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)

Isoflurane (ISO) was examined as an alternative hypotensive agent to nitroprusside (SNP) in 16 patients (mean age: 60 years) anaesthetized for total hip arthroplasty. MAP was decreased to 50 per cent of the awake level by infusion of SNP in Group I (n = 8) and with ISO in Group II (n = 8). Fentanyl (10-16 micrograms X kg-1) was administered to both groups. Haemodynamic measurements were repeated in the lateral position before, during and after hypotension. Polygeline and fresh frozen plasma were infused throughout the study period in volumes sufficient to maintain pulmonary capillary wedge pressure in the 7-9 mmHg range. The MAP decrease was the same in both groups, as were perioperative blood replacement (mean 500 ml), and postoperative haematocrits. Total perioperative fluid replacement was higher (p less than 0.01) in Group I (mean 2500 ml) than in Group II (mean 1300 ml). Venous tone was more affected by SNP than by ISO. ISO decreased the systemic vascular resistance index and oxygen consumption (VO2) without any change in CI or in Qs/Qt, in contrast to SNP which increased CI, VO2 and Qs/Qt.
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PMID:Systemic haemodynamic and metabolic effects of deliberate hypotension with isoflurane anaesthesia or sodium nitroprusside during total hip arthroplasty. 382 98

Activation of the sympathetic nervous system occurs in response to desflurane, causing tachycardia and hypertension. Fentanyl partially blunts the hemodynamic effects of desflurane but fails to attenuate the sympathetic response. This study determined the clinical effectiveness and dose response of alfentanil on the neurocirculatory responses to desflurane. Twenty-five healthy, male volunteers were randomized into one of three groups to receive either placebo (n = 9), 10 micrograms/kg intravenous (IV) bolus alfentanil (n = 9), or 20 micrograms/kg IV bolus alfentanil (n = 7) in conjunction with anesthetic induction by propofol, 2.5 mg/kg. Mean arterial pressure (MAP, radial artery), heart rate (HR), and efferent muscle sympathetic nerve activity (SNA, peroneal nerve) were recorded. After conscious baseline measurements, anesthesia was induced by propofol and alfentanil/placebo. One minute later, the desflurane vaporizer was activated at 11%. Neurocirculatory measurements were recorded for 11 min. There were no differences between the groups at conscious baseline. Induction of anesthesia was associated with significantly decreased MAP in the placebo and the 10 micrograms/kg alfentanil groups and increased HR in all groups with little change in SNA. In placebo subjects, desflurane administration increased HR and MAP above baseline. In both alfentanil groups, during desflurane administration HR and MAP never increased significantly above baseline. However, SNA was significantly increased in both groups. Alfentanil effectively blunts the hemodynamic changes but not the sympathetic responses associated with rapid increases in the inspired concentration of desflurane.
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PMID:Alfentanil modifies the neurocirculatory responses to desflurane. 871 95

Despite opioids are routinely used for analgesia in head injured patients, the effects of such drugs on ICP and cerebral hemodynamics remain controversial. Cerebrovascular autoregulation (CAR) could be an important factor in the ICP increases reported after opioid administration. In order to describe the effects on intracranial pressure of fentanyl and correlated such effects with autoregulation status, we studied 30 consecutive severe head injury patients who received fentanyl (2 micrograms/kg) intravenously over one minute. Prior to study, CAR was assessed. Monitoring included MAP, HR, SaO2, ETCO2, SjO2 and ICP. Changes in cerebral blood flow (CBF) were estimated from relative changes in AVDO2. Patients mean GCS was 5.7 +/- 1.7 (mean +/- STD) and mean ICP on admission was 23.8 +/- 16.3 mmHg. Fentanyl caused significant increases in ICP and decreases in MAP and CPP, but CBF remained unchanged when estimated by AVDO2. In patients with preserved CAR (34.5%), opioid-induced ICP increase was greater (but not statistically significant) than in those with impaired CAR (65.5%). We conclude than fentanyl moderately increased ICP and decreased MAP and CPP. Our data suggests that in patients with preserved CAR, potent opioids could cause greater increases of ICP, probably due to activation of the vasodilatadory cascade.
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PMID:Effects on intracranial pressure of fentanyl in severe head injured patients. 977 29

Hypotension after traumatic brain injury (TBI) has been associated with significant reductions in cerebral blood flow (CBF) in experimental animals. In humans, posttraumatic hypotension is associated with significantly worsened outcome, possibly because of cerebral hypoperfusion. The existence of opioid receptor-mediated cerebrovascular dilatory effects in humans has been theorized. We studied the systemic and cerebral vascular effects of fentanyl after fluid-percussion injury (FPI) TBI in isoflurane-anesthetized cats. In an approved protocol, 17 fasted cats were anesthetized, mechanically ventilated with 1-1.5% isoflurane in 70% N2O/30% O2, and prepared for FPI. Electroencephalogram (EEG) and intracranial pressure (ICP) were monitored. Cerebral blood flow and cardiac output were measured with radiolabelled microspheres. Animals received moderate FPI (2.2 atm) followed by 15 min of stabilization. Cats were then randomized to control (isoflurane anesthesia plus saline placebo) or fentanyl (isoflurane anesthesia plus fentanyl 50 microg x kg(-1) h(-1)) groups. CBF, EEG, and ICP were recorded at baseline (Baseline), 15 min post-FPI (post-FPI), and at 15, 75, and 135 min after beginning fentanyl or saline placebo infusions (INF 15, INF 75, INF 135). EEG, ICP, PaCO2, PaO2, pH, and temperature were similar between groups. Mean arterial pressure was significantly lower than in the control group after fentanyl administration, while total CBF was not significantly different from control values. In a previous study, decreasing MAP to 80 mm Hg after TBI in isoflurane-anesthetized cats resulted in a 30% decrease in CBF. In this study, fentanyl after TBI significantly decreased MAP but not CBF. Fentanyl administration was associated with preservation of CBF despite hypotension. Further research is necessary to evaluate the effects of fentanyl on cerebral autoregulation after TBI.
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PMID:Fentanyl infusion preserves cerebral blood flow during decreased arterial blood pressure after traumatic brain injury in cats. 984 Jul 71