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

Although lidocaine HCl is often given to critically ill patients with ventricular tachyarrhythmias, it use is not without hazard. To investigate whether acid-base disturbances and their subsequent effects on molecular ioization influence cardiovascular (CV) response to lidocaine, dogs in normal acid-base balance, metabolic acidosis, respiratory acidosis, and respiratory alkalosis were given 2 or 4 mg/kg lidocaine IV. Heart rate (HR), PR and QT intervals, MAP, LVEDP, LV dp/dt, and LV dp/dt divided by CPIP were measured at intervals. In all groups a slight increase in mean HR occurred after 2 mg/kg. Generally, myocardial contractile force was depressed in direct proportion to dose. Essentially, the CV response to lidocaine was not altered by any clinically remarkable degree by pH disturbances. Responses differing from those observed during normal acid-base conditions could not be significantly correlated with changes in pH or PaCO2. Results suggest that, in the intact animal, the CV effects of lidocaine, administered in therapeutic doses, are not appreciably influenced by clinically encountered states of acid-base imbalance.
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PMID:Crdiovascular effects of lidocaine during acid-base imbalance. 103 6

Human skin blood flow (SkBF) is controlled by both an alpha-adrenergic vasoconstrictor system and an active vasodilator system. During upright dynamic exercise, SkBF increases linearly with increasing body core temperature (Tc) until higher (i.e., greater than 38 degrees C) Tcs, beyond which little further increase in SkBF occurs. To examine the role of the two efferent control arms in this attenuated SkBF rise, we tested nine men (aged 25-53 yr) with and without (placebo) orally administered prazosin HCl (an alpha 1-adrenergic antagonist) during 1 h of moderate cycle exercise (100 W) in a warm (36 degrees C, 45% relative humidity) environment. Blockade of reflex vasoconstriction was verified via a cold challenge. During exercise, mean arterial pressure (MAP, brachial auscultation) was significantly lower (P less than 0.03) and heart rate significantly higher (P less than 0.02) during the prazosin trials; plasma catecholamine concentrations were unaffected. Neither esophageal temperature (Tes) nor mean skin temperature was affected by the drug during exercise. Forearm vascular conductance (FVC) was calculated from forearm blood flow (FBF, venous occlusion plethysmography) and MAP (FVC = FBF/MAP). FVC plotted as a function of time or Tes resulted in coincident response patterns for the placebo and prazosin treatments, reaching a plateau at a Tes of about 38 degrees C. The responses of the older men were not selectively altered by prazosin treatment, indicating that the lower FBF responses previously seen in older subjects during exercise in the heat does not appear to be the result of an increased alpha 1-adrenergic tone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha 1-adrenergic blockade does not alter control of skin blood flow during exercise. 167 54

Experiments were performed on spinalized rats transected at C1. Intravenous administration of 2-phenylethylamine-HCl (PEA-HCl) (0.3 and 1 mg/kg, i.v.) and methamphetamine-HCl (MAP-HCl) (0.1 and 0.3 mg/kg, i.v.) increased the amplitude of the monosynaptic reflex (MSR). The increase of the MSR caused by PEA and MAP was antagonized by prazosin-HCl and abolished by the pretreatment with reserpine (i.p.) and 6-hydroxydopamine (intracisternally, 14 days previously). A dopamine D1 antagonist, SK&F 83566-HBr (0.01 mg/kg, i.v.), and a D2 antagonist. YM-09151-2 (0.3 mg/kg, i.v.), did not antagonize the increasing effects produced by PEA and MAP. An inhibitor of type-B monoamine oxidase, (-)deprenyl-HCl (1 mg/kg, i.v.), prolonged the effect of PEA but not that of MAP, suggesting that PEA alone, and not its metabolites, enhanced the MSR. These results suggest that PEA and MAP increase the amplitude of the MSR by releasing noradrenaline from the terminals of descending noradrenergic fibers, and that PEA, an endogenous trace amine, has a mechanism of action similar to that of MAP.
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PMID:2-phenylethylamine and methamphetamine enhance the spinal monosynaptic reflex by releasing noradrenaline from the terminals of descending fibers. 183 Mar 50

Administration of 20, 4 or 2.5 micrograms/kg of atriopeptin III (AT III) into the fourth ventricle of the brain of spontaneously hypertensive rats produced a 13, 14 and 7 mm Hg decrease in MAP respectively, while 1 microgram/kg had no effect on MAP and was significantly different from 20 or 4 micrograms/kg (p less than 0.025). In contrast, injection of AT III 20 micrograms/kg into the lateral ventricle did not produce a change in MAP. To examine an interaction of AT III with the opioidergic system, the opiate antagonist, naloxone HCl, 10 micrograms, was given by ICV injection 10 minutes prior to AT III, and significantly prevented the depressor response to AT III (p less than 0.025 compared with AT III alone). Injection of specific anti-sera to beta-endorphin failed to prevent the AT III-induced depressor response. Our results demonstrate that AT III can act within the central nervous system to decrease the MAP of rats, most likely at a locus in proximity to the fourth ventricle of the brain. Further, an interaction with the central opioidergic nervous system underlies the central effects of AT III.
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PMID:Central nervous system mediated vasodepressor action of atrial natriuretic factor. 252 18

Previous studies have reported haemodynamic interactions between dihydropyridine calcium antagonists and general anaesthesia. During anaesthesia for intracranial aneurysm surgery, we prospectively compared haemodynamic values obtained from 13 patients being treated with nicardipine HCl (0.15 mg.kg-1.hr-1 IV) for cerebral vasospasm against values obtained from 11 untreated controls. Prior to induction of anaesthesia, nicardipine-treated patients had significantly elevated mean +/- SD cardiac index (5.67 +/- 1.30 vs 3.99 +/- 0.73 L.min-1.m-2) while MAP (86 +/- 10 vs 99 +/- 14 mmHg) and systemic vascular resistance (647 +/- 227 vs 1141 +/- 404 dynes.sec-1.cm-5) were reduced. Heart rate, CVP, and PACWP were similar between groups. Anaesthesia induction and tracheal intubation resulted in similar haemodynamic values between groups with the exception of CVP (10 +/- 5 vs 5 +/- 2 mmHg) and PACWP (15 +/- 5 vs 8 +/- 3 mmHg) which were elevated in the nicardipine group (P less than 0.01). Mannitol infusion and deliberate hypotension resulted in nearly identical haemodynamic responses in both groups. Nicardipine-treated patients required more intravenous fluids during the operative procedure (2.4 +/- 0.3 L vs 1.5 +/- 0.4 L, P less than 0.05) and were less likely to require isoflurane supplementation to morphine sulphate/nitrous oxide anaesthesia (P less than 0.01). In summary, our experience with nicardipine HCl revealed no major untoward effects with respect to maintenance of intraoperative haemodynamic stability despite continuous antivasospasm therapy with this vasodilator.
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PMID:Nicardipine HCl: clinical experience in patients undergoing anaesthesia for intracranial aneurysm clipping. 270 15

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ~0.5 degrees C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [DeltaMAP 8.4 +/- 1.2 mmHg; DeltaTPR 0.96 +/- 0.85 peripheral resistance units (PRU)] compared with normothermia (DeltaMAP 15.4 +/- 1.4 mmHg, DeltaTPR 7.13 +/- 1.18 PRU; all P < 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.
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PMID:Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans. 1237 16

This paper presents a recycle MAP process (magnesium ammonium phosphate) to remove NH4-N from a typical rare-earth wastewater. The optimum conditions for the MAP precipitation and recycle use of the MAP with a newly-designed process were investigated in laboratory. The results showed that the pH value and dosages of P (phosphate) and Mg reagents have a significant influence on NH4-N removal, with a maximum removal efficiency of 99.4% at the conditions of pH=9 and Mg:N:P molar ratio=1.2:1:1.2. In the process of recycle use of the MAP, adding some HCl to dissolve MAP decomposition residues could effectively enhance NH4-N removal. The NH4-N removal efficiency reached 99.6% by adding an HCl amount of H+:OH- molar ratio=0.8 into the reused MAP decomposition residues, whereas the NH4-N removal efficiency without addition of HCl was only 96.4%. Moreover, the residual PO4-P from the end of reaction was recovered and the optimum recovery efficiency was achieved at a Mg:P molar ratio=6 and pH=10. Under these optimum conditions, the residual NH4-N and PO4-P concentrations in the treated wastewater, through 6 times of the recycling, were less than 15 mg/L and 1 mg/L, respectively. On the basis of this, an economic evaluation of the recycling MAP was made, and this recycle process could save 48.6% cost used in the chemicals for treating per cubic meter of the rare-earth wastewater, compared to the conventional MAP process.
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PMID:Recycle use of magnesium ammonium phosphate to remove ammonium nitrogen from rare-earth wastewater. 1934 4

Semisynthetic analogues of fumagillin, 1, inhibit methionine aminopeptidase-2 (MetAP2) and have entered the clinic for the treatment of cancer. An optimized fumagillin analogue, 3 (PPI-2458), was found to be orally active, despite containing a spiroepoxide function that formed a covalent linkage to the target protein. In aqueous acid, 3 underwent ring-opening addition of water and HCl, leading to four products, 4-7, which were characterized in detail. The chlorohydrin, but not the diol, products inhibited MetAP2 under weakly basic conditions, suggesting reversion to epoxide as a step in the mechanism. In agreement, chlorohydrin 6 was shown to revert rapidly to 3 in rat plasma. In an ex vivo assay, rats treated with purified acid degradants demonstrated inhibition of MetAP2 that correlated with the biochemical activity of the compounds. Taken together, the results indicate that degradation of the parent compound was compensated by the formation of active equivalents leading to a pharmacologically useful level of MetAP2 inhibition.
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PMID:Orally active fumagillin analogues: transformations of a reactive warhead in the gastric environment. 2490 Jun 82