesthesia, ataranalgesic combinations of benzodiazepines and ketamine have been reported to be advantageous alternatives to inhalation agents or high-dose opioids. In this study, the influence of midazolam-ketamine-N2O/O2 anesthesia on the endocrine metabolic response of patients during the course of reconstructive orthopedic surgery (n = 8) was investigated. METHODS. The dosage of anesthetic agents was calculated according to body weight. Thus, the amount of ketamine given in young adults (mean age = 24.1 years) was 30 micrograms/kg per minute. Pre-, intra-, and postoperatively, each of following hormones was measured by either radioimmunoassay or radioenzyme-linked assay: ACTH, aldosterone, cortisol, 17-dehydroepiandrosterone (17-DHEA), prolactin, insulin, T3, T4, thyroxine-binding globulin (TGB), epinephrine, norepinephrine, and dopamine. Additionally, the metabolites glucose, lactate, and free glycerin were measured perioperatively. RESULTS and CONCLUSION. The circulation remained relatively stable under midazolam-ketamine-N2O/O2 anesthesia (MAP +23%; HR +17%). ACTH secretion and prolactin secretion showed a significant rise (p less than 0.01) even before skin incision (Figs. 1, 3). A significant rise in cortisol levels occurred intraoperatively (+80%; p less than 0.01). Secretion of aldosterone (+246%; p less than 0.05) and 17-DHEA (+49%; p less than 0.05) essentially followed the secretory profile of cortisol, while insulin secretion did not rise significantly under acute surgical stress (Fig. 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Combined midazolam-ketamine anesthesia in traumatologic interventions. Patterns of endocrine reactions]. 340 94

In urethane-anesthetized rats, removal of about 50% of the total blood volume over a period of 25-30 min caused hypovolemic shock, with extreme hypotension (MAP = 18-25 mm Hg and death of all animals within 22 +/- 5 min. The i.v. injection of ACTH-(1-24) in the dose range of 40-160 micrograms/kg induced a sustained, dose-dependent, and, at the highest dose used, an almost complete recovery of blood pressure, and 100% survival, at least for 2 h after treatment. The effect of ACTH-(1-24) was completely prevented by reserpine (5 mg/kg) and clonidine (0.1 mg/kg), significantly reduced by prazosin (0.1 mg/kg), dibenamine (15 mg/kg) and i.v. yohimbine (1 mg/kg) and unaffected by i.c.v. yohimbine (0.2 mg/kg) and i.v. practolol (15 mg/kg). These data suggest that the effect of ACTH-(1-24) in hypovolemic shock depends on the functional integrity of the sympathetic nervous system and is mediated through an activation of peripheral alpha-adrenoceptors.
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PMID:Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats. 341 92

Based upon preliminary observations that tumor response to MPA was correlated to cortisol suppression 42 patients were treated with MPA at different dose levels. 1500 mg MPA p.o. almost completely suppressed endogenous cortisol production in 23 out of 23 patients. Consequently, 51 patients with advanced stage metastatic breast cancer were treated with Medroxyprogesteroneacetate (HD-MAP) at a dosage of 1500 mg p.o. daily or 500 mg i.m. on 5 days per week. There were 5 complete and 7 partical remissions, 23 patients with no change and 10 with progressive disease. 7 patients were not evaluable. Clinical results correlated to plasma cortisol and prolactin blood levels bot not to LH, FSH, TSH, TBI, T3, T4, ACTH and aldosterone measurements. There was no patient with relapse and suppressed cortisol or normal prolactin measurements. The development of pituituary resistance to MPA is suggested. HD-MPA was equally effective in estrogen and/or progesterone receptor positive as in receptor negative patients. It is proposed that cortisol and prolactin determinations are useful to monitor for effective MPA treatment and the early detection of MPA resistance.
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PMID:[High dose medroxyprogesteroneacetate in metastasizing breast cancer: correlations between course of the disease and hormone profiles]. 622 46

One of the central effects of MAP is the intrinsic glucocorticoid activity. In the therapy of metastatic breast cancer with high dose MAP the cortisol like effect could be shown even in long term treatment. The cortisol like activity of MAP leads via the suppression of ACTH to a decrease of endogenous cortisol secretion. This cortisol like activity of MAP is sufficient to replace the obligate cortisol substitution in the therapy of metastatic breast cancer with aminoglutethimide. Thus within the therapy of metastatic breast cancer the combination of two endocrine acting drugs is possible.
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PMID:[Medroxyprogesterone acetate as glucocorticoid in combination with aminoglutethimide in the treatment of metastatic breast cancer]. 629 Sep 55

Effects of the GABAergic drug diazepam (0.15 mg kg-1, i.v.) on cardiovascular and endocrine responses to 50 degrees head-up tilt were evaluated in seven men. During the initial phase of tilt (normotensive phase), increases in heart rate (HR) and total peripheral resistance (TPR) and decreases in cardiac output were unaffected by diazepam. Also the associated increase in plasma noradrenaline did not change, while response in plasma ACTH was diminished and in plasma cortisol abolished by diazepam (F(1,10) = 6.45; P < 0.03). After 42 +/- 4 min of sustained tilt with saline (control) and 47 +/- 6 min (n.s.) after diazepam, presyncopal symptoms appeared (hypotensive phase) associated with decreases in HR, MAP, and TPR (P < 0.01). This episode induced a 2-3-fold increase in plasma ACTH, beta-endorphin, prolactin, cortisol (< 0.01), and a moderate increase in plasma adrenaline (P < 0.05). Diazepam did not significantly change cardiovascular and endocrine responses to the hypotensive phase of tilt. Results indicate that diazepam attenuates the cortisol part of pituitary-adrenal responses to moderate, but not to severe, central hypovolaemia in humans with no effect on cardiovascular tolerance.
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PMID:Effect of diazepam on endocrine and cardiovascular responses to head-up tilt in humans. 835 26

In humans, the head-up tilted position results in central hypovolaemia which mimicks haemorrhage and is associated with cardiovascular changes that can be divided into two stages. 1) One stage with increase in HR and vascular resistance and a slight increase in MAP. 2) Another stage with decrease in HR, vascular resistance and MAP and appearance of presyncopal symptoms (hypovolaemic shock). The first stage is "sympathoexcitatory" as plasma NA originating from postganglionic vasoconstrictory sympathetic neurons increase. Limb vascular resistance contributes to the increase in TPR at this time. The second stage is "sympathoinhibitory" in nature as plasma NA slightly decreases, or remains unchanged, while plasma A, originating from the adrenal medulla, raises. This pattern is a reflection of a differentiated sympathetic response as an increase in the activity of the nerves innervating the adrenals and decrease in renal sympathetic nerves has been reported by others. There is a decrease in limb as well as total vascular resistance. The secretion of potent vasoactive peptides may contribute to the circulatory changes taken place during head-up tilt. The head-up tilted position is associated with central hypovolaemia which is reliably monitored by electrical impedance. There is a close relation between the increase in thoracic electrical impedance and the decrease in plasma ANP which is regulated by atrial stretch. Also, from recording of technetium labeled red blood cells and measurements of haematocrite the decrease in CBV is reflected by thoracic electrical impedance. In contrast, CVP reflects changes in CBV during the initial head-up tilt only, whereafter CVP usually is unchanged or may even increase. After the initial head-up tilt the decrease in the CBV is caused by further reduction in plasma volume as shown by increase in haematocrite and unchanged distribution of labeled red blood cells. This mechanism is reflected by application of regional electrical impedance measurements at a low and high frequency current. The low frequency current, passing extracellular fluid only, changing more than the high frequency current that passes extra as well as intracellular fluid. Central hypovolaemia was found to stimulate the pituitary-adrenal axis, and the development of hypotension strongly increases plasma ACTH, beta-END, cortisol and PRL. Blocking histaminergic receptors did not change the pituitary-adrenal response to central hypovolaemia, while the sympathoadrenal response was affected by histaminergic receptor blockade. The H2-receptor antagonist cimetidine inhibited plasma A, while the H1-receptor antagonist mepyramine attenuated plasma NA and reduced cardiovascular tolerance, and also induced some sedation. A possible effect of sedation and anxiolysis was investigated by administration of the GABAergic drug diazepam. This drug did not change the cardiovascular response to head-up tilt, but reduced the increase in plasma cortisol. This indicates that the appearance of presyncopal symptoms is not related to "stress" but associated with the cardiovascular effects of central hypovolaemia. Another endogenous substance, serotonin (5-HT), may be also involved in cardiovascular as well as endocrine regulation. We investigated the effect of blocking three main receptors on the development and effects of hypovolaemic shock. Methysergide (5-Ht1+2-receptor antagonist) attenuated plasma NA, beta-END, PRL and PRA during tilt with a slight reduction of cardiovascular tolerance. The 5-HT2-receptor antagonist ketanserin reduced cardiovascular tolerance without significant effects on the hormonal responses. The 5-HT3-receptor antagonist ondansetron inhibited the plasma CGRP and adrenalin response to central hypovolaemia without influencing cardiovascular tolerance. It is concluded that the head-up tilted model in humans can be applied to study cardiovascular and endocrine mechanisms until the development of hypovolaemic shock.(ABSTRACT TRUNCATED)
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PMID:Neuroendocrine mechanisms during reversible hypovolaemic shock in humans with emphasis on the histaminergic and serotonergic system. 880 74

To determine whether the immune Fab fragment of digoxin antibody (digibind) attenuates established corticotropin (ACTH) hypertension, rats were given ACTH sham control (0.1 mL normal saline, twice daily, subcutaneously, n = 18) or ACTH treatment (2.5 microg/kg in 0.1 mL normal saline, twice daily, subcutaneously; n = 27) for 10 days. Acute hemodynamic effects of digibind (30 mg/kg, intravenous bolus injection) were examined after 10 days of sham control or ACTH treatment. Rats were divided into 7 groups: digibind (30 mg/kg, in 1 mL 0.9% NaCl intravenous bolus injection) plus sham (n = 6) or ACTH (n = 8), sham digibind (1 mL 0.9% NaCl intravenous bolus) plus ACTH (n = 7), digibind vehicle (sorbitol 1.8 mg in 1 mL 0.9% NaCl, intravenous bolus) plus sham (n = 6), preimmune sheep IgG (30 mg/kg in 1 mL 0.9% NaCl intravenous bolus) plus sham (n = 6) or ACTH (n = 6) and preimmune sheep IgG (Fab)2 fragment (30 mg/kg in 1 mL 0.9% NaCl intravenous bolus) plus ACTH (n = 6). ACTH increased systolic blood pressure (SBP) from 118 +/- 2 to 132 +/- 3 mm Hg on treatment day 10. BP was unchanged in sham treated rats. The acute administration of digibind decreased MAP (-14 +/- 3 mm Hg, P <.001) in ACTH hypertensive rats, but not in ACTH sham control normotensive rats (+2 +/- 3 mm Hg). Blood pressure reached a minimum after 14 +/- 3 min and the effect lasted more than 30 min. No significant change of blood pressure was found in ACTH treated rats receiving sham (0.9% NaCl) digibind injection (+2 +/- 2 mm Hg). However, both preimmune sheep IgG and IgG (Fab)2 fragment caused a decrease of blood pressure in both sham or ACTH treated rats. Although these data that digibind decreases BP in ACTH but not sham treated rats are consistent with the notion that digitalis-like substances may play a role in ACTH induced hypertension, the evidence that both preimmune sheep IgG and IgG (Fab)2 fragments also decreased blood pressure in rats suggests caution in interpretation of studies that employ digibind preparations.
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PMID:Hemodynamic effects of the Fab fragment of digoxin antibody (digibind) in corticotropin (ACTH)-induced hypertension. 905 91


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