Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-two adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-fentanyl-thiopentone (BAL group) or nitrous oxide-halothane (HAL group) anaesthesia. Eighteen patients in the BAL group received an initial bolus of mivacurium, either the ED25 (n = 9) or the ED50 (n = 9) (0.03 and 0.05 mg kg-1). These doses were based on the assumption that the slope of the dose-response curve during nitrous oxide-opioid anaesthesia would be approximately the same as the slope of the neuromuscular response from the first human studies with mivacurium. Twenty-seven additional patients were allocated to subgroups of nine patients to receive mivacurium 0.04, 0.08 or 0.15 mg kg-1. Twenty-seven patients in the HAL group were allocated also to subgroups of nine patients to receive mivacurium 0.03, 0.04 or 0.15 mg kg-1. During stable anaesthesia, mean endtidal halothane concentrations were maintained at 0.49 +/- 0.01%. The estimated ED50, ED75 and ED95 for BAL and HAL groups were 0.039, 0.05 and 0.073 mg kg-1 and 0.040, 0.053 and 0.081 mg kg-1, respectively. Halothane did not potentiate maximum block or time to maximum block. Halothane did affect spontaneous recovery. With the 0.15-mg kg-1 dose, time to 95% recovery was prolonged significantly in the HAL group (30.0 (SEM 1.4) min) compared with the BAL group (24.1 (1.5) min). Recovery index from 25% to 75% recovery was also prolonged significantly in the HAL group (7.0 (0.4) min) compared with the BAL group (5.4 (0.4) min). There were no significant haemodynamic changes in groups given mivacurium doses up to and including 2 x ED95 by bolus i.v. administration.
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PMID:Neuromuscular and cardiovascular effects of mivacurium chloride (BW B1090U) during nitrous oxide-fentanyl-thiopentone and nitrous oxide-halothane anaesthesia. 213 90

In an attempt to clarify the regulatory role in GH secretion of central alpha-adrenergic and dopaminergic mechanisms, the effects of iv administration of alpha 1- and alpha 2-adrenergic antagonists and dopaminergic antagonists were investigated in undisturbed conscious male rabbits. During a 6-h observation period (1030-1630 h), control animals demonstrated spontaneous pulsatile GH secretion with mean (+/- SEM) 6-h GH levels of 6.49 +/- 0.54 ng/ml (n = 16). Intravenous injection of yohimbine (YOM; an alpha 2-antagonist), chlorpromazine (CPZ), and haloperidol (HAL; dopamine and alpha-adrenergic antagonists) completely suppressed this pulsatile GH secretion (mean 6-h GH levels, 2.98 +/- 0.24, 3.48 +/- 0.24, and 2.91 +/- 0.29 ng/ml, respectively; P less than 0.001), whereas prazosin (an alpha 1-antagonist), pimozide (a selective dopamine antagonist), sulpiride, and YM-09151-2 (YM; D2-specific antagonists) failed to affect the GH secretory pattern (mean 6-h GH levels, 6.61 +/- 0.73, 6.71 +/- 0.56, 5.44 +/- 0.44, and 6.87 +/- 1.44 ng/ml, respectively). While an iv injection of 2 micrograms synthetic human GH-releasing factor-(1-44)-NH2 (hGRF) induced GH rises in prazosin-, HAL-, pimozide-, sulpiride-, and YM-treated rabbits as well as control rabbits, YOM and CPZ completely abolished these GH responses to hGRF injection. An iv injection of 10 ml antisomatostatin gamma-globulin caused a prompt and transient GH rise, followed by a sustained elevation of GH trough levels in normal control rabbits. YOM treatment completely abolished this highly oscillated GH release. However, suppression by YOM or CPZ of hGRF-induced GH rises was significantly reversed by iv administration of 10 ml antisomatostatin gamma-globulin. Therefore, the inhibitory effect of YOM and CPZ on both episodic GH release and hGRF-induced GH rises is due to the enhanced release of somatostatin, with a simultaneous suppression of endogenous GRF. On the other hand, HAL, possessing a weaker alpha-blocking action than CPZ, blunted pulsatile GH secretion, but only modestly suppressed hGRF-induced GH rises. These results suggest the following. 1) Central alpha 2-adrenergic mechanisms play a more important role in the regulation of GH secretion than alpha 1-adrenergic mechanisms in the rabbit as well as in other species. 2) The alpha 2-adrenergic blockade causes suppression of the release of hypothalamic GRF and enhanced release of endogenous somatostatin, thereby suppressing GH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alpha 2-adrenergic control of growth hormone (GH) secretion in conscious male rabbits: involvement of endogenous GH-releasing factor and somatostatin. 247 28

The effects of haloperidol on circling and spying behaviors induced by electrical stimulation of the medial prefrontal cortex (PFC) were evaluated. Male Wistar rats with an electrode implanted into the left medial PFC (B: 2.5 mm A, 0.6 mm L and 2.7 mm V) were electrically stimulated in a sequence of ten 30-sec trains separated by 30-sec intervals (60 Hz) in each session, and simultaneously observed in the open field. The animals with circling (CI) and spying (SP) behaviors were treated with intraperitoneal haloperidol (HAL ip, 5 mg/kg, N = 6) and saline (SAL ip, N = 7) or intracortical HAL (ic, 5 micrograms, N = 6) and SAL (ic, N = 9), 20 min before the session of electrical stimulation. HAL ic significantly decreased (P < 0.05) CI (mean frequency +/- SEM: 0.5 +/- 0.16) and nonsignificantly decreased SP behavior (0.6 +/- 0.17) compared to SAL ic (CI: 0.9 0.02, SP: 1 +/- 0). HAL ip full abolished these behaviors (P < 0.05) (CI: 0.02 +/- 0, SP: 1 +/- 0) compared to SAL ip (CI: 0.86 +/- 0.06, SP: 0:93 +/- 0.06). These results show that haloperidol, a dopaminergic antagonist and antipsychotic agent, interfered significantly with the expression of behaviors induced by electrical stimulation of the left medial PFC, suggesting that the induction of these behaviors may involve the dopaminergic neurotransmission.
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PMID:Effects of haloperidol on behavioral responses induced by electrical stimulation of medial prefrontal cortex. 918 Nov 8

There is a great demand of Hydroxyapatite (HA) material in Orthopaedics and Dental applications due to its similarity to human bone. However, the lack of availability and due to high import cost of this material in Malaysia, research in producing synthetic HA locally is therefore timely. The use of local resources as the raw materials for the production of HA is also desirable in reducing the overall cost of HA. In this study, two HA materials were synthesised from different starting precursors, i.e. commercial pure Ca(OH)2 (HAS) and Ca(OH)2 directly from a local natural limestone deposit (HAL). Whereas a commercially available HA "Captal 60" (HAC) was used as reference. The synthesised powders obtained were fired at 1000 degrees C and at 1250 degrees C. Characterisation evaluations on bulk properties were carried out using XRD, SEM-EDX, ICP and FTIR. The results indicate that both HAS and HAL are comparable to HAC even at 1000 degrees C. Thus, the local natural limestone can be used to form HA. However, the overall appearance of these materials are quite different (HAC - blue, HAS - greenish and HAL - light green). The reasons for this and the subsequent mechanical and bioactive effects of these materials are currently being investigated.
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PMID:Comparison of hydroxyapatite powders derived from different resources. 1546 27