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)

The aim of the work was to check if cerebrospinal fluid drainage performed under general anaesthesia altered in time the permeability of the blood/cerebrospinal fluid barrier (BCSFB), the part of blood-brain barrier. Twelve adult Chinchilla rabbits were included into the study. The animals were divided into 2 groups: control and investigated. The cerebrospinal fluid drainage was performed in animals from the studied group. Gentamycin was applied as the marker of tightness of BCSFB; under normal circumstances BCSFB prevented or limited the passage of gentamycin to the cerebrospinal fluid after intravenous administration. Heart rate (HR), arterial blood pressure (SAP, DAP, MAP), central venous pressure (CVP), blood-gas analysis (BGA), end-expiratory CO2 pressure (et CO2), hemoglobin, hematocrit, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were recorded. General anaesthesia was performed under circumstances that excluded the influence of any additional factor on the permeability of the BCSFB and haemodynamic, haematologic and gasometric parameters were stable in all animals. The influence of the cerebrospinal fluid drainage on the permeability of the BCSFB was evaluated using gentamycin concentration levels in blood and cerebrospinal fluid. Mean haemodynamic, haematologic and gasometric parameter values showed no within-group and between-group differences. In the investigated group the cerebrospinal fluid drainage was followed by a decrease in intracranial pressure (Tab. 1, Fig 1.) without changes in cerebral perfusion pressure (Tab. 2, Fig. 2). No significant changes in gentamycin permeability indexes were stated (Tab. 3, Fig. 3). Cerebrospinal fluid drainage performed under general anaesthesia caused no increase of the permeability of the BCSFB. A decrease of the intracranial pressure without changes of the cerebral perfusion pressure followed the cerebrospinal fluid drainage.
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PMID:[The effect of cerebrospinal fluid drainage on the permeability of the blood-brain barrier for gentamycin under general anesthesia conditions in the rabbit]. 947 17

Recently we have found that hypercapnia induces nuclear protein (FOS) expression in the brainstem chemosensitive neurons, including catecholamine-containing cells. In the present studies we examined the role of protein kinase C (PKC) pathway in CO2-induced c-fos expression. Because of the complexity of the CNS system, experiments were performed in pheochromocytoma cells (PC12 cells). These cells originate from neuronal crest and express catecholaminergic traits. We depleted PKC from PC12 cells by prolonged (48 h) exposure to high concentration of phorbol 12-myristate, 13-acetate (PMA, 100 nM), and then determined the expression of: (1) c-fos mRNA by Northern blot (2) PKC isoforms, tyrosine phosphorylated and unphosphorylated MAP (mitogen activated protein) kinases by Western blot. Depletion of PKC abolished the effect of CO2 on c-fos mRNA expression, inhibited MAP kinases tyrosine phosphorylation and suppressed the expression of PKC(alpha) and PKC(zeta). These results suggest that MAP kinases, PKC(alpha) and/or PKC(beta) might be involved in CO2-induced c-fos mRNA expression.
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PMID:A possible role for protein kinase C in CO2/H+-induced c-fos mRNA expression in PC12 cells. 957 65

The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.
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PMID:Role of hypoxemia and hypercapnia in acute cardiovascular response to periodic apneas in sedated pigs. 962 31

Eight healthy horses premedicated with xylazine and induced with ketamine were used to evaluate sevoflurane in oxygen for maintenance of anaesthesia during elective exploratory laparotomy. After orotracheal intubation, horses were hoisted, placed in dorsal recumbency on a padded surgery table, and received sevoflurane in oxygen for maintenance of anaesthesia. The horses were allowed to breathe spontaneously until instrumented; then, they were mechanically ventilated to maintain the PaCO2 between 35 and 45 mmHg. Systolic (SAP), diastolic (DAP), and mean (MAP) arterial blood pressures, heart rate (HR), ECG, respiratory rate, an estimation of the saturation of haemoglobin with oxygen in peripheral arterial blood (S(p)O2), nasal temperature, end-tidal CO2(ET(CO2)), end-tidal sevoflurane (ET(SEVO)), and vaporiser concentration were recorded every 5 min post induction; arterial blood samples were obtained soon after induction, at 30 min after induction, and every hour thereafter until surgery was completed. Recovery data including times from the sevoflurane vaporiser being turned off to first movement, to sternal recumbency, and to standing, number of attempts to stand, and recovery score (between 1 = safe, smooth and 6 = stormy, major injury to horse) were collected. Analysis of variance was performed using physiological data collected over 195 min of anaesthesia, the longest time period during which all 8 horses were instrumented. Time effects (P<0.05) for HR, SAP, DAP, MAP, and nasal temperature were identified. Heart rate peaked at 45 min and declined over the course of the procedure. Arterial blood pressure generally decreased over time. Body temperature decreased over time. From 15 to 195 min mean ET(SEVO)concentration ranged from 2.0 to 3.3%, while mean vaporiser settings ranged from 3.7 to 5.5%. Three horses received intra-operative ketamine; all horses received dobutamine infusions; and 2 horses received intra-operative calcium-dextrose. Total anaesthesia time was 222-316 min (mean+/-s.d.269+/-31 min). Time from turning the sevoflurane vaporiser off to first movement was mean +/-s.d.18+/-15 min; to sternal recumbency was 54+/-22 min; to standing was 65+/-27 min; and to returning the horse to the stall in the ward was 78+/-24 min. Six horses stood on the first attempt; 2 horses stood on the second attempt. The median recovery score was one (1-3). In conclusion, sevoflurane provided a stable, easily controllable anaesthetic plane during prolonged exploratory laparotomies; horses experienced smooth, safe recoveries after maintenance of anaesthesia with sevoflurane following routine anaesthetic induction and post operative xyalzine administration.
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PMID:Maintenance of anaesthesia with sevoflurane and oxygen in mechanically-ventilated horses subjected to exploratory laparotomy treated with intra- and post operative anaesthetic adjuncts. 975 97

Cold pressor test (CPT) evokes generalized activation of the sympathetic nervous system (SNS). The activity of SNS may be estimated by monitoring the mean blood velocity (v(m)) in the middle cerebral artery (MCA) by using a transcranial Doppler monitoring system (TCD). To determine the response of SNS, we studied the v(m) during CPT. Thirty-four healthy volunteers, 13 female and 21 male (mean age 34 +/- 9.5 years, range 18 to 55 years) participated in our study. The experiment consisted of a 5-min baseline period followed by a 3-min immersion of the right hand in ice water. Blood velocity in both MCA's was monitored by bitemporal 2 MHz probes by using a Multi-Dop X4. MAP and heart rate (HR) were measured simultaneously by a Finapres non-invasive blood pressure monitor and a computerized ECG system. End-tidal CO2 (Et-CO2) was measured with an infrared capnograph. To determine v(m) over a chosen time interval the TCD-8 software was utilized. The results showed that during CPT v(m), MAP, and HR increased significantly (P < 0.01) for 9.8%, 18.5%, and 3.6%, respectively. Et-CO2 did not change significantly (P > 0.05). The increase of v(m) was also significantly higher in the stimulated hemispheres (P = 0.005) regarding to unstimulated ones. The increase of v(m) during CPT was not gender dependent. To establish the association between variables the models of multivariate regression were used. Multiple regression CPT model was significant (P < 0.01) and fitted data moderately well (R2 = 0.28). MAP and Et-CO2 were significant in the model (P < 0.01). It seems that the reactivity of the SNS can be estimated by measuring v(m) with TCD during CPT.
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PMID:Influence of the cold pressor test on the middle cerebral artery circulation. 991 34

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.
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PMID:Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs. 991 31

The effect of aerobic, modified atmosphere packaging (MAP; 40% CO2/30% O2/30% N2) and vacuum packaging (VP) on the growth/survival of Listeria monocytogenes on sterile and naturally contaminated beef meat fillets was studied in relation to film permeability and oregano essential oil. The dominant micro-organism(s) and the effect of the endogenous flora on the growth/survival of L. monocytogenes were dependent on the type of packaging film. The fact that L. monocytogenes increased whenever pseudomonads dominated, i.e. aerobic storage and MAP/VP in high-permeability film, and even earlier than on sterile tissue, suggests that this spoilage group enhanced growth of the pathogen. Brochothrix thermosphacta constituted the major proportion of the total microflora in MAP/VP within the low-permeability film, where no growth of L. monocytogenes was detected either on naturally contaminated or sterile meat fillets. The addition of 0.8% (v/w) oregano essential oil resulted in: (i) an initial reduction of 2-3 log10 of the majority of the bacterial population, with lactic acid bacteria and L. monocytogenes indicating the most apparent decrease in all gaseous environments, and (ii) limited growth aerobically and survival/death of L. monocytogenes in MAP/VP, regardless of film permeability.
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PMID:Behaviour of Listeria monocytogenes and autochthonous flora on meat stored under aerobic, vacuum and modified atmosphere packaging conditions with or without the presence of oregano essential oil at 5 degrees C. 1112 63

Biogenic amines are formed in foods as a result of amino acid decarboxylation catalyzed by bacterial enzymes. When consumed in sufficient quantities, these compounds will cause headache, hypertension, fever, and heart failure. Technologies such as vacuum packaging and carbon dioxide-modified atmosphere packaging (CO2-MAP), when combined with low-temperature storage (-1.5 degrees C), allow fresh pork to have a storage life long enough for export to overseas markets. During low-temperature storage of pork in these packaging systems, the lactic acid bacteria (LAB), which possess the enzymes for biogenic amine formation, dominate the microflora. The objectives of this study were to determine the quantities of biogenic amines in packaged fresh pork, to monitor LAB growth, and to determine the storage life by sensory evaluation. Vacuum-packaged and CO2-MAP pork were stored at -1.5+/-0.5 degrees C for 9 and 13 weeks, respectively. Phenylethylamine, putrescine, cadaverine, histamine, tyramine, spermidine, and spermine concentrations were determined weekly by high-performance liquid chromatography and capillary gel electrophoresis. LAB and carnobacteria were enumerated weekly. Samples were evaluated for odor and appearance. The CO2-MAP was successful in delaying bacterial growth and the development of unacceptable off-odors compared with the vacuum packaging. The storage lives of the vacuum-packaged and CO2-MAP pork were 5 and 13 weeks, respectively. High-performance liquid chromatography was the superior method for biogenic amine quantification. Tyramine and phenylethylamine in pork of both packaging treatments approached levels considered to be potentially toxic. Given Canada's increasing role in the export of fresh meat to foreign markets, it is recommended that the formation of biogenic amines in vacuum-packaged and CO2-MAP pork be further investigated.
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PMID:Biogenic amines in vacuum-packaged and carbon dioxide-controlled atmosphere-packaged fresh pork stored at -1.50 degrees C. 1127 71

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2. In six healthy human subjects at rest, we measured leg blood flow (.Q(L)) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3-10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P(M)) and a prolonged duty cycle (T(I)/T(TOT) = 0.7); and (ii) 60 % maximal P(M) and a T(I)/T(TOT) of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P(CO2) was maintained by increasing the inspired CO(2) fraction (F(I,CO2)) as needed. Both trials caused a 25-40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. .Q(L) and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, .Q(L) subsequently decreased (-30 %) and LVR increased (50-60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4-13 mmHg) and heart rate (+16-20 beats min(-1)) increased during fatiguing diaphragm contractions. 4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 x eupnoea), .Q(L), MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in .Q(L). 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and .Q(L) increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume. 6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on .Q(L) and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in .Q(L) and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and .Q(L).
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PMID:Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans. 1171 55

The aim of the present study was to assess the veno-arterial difference in pCO2 (delta pCO2) as an indicator of ischemia compared to the arteriovenous O2 difference (AVDO2). Staircase cerebral blood flow (CBF) reductions were obtained in seven domestic pigs by inducing intracranial hypertension: CBF 100%, 50-60% of baseline, 20-30% of baseline. ICP, MAP, CPP and CBF (Laser-Doppler method) were continuously recorded. The superior sagittal sinus was punctured to determine AVDO2 and delta pCO2. AVDO2 was 5.9 (+/- 1.78, range 3.3-7.4), 7.01 (+/- 1.31, range 5-8.9) and 8.17 (+/- 1.51, range 6.0-11.3) ml/100 ml in the three CBF steps (p = 0.001). CBF impairment was accompanied by the following increases in delta pCO2: from 10 (+/- 4, range 4-15) mmHg to 14.5 (+/- 4.11, range 10-27) mmHg, and to 31.2 (+/- 9.0, range 17-39) mmHg (p < 0.001). When CBF declines AVDO2 increases, indicating greater extraction of O2 to satisfy the aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. delta pCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is impressive during marked CBF impairment when anaerobic metabolism takes place with proton buffering in CO2 and H2O. Therefore, when the brain's ability to compensate for low blood flow is exceeded, CO2 production outweighs O2 extraction.
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PMID:Cerebral veno-arterial pCO2 difference as an estimator of uncompensated cerebral hypoperfusion. 1216 4


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