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 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

Thirty years after its first description metabolic suppressive therapy is still controversial in patients with intractable intracranial hypertension. In this study high dose propofol was used to induce metabolic suppression. The effects on intracranial pressure (ICP) and the cerebral metabolic rates for oxygen and glucose (CMRO2 and CMRGlc) are reported. A total of 28 studies were performed on 14 head injured patients. A Xenon133 cerebral blood flow (CBF) and a CO2-reactivity (CO2R) test were performed prior to induction of metabolic suppression. The following parameters were continuously monitored: EEG, etCO2, SjvO2, ICP, MAP and bilateral MCA flow velocity (VMCA). PCO2 was obtained before and during propofol-induced EEG burst-suppression in arterial and jugular-venous blood. CMRO2, CMRGlc and Metabolic Ratio (MR = CMRO2/CMRGlc) were calculated. MR < 0.6 was defined as relative hyperglycolysis. ICP decreased by 24.1 +/- 29.0% during burst-suppression. Arterial, jugular-venous and etCO2 also decreased. Multiple regression analysis revealed that CO2 was the strongest predictor for ICP. Lower baseline ICP and normal CO2 reactivity were predictors for normal metabolic suppression reactivity. In studies with normal metabolic ratio, ICP reduction was associated with a reduction in CMRO2. In studies with hyperglycolysis, ICP reduction was poor but CMRGlc decreased significantly. In conclusion, intact CO2R, normal or only moderately elevated ICP and normal MR are predictive of ICP reduction with high dose propofol after head injury.
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PMID:Metabolic suppressive therapy as a treatment for intracranial hypertension--why it works and when it fails. 1216 59

Methods of laser Doppler perfusion monitoring (LDPM) and imaging (LDPI) have been validated and found useful for measurements of brain blood flow in several studies. The present work was undertaken to examine the cortical blood flow autoregulatory phenomenon as it has lately been questioned and claimed to be method-dependent and related to sample volume. Spatial variations in cerebral cortical blood flow (CBF(cortex)) in the pressure range 20-140 mmHg (static cerebral autoregulation; caval block/angiotensin infusion) were studied in six mechanically ventilated (hypocapnic, normocapnic and hypercapnic) pigs anaesthetized with propofol and fentanyl. Although the cortical blood flow values sampled were highly heterogeneously distributed, they were strongly pressure-dependent as well as CO2-dependent (P < 0.001). A cumulative cerebral blood flow (CBF)-pressure (MAP) plot comprising all values obtained indicated a pressure range between 70 and 120 mmHg where CBF remained almost constant. However, at the local level in the cortex (mm2) the same type of 'classic' autoregulatory flow : pressure graphs (FPG) were found in only a few of the cases of the cortical areas examined (n = 96). Alterations in blood P(a)CO2 saturation did not affect the pressure : flow relationship at low perfusion pressures, whereas at normal or above normal values, and as anticipated, hypercapnia considerably increased CBF (P < 0.001). 'Classic' autoregulatory FPGs were found only when all values sampled were clustered together, whereas, as a new finding, data are presented indicating that autoregulatory capacity is lacking at the local level at some cortical surface areas.
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PMID:Cortical blood flow autoregulation revisited using laser Doppler perfusion imaging. 1244 30

We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PET(CO2)) from approximately 40 to approximately 58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PET(CO2) (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16 +/- 3 mmHg) and hyperoxia (17 +/- 2 mmHg PET(CO2)). The increase in cardiac output (Q) at 55 mmHg PET(CO2) was greater in hypoxia (2.61 +/- 0.7 L/min) versus hyperoxia (1.09 +/- 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (> 50 mmHg PET(CO2)) than hyperoxia (> 55 mmHg). MSNA increased earlier during hypoxic hypercapnia (> 45 mmHg) compared with hyperoxic hypercapnia (> 55 mmHg). Thus, in these conscious humans, the dose-response effect of PET(CO2) on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia.
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PMID:Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia. 1256 39

The stress-inducible gene heme oxygenase (HO-1) has previously been shown to provide cytoprotection against oxidative stress. The mechanism(s) by which HO-1 provides this cytoprotection is poorly understood. We demonstrate here that carbon monoxide (CO), a byproduct released during the degradation of heme by HO, plays a major role in mediating the cytoprotection against oxidant-induced lung injury. We show in vitro that CO protects cultured epithelial cells from hyperoxic damage. By using dominant negative mutants and mice deficient in the genes for the various MAP kinases, we demonstrate that the cytoprotective effects of CO are mediated by selective activation of the MKK3/p38 beta protein MAP kinase pathway. In vivo, our experiments demonstrate that CO at a low concentration protects the lungs, extends the survival of the animals, and exerts potent anti-inflammatory effects with reduced inflammatory cell influx into the lungs and marked attenuation in the expression of pro-inflammatory cytokines.
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PMID:MKK3 mitogen-activated protein kinase pathway mediates carbon monoxide-induced protection against oxidant-induced lung injury. 1463 27

The effect of prestorage treatments, such as immersion in a sorbate solution (5%, wt/vol), heating (60 degrees C, 1 min), and a combination of the two treatments, and the subsequent storage in air or under modified atmosphere packaging (MAP; 40% CO2, 30% O2, and 30% N2) at chill temperatures (0 +/- 1 degrees C), on Listeria monocytogenes and Salmonella Enteritidis PT4 was studied. The prestorage treatments affected the pathogenic bacteria, and in all cases, there was a decrease in their population, with the sorbate and combination (hot water and sorbate) treatment being most effective. The beneficial effect of the prestorage treatments, which was more pronounced in storage under MAP conditions, suggests an interaction of the treatments with the CO2 of MAP against injured bacterial cells.
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PMID:Effect of prestorage treatmlents and storage conditions on the survival of Salmonella enteritidis PT4 and Listeria monocytogenes on fresh marine and freshwater aquaaculture fish. 1471 74

The cardiopulmonary effects of desflurane and sevoflurane anesthesia were compared in cats breathing spontaneously. Heart (HR) and respiratory (RR) rates; systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressures; partial pressure of end tidal carbon dioxide (PETCO2), arterial blood pH (pH), arterial partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2); base deficit (BD), arterial oxygen saturation (SaO2) and bicarbonate ion concentration (HCO3) were measured. Anesthesia was induced with propofol (8+/-2.3mg/kg IV) and maintained with desflurane (GD) or sevoflurane (GS), both at 1.3 MAC. Data were analyzed by analysis of variance (ANOVA), followed by the Tukey test (P<0.05). Both anesthetics showed similar effects. HR and RR decreased when compared to the basal values, but remained constant during inhalant anesthesia and PETCO2 increased with time. Both anesthetics caused acidemia and hypercapnia, but BD stayed within normal limits. Therefore, despite reducing HR and SAP (GD) when compared to the basal values, desflurane and sevoflurane provide good stability of the cardiovascular parameters during a short period of inhalant anesthesia (T20-T60). However, both volatile anesthetics cause acute respiratory acidosis in cats breathing spontaneously.
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PMID:Cardiopulmonary and acid-base effects of desflurane and sevoflurane in spontaneously breathing cats. 1577 45

The relative importance of CO2 and sympathetic stimulation in the regulation of cerebral and peripheral vasculatures has not been previously studied in humans. We investigated the effect of sympathetic activation, produced by isometric handgrip (HG) exercise, on cerebral and femoral vasculatures during periods of isocapnia and hypercapnia. In 14 healthy males (28.1 +/- 3.7 (mean +/- S.D.) years), we measured flow velocity (VP; transcranial Doppler ultrasound) in the middle cerebral artery during euoxic isocapnia (ISO, +1 mmHg above rest) and two levels of euoxic hypercapnia (HC5, end-tidal P(CO(2)), P(ET,CO2), = +5 mmHg above ISO; HC10, P(ET,CO2) = +10 above ISO). Each P(ET,CO2) level was maintained for 10 min using the dynamic end-tidal forcing technique, during which increases in sympathetic activity were elicited by a 2-min HG at 30% of maximal voluntary contraction. Femoral blood flow (FBF; Doppler ultrasound), muscle sympathetic nerve activity (MSNA; microneurography) and mean arterial pressure (MAP; Portapres) were also measured. Hypercapnia increased VP and FBF by 5.0 and 0.6% mmHg-1, respectively, and MSNA by 20-220%. Isometric HG increased MSNA by 50% and MAP by 20%, with no differences between ISO, HC5 and HC10. During the ISO HG there was an increase in cerebral vascular resistance (CVR; 20 +/- 11%), while VP remained unchanged. During HC5 and HC10 HG, VP increased (13% and 14%, respectively), but CVR was unchanged. In contrast, HG-induced sympathetic stimulation increased femoral vascular resistance (FVR) during ISO, HC5 and HC10 (17-41%), while there was a general decrease in FBF below ISO. The HG-induced increases in MSNA were associated with increases in FVR in all conditions (r = 0.76-0.87), whereas increases in MSNA were associated with increases in CVR only during ISO (r = 0.91). In summary, in the absence of hypercapnia, HG exercise caused cerebral vasoconstriction, myogenically and/or neurally, which was reflected by increases in CVR and a maintained VP. In contrast, HG increased FVR during conditions of ISO, HC5 and HC10. Therefore, the cerebral circulation is more responsive to alterations in PCO2, and less responsive to sympathetic stimulation than the femoral circulation.
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PMID:Differential responses to CO2 and sympathetic stimulation in the cerebral and femoral circulations in humans. 1589 Jun 97

According to a previous study, a pathologically increased intraabdominal pressure (IAP) reduces cardiac output (CO) and results in medium- to high-grade organ damage in a porcine model of the abdominal compartment syndrome (ACS). The purpose of this study was to evaluate whether fluid resuscitation can preserve organ integrity together with CO. We examined 12 domestic pigs with a mean body weight of 48 kg. We used a CO2 pneumoperitoneum to increase the IAP to 30 mmHg in 6 animals, and the others served as control group. The investigation period was 24 h. In addition to a standard infusion regimen, Ringer's solution was infused to maintain CO at the level of control animals. Hemodynamic parameters (ITBV, EVLW, MAP, CVP), urine output, inspiratory pressure, as well as serum parameters (e.g., ALT, lipase, AP, lactate, creatinine) were recorded. In the end histological examination of liver, bowel, kidney, and lung was performed. CO, ITBV, EVLW, and urine output did not change when compared with control. Fluid intake was increased (P < 0.01) when compared with control (10,570 +/- 1,928 vs. 3,918 +/- 1,042 mL). CVP, MAP, and inspiratory pressure were increased. Serum parameters did not change. Acidosis occurred in the study group. Liver, bowel, kidney, and lung displayed mean- to high-grade damage (P < 0.01). Although extensive fluid resuscitation preserved CO, diuresis, and serum parameters in this previously described model of the ACS, organ damage occurred. In the clinical regard, these results support decompressive treatment in the presence of pathologically high IAP despite "normalized" parameters.
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PMID:Fluid resuscitation preserves cardiac output but cannot prevent organ damage in a porcine model during 24 h of intraabdominal hypertension. 1604 86

The color of food, especially meat and meat products, is a parameter that strongly influences consumer choice. In Italy, repeated cases of darkening in deboned thigh meat of male turkeys packaged in modified atmosphere (MAP; 80% 02, 20% CO2) have been reported. The pH, lipid oxidation (TBARS), heme proteins, and iron content were investigated in MAP samples of turkey males, females, and in oxygen-permeable film-packaged males. Furthermore, the absorbance spectrum (400 to 700 nm) of the meat extracts was analyzed to better delineate the evolution and characteristics of the darkening process. Results showed that darkening occurred only in males with higher content of total iron, independently of the content of heme proteins, which differs only between males and females. Furthermore, pH was higher in muscles taken as controls, with respect to muscles involved in the darkening, as well as in females. Finally, TBARS values were found to be higher in darkened regions than in not darkened ones, as well as in MAP samples with respect to oxygen-permeable film-packaged samples. These findings suggest that darkening occurrence might depend on kind of muscle, sex, and individual characteristics of the animals raised under the same breeding conditions.
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PMID:Biochemical survey on episodic localized darkening in turkey deboned thigh meat packaged in modified atmosphere. 1661 64


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