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)

We measured rat brain cortex PO2 (PtO2) with gold microelectrodes (tip diameter 5--10 micron) for up to 2 hours after 16 min of transient global brain ischemia with and without thiopental 90 mg/kg infused iv over 60 min beginning at 5 min postischemia. Seventeen rats were immobilized and mechanically ventilated on 1% halothane in oxygen with continuous monitoring of PtO2, ECG, end-expiratory CO2, rectal temperature, and arterial blood pressure. Global ischemia was induced by trimethaphan hypotension to an MAP of about 50 torr and a neck tourniquet inflated to 1500 torr. Postischemia, nine control rats (11 PtO2 measurements) were untreated and eight rats (8 PtO2 measurements) received thiopental 90 mg/kg. Preischemia, PtO2 values in both groups ranged from less than 5--70 torr with values of greatest frequency between 10 and 15 torr. Postischemia, PtO2 in control rats peaked at 45 +/- 8 (SEM) torr at 20 min. In thiopental treated rats, peak PtO2 was 24 +/- 6 torr at 10 min postischemia. Relative frequency histograms of PtO2 revealed that PtO2 in thiopental treated rats was lower (p less than 0.05) between 15 and 30 min postischemia. The magnitude of the decrease in PtO2 between 105 and 120 min postischemia appeared to correlate directly with the absolute preischemic value (i.e., the higher the preischemic PtO2, the greater the decrease in PtO2 postischemia). These results suggest that thiopental administered in large doses in early postischemia does not improve brain oxygenation secondary to a reduction in brain oxygen consumption. The relevance of the correlation between the magnitude of the fall in PtO2 postischemia and the magnitude of the preischemic value is discussed.
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PMID:Postischemic brain oxygenation with barbiturate therapy in rats. 3 43

Over the last ten years the survival of infants born with congenital diaphragmatic hernia who reach the Intensive Care Unit of the Royal Children's Hospital, Melbourne has been constant at 56 +/- 6%. Experimental therapies such as extracorporeal membrane oxygenation, high-frequency oscillation and lung transplantation are now being considered as therapeutic options, and as such the ability to predict survival or death of these infants is increasingly important. The records of all infants with congenital diaphragmatic hernia admitted to the Intensive Care Unit between 1 January 1980 and 30 April 1989 were reviewed; blood gas, ventilatory details, and outcome information was obtained. Receiver operating curve analysis was used to determine the best predictor of death. An oxygenation index (MAP x FiO2/PaO2) > 0.3 or ventilation index (PIP x RR x CO2/1000) > 70 predicted a 94% mortality with a specificity of 96% and a sensitivity of 82%.
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PMID:Mortality prediction in infants with congenital diaphragmatic hernia: potential criteria for ECMO. 146 69

Changes in pre-bypass and post-bypass P(a-ET)CO2 gradients were evaluated regarding the type of bypass flow (pulsatile or nonpulsatile) and oxygenator (membrane or bubble). Duration of bypass and hemodynamic changes were analyzed also to determine their possible influence on PaCO2, PETCO2, and P(a-ET)CO2. A total of 36 adult patients undergoing cardiopulmonary bypass were anesthetized using a sufentanil-pancuronium-oxygen technique. Patients were divided into three groups based on the type of oxygenator and pump flow: group 1 (control group) consisted of a bubble oxygenator with nonpulsatile flow (BN), group 2 consisted of a bubble oxygenator with pulsatile flow (BP), and group 3 consisted of a membrane oxygenator with nonpulsatile flow (MN). Cardiac parameters (MAP, CI, SVR, and PVR) PaCO2, PETCO2, and P(a-ET)CO2 were determined pre-bypass and post-bypass following steady-state conditions. For the entire group there was a trend for the P(a-ET)CO2 gradient to increase in the post-bypass period (pre-bypass = 3.5 +/- 0.5 mm Hg, post-bypass = 4.3 +/- 0.5 mm Hg.). However, this increase was not statistically significant. Pulsatile flow (group 2) demonstrated a significant correlation with the change in P(a-ET)CO2 gradients from the pre-bypass to the post-bypass period (r = 0.85) when compared with the other two groups (group 1: r = -0.09 and group 3: r = 0.37). Thus, the P(a-ET)CO2 gradient tended to remain constant from the pre-bypass to the post-bypass period in group 2, whereas it increased in groups 1 and 3. Changes in MAP, CI, SVR, and PVR and the duration of CPB did not influence the P(a-ET)CO2 gradient.
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PMID:Effect of oxygenator type and bypass flow pattern on the P(a-ET)CO2 gradient. 154 53

The cerebral vasomotor reactivity to carbon dioxide was studied, using a thermal gradient blood flow meter in 43 patients with intracranial cerebral aneurysm under deliberate hypotension induced by prostaglandin E1 (PGE1) infusion. The patients were divided into three groups according to the neurological status. Patients in Groups A and B had subarachnoid haemorrhage due to ruptured cerebral aneurysms. Group A consisted of 23 patients with a neurological grade of I-II and Group B consisted of 11 patients with a grade of III-V. Nine patients with non-ruptured cerebral aneurysm served as controls (Group C). After the dura was opened, local cerebral blood flow (LCBF) was measured. The PGE1 was started with an initial dose of 0.1 microgram.-kg-1.min-1 and the dose was adjusted to maintain MAP at about 70 mmHg. The LCBF and carbon dioxide (CO2) reactivity were estimated during and after PGE1 administration. The LCBF did not change among groups throughout the study period. Carbon dioxide reactivity was estimated as follows: absolute; delta LCBF/delta PaCO2, and relative; % delta LCBF/delta PaCO2 after changing PaCO2 by increasing minute ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery. 155 Nov 57

The effects of hypoxia on the myocardial uptake and pharmacodynamics of quinidine were studied in isolated perfused rabbit hearts. Hearts were perfused with a modified Krebs-Henseleit buffer that was equilibrated with either 95% O2-5% CO2 (normoxia) or 95% N2-5% CO2 (hypoxia). The myocardial quinidine accumulation was determined from concentration differences in aortic perfusate and coronary sinus effluent. Under hypoxic conditions, the myocardial concentration of quinidine (12.0 +/- 3.6 micrograms/g) was significantly reduced compared to normoxic conditions (24.8 +/- 8.5 micrograms/g, p less than 0.01). Greater increases in QRS complex duration were observed during hypoxia (10.0 +/- 1.0 ms) compared to normoxia (7.5 +/- 1.3 ms; p less than 0.05). Greater increases in MAP duration were also observed during hypoxia (64 +/- 14 ms) compared to normoxia (37 +/- 14 ms; p less than 0.01). The myocardial concentration-effect relationships describing changes in QRS complex duration, QT interval, MAP duration, and ventricular effective refractory periods were linear in both groups. The curves of the concentration-effect relationships observed during hypoxia were shifted to the left compared to those observed during normoxia and the slopes of these relationships were also significantly greater (p less than 0.05). These pharmacokinetic and pharmacodynamic interactions may be explained by the development of acidosis during hypoxia since the pH of the coronary sinus effluent decreased significantly during hypoxia (7.10 +/- 0.04) compared to the normoxic group (7.25 +/- 0.04, p less than 0.001). Thus, although hypoxia reduces the myocardial accumulation of quinidine, greater electrophysiologic effects are observed compared to normoxic conditions. These observations likely relate to a change in responsiveness of acidotic tissue to quinidine.
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PMID:Influence of hypoxia on the myocardial uptake and pharmacodynamics of quinidine in isolated perfused rabbit hearts. 170 29

Anesthesia may compromise the regulation of systemic and cerebral hemodynamics following changes in body position. Sudden decreases in cerebral perfusion pressure due to changes from a horizontal to a head-elevated position may cause decreases in cerebral blood flow (CBF), particularly in patients with preexisting cerebrovascular disease. Transcranial Doppler sonography (TCD) permits on-line measurement of blood flow velocity (BFV) in human basal cerebral arteries, and there is evidence that monitoring of BFV may indicate relative changes in CBF. The present study compares the effects of changes from a horizontal to a head-elevated position on blood flow velocity in the middle cerebral artery (MCA) in 30 patients (ASA I) with different levels of steady state anesthesia (group A: n = 20, isoflurane = 1.0 vol% end-tidal; group B: n = 10, isoflurane = 0.4 vol% end-tidal; O2/N2O; FiO2: 0.3; 6 1/min). The MCA was insonated by transtemporal approach using a 2 MHz Doppler ultrasound system (TC2-64 B, EME) with a range-gating mechanism, adjustable sample volume depth, and flow direction discrimination. Systolic (Vsyst, cm/s) and mean flow velocity (Vmean, cm/s), pulsatility index (PI), mean arterial blood pressure (MAP, mmHg), heart rate (HR, b/min) and end-tidal CO2 (pet-CO2, mmHg) were recorded with the subjects lying flat (baseline values) and for 5 min following adjustment to a 35-40 degrees head-elevated position. There was a significant reduction of 25% for Vsyst from 79 +/- 17 cm/s (baseline) to 59 +/- 13 cm/s and a 33% decrease for Vmean from 52 +/- 9 cm/s (baseline) to 35 +/- 9 cm/s in group A immediately after repositioning.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of postural changes on cerebral hemodynamics during general anesthesia]. 224 May 63

In a porcine endotoxin shock model employing a continuous intravenous administration of Salmonella abortus equi endotoxin the cardiorespiratory and metabolic parameters were studied with main emphasis on the effect of hemofiltration (HF) as the only therapeutical measurement on the enhancement of survival time. Arachidonic acid (AA) metabolites Thromboxan B2 and 6-Keto-PGF 1-alpha could be lowered significantly by hemofiltration. Measuring the inadequacy of the supply and delivery systems in terms of O2-uptake, CO2 production, lung mechanics, TPR, CO, heart rate and MAP the control group seemed to be more severely compromised than the hemofiltrated groups, although the final outcome as for survival time could not be increased significantly. HF can nonselectively counteract some toxic effects of shock mediators without depriving the organism of beneficial components of a protective system being stimulated at the same time. Once the AA cascade is initiated, pharmacologic inhibition is of limited value as long as a direct specific therapeutic manipulation is still not available. Elimination of mediators by HF helps to combat the overstimulation of host defense mechanisms in ET shock which represents the ultimate threat to the host.
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PMID:Can hemofiltration increase survival time in acute endotoxemia--a porcine shock model. 250 78

The ventilatory response to exercise induced by stimulation of the peripheral ends of severed sciatic nerves was studied in seven anesthetized dogs. In response to exercise (n = 23) there were increases in expired minute ventilation (delta VE = 4.09 l/min), arterial CO2 partial pressure (delta PaCO2 = 3.06 Torr), and carotid artery temperature (delta Tca = 0.26 degrees C). There was also a concomitant decrease in mean arterial blood pressure (delta MAP = -6.28 Torr). Since the neural pathways from the exercising limbs to the central nervous system had been eliminated by nerve section, the significant increase in PaCO2 during exercise indicates that humoral factors alone cannot produce the normal exercise response, i.e., an isocapnic hyperpnea. Therefore, neural pathways may play a fundamental role in the ventilatory response to exercise in intact animals.
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PMID:A role for neural pathways in exercise hyperpnea. 642 6

The authors investigated in 24 patients with ASA I or II who were subjected to elective laparoscopic cholecystectomy haemodynamic parameters (CI, SI, HR, MAP, SVRI, EF and LCWI), assessed by transthoracic electric bioimpendance. They used a BoMED NCCOM3 apparatus and evaluated data from the period before induction of anaesthesia (considered as control data), after induction of anaesthesia, immediately after insufflation of CO2 into the peritoneum, 30 minutes after insufflation and after desufflation. Insufflation of CO2 into the peritoneum caused a statistically significant drop of CI (p < 0.05), reduction of HR (p < 0.05), a drop of EF (p < 0.05), reduction of LCWI (p < 0.05) and a statistically significant rise of SVRI (p < 0.001). Thirty minutes after insufflation another significant drop of CI occurred and also for the first time of SI (p < 0.05 and p < 0.05 resp.); the mean values of HR and MAP did not differ significantly from control values, SVRI remained elevated (p < 0.05) and EF was permanently reduced (p < 0.05). After desufflation all haemodynamic values with the exception of EF did not differ significantly from control values. The reduced EF (p < 0.05), however, reached as to its absolute value the lower borderline of the physiological range. Based on these results, the authors assume that in patients with a compromised cardiovascular apparatus circulatory complications could develop. In these patients laparoscopic cholecystectomy should be indicated after due consideration.
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PMID:[Hemodynamic changes during laparoscopic cholecystectomy]. 765 12

The present study compared the effects of propofol/alfentanil versus isoflurane anaesthesia on cerebral vascular reactivity to changes in carbon dioxide (CO2) using transcranial Doppler sonography (TCD). METHODS. Seventeen ASA class I patients undergoing minor elective surgery were studied following IRB approval and informed consent. In group 1 (n = 10), anaesthesia was induced with thiopental 4 mg/kg and alfentanil 15 micrograms/kg. Endotracheal intubation was facilitated by vecuronium 0.1 mg/kg. Anaesthesia was maintained with 1% end-tidal isoflurane and nitrous oxide (N2O) in oxygen O2 (6 l/min; FiO2 0.3). In group 2 (n = 7), anaesthesia was induced with propofol 2 mg/kg, alfentanil 15 micrograms/kg, and vecuronium 0.1 mg/kg for endotracheal intubation and maintained by infusion of propofol, alfentanil, and N2O-O2 (6 l/min; FiO2 0.3) according to the following protocol: propofol: 10, 8, and 6 mg/kg.h for 10 min each followed by 4 mg/kg.h; alfentanil: 55 micrograms/kg.h. Monitoring included measurement of mean arterial blood pressure (MAP, mm Hg), heart rate (HR), body temperature (T), end-tidal CO2 (PetCO2, mm Hg), isoflurane concentrations, and arterial O2 saturation (SaO2, %). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a bidirectional 2-MHz TCD system (TranspectT, Medasonics). Mechanical ventilation was adjusted to achieve PetCO2 levels of 40-50-40-30 and 40 mm Hg. Ten minutes of equilibration were allowed at each PetCO2 level. The CO2 reactivity index was calculated as delta Vmean/delta PetCO2 (cm/s.mm Hg). RESULTS. MAP, HR, T, and SaO2 were constant over time and were not different between groups. The CO2 reactivity index over the CO2 range of 30-50 mm Hg was higher in isoflurane (2.32 +/- 1.51 delta cm/s.mm Hg) compared to propofol/alfentanil patients (1.15 +/- 0.77 delta cm/s.mm Hg) (mean +/- SD, P < 0.05). CONCLUSIONS. The data show that although CO2 reactivity is maintained during both isoflurane and propofol/alfentanil anaesthesia, the cerebral vascular response to CO2 was lower in propofol/alfentanil compared to isoflurane patients. This is likely due to propofol/alfentanil-induced cerebral vasoconstriction. These data suggest that CO2 reactivity is a function of the pre-existing cerebral vascular tone induced by the anaesthetic.
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PMID:[Propofol-alfentanil reduced cerebrovascular CO2 reactivity in comparison with isoflurane]. 765 93


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