Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phencyclidine derivative ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist with the thalamo-neocortical projection system as the primary site of action. Racemic ketamine consists of the enantiomers S(+)-ketamine and R(-)-ketamine. Racemic ketamine has never been considered an adequate anaesthetic agent in neurosurgical patients since it produces regionally specific stimulation of cerebral metabolism (CMRO2) and increases cerebral blood flow (CBF) and intracranial pressure (ICP). However, recent experiments suggest that both tracemic ketamine and S(+)-ketamine may reduce infarct size in animal models of incomplete cerebral ischaemia and brain injury. This experimental protective effect appears to be related to decreases in Ca++ influx and maintenance of brain tissue magnesium levels due to NMDA and quisqualate receptor blockade by ketamine. Studies in dogs have shown that racemic ketamine (2.0 mg/kg) increases CBF in the presence of the cerebral vasodilator N2O. In contrast, studies in rats without background anaesthesia showed increases in CBF after racemic ketamine (100 mg/kg i.p.). This suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Cerebrovascular CO2 reactivity was maintained regardless of the baseline cerebrovascular resistance. There are several mechanisms by which racemic ketamine may increase CBF. It induces dose-dependent respiratory depression with consequent mild hypercapnia in spontaneously ventilating subjects. This produces vasodilation due to the intact cerebrovascular CO2 reactivity. Racemic ketamine also induces regional neuroexcitation, which leads to stimulation of cerebral glucose consumption in the limbic, extrapyramidal, auditory, and sensory-motor systems. This regional neuroexcitation with increased CMRO2 produces increases in CBF that can be blocked by infusion of barbiturates or benzodiazepines. However, increases in CBF with racemic ketamine (1 mg/kg) may also occur during normocapnia and without changes in CMRO2. This effect is related to some additional direct cerebral vasodilating potency of racemic ketamine based on a mechanism involving blockade of Ca++ channels. The effects of racemic ketamine on CBF autoregulation have not been investigated systematically. However, studies in rats have shown that CBF autoregulation was maintained with low- and high-dose S(+)-ketamine. Infusion of racemic ketamine alters intracranial volume and ICP. Studies in spontaneously ventilating pigs with and without intracranial hypertension have shown that racemic ketamine (0.5-5.0 mg/kg) produces increases in PaCO2 and ICP. In contrast, identical experiments with mechanical ventilation and controlled PaCO2 showed no changes in ICP following racemic ketamine infusion. This implies that increases in ICP are related to inadequate ventilation with consecutive hypercapnia and increases in intracranial blood volume. However, mechanical ventilation may not be sufficient to control ICP following racemic ketamine. Experiments in mechanically ventilated dogs indicate that racemic ketamine (2 mg/kg) increases cerebral blood volume and ICP even in the presence of normoventilation, a response that is reversible by hyperventilation or the administration of diazepam. Studies in patients have shown that racemic ketamine (2.0 mg/kg) reduces CBF in the presence of cerebral vasodilators like halothane or N2O. In contrast, studies in unanaesthetised humans showed increases in CBF after racemic ketamine (2-3 mg/kg). This observation is consistent with animal studies and suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Studies in humans with and without intracranial pathology confirm the data from animal experiments. (ABSTRACT TRUNCATED)
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PMID:[Ketamine racemate and S-(+)-ketamine. Cerebrovascular effects and neuroprotection following focal ischemia]. 916 80

Desflurane has been reported to cause tachycardia and hypertension during induction of anaesthesia. The aim of this study was to determine the effects of desflurane on cerebral blood flow (CBF) velocity using transcranial Doppler ultrasonography in a setting that closely resembled usual clinical practice. In two groups (n = 9 in each) ASA Grade I or II patients, anaesthesia was induced with etomidate and vecuronium intravenously (i.v.), sufentanil (0.3 microgram kg-1 i.v.) was added in the second group. Patients were ventilated by facemask for 2 min before desflurane was administered in steps of 0.5 MAC min-1 until 1.5 MAC was reached and maintained for 7 min. Haemodynamic variables and CBF velocity in the middle cerebral artery (MCA) were monitored throughout the study period. In group 1 heart rate increased to 108 +/- 2 b.p.m. (37% increase) whereas MAP increased to 114 +/- 6 mmHg after administration of desflurane (33% increase). CBF velocity increased to 86 +/- 7 cm s-1 (69% increase). In group 2 no significant changes in systemic haemodynamic responses were measured after desflurane administration; however, CBF velocity increased to 73 +/- 5 cm s-1 (59% increase). The results indicate that desflurane increases CBF velocity concurrently with induction of tachycardia and hypertension. Although sufentanil and N2O attenuate the systemic haemodynamic alterations caused by desflurane, the CBF velocity increases. These data suggest that the abrupt addition of desflurane may have adverse consequences in patients at risk for intracranial hypertension.
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PMID:Administration of sufentanil and nitrous oxide blunts cardiovascular effects of desflurane but does not prevent an increase in middle cerebral artery blood flow velocity. 925 67

Effects of some methods of total anesthesia on the cerebral bloodflow and cerebrovascular reactivity was studied by transcranial dopplerography. Ketamine appreciably increases the cerebral bloodflow if no benzodiazepines are injected simultaneously. In patients with intracranial abnormalities ketamine can increase intracranial hypertension and disorder the cerebral perfusion. Despite the manifest hypotensive effect of diprivan, the autoregulation reserve of the cerebral bloodflow is not changed, probably due to the indirect vasoconstrictive effect of the drug. Total anesthesia with N2O and fentanyl virtually does not influence brain circulation.
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PMID:[Effects of several methods of general anesthesia on the cerebral blood flow and cerebrovascular reactivity: transcranial dopplerography data]. 961 69

In the past several years, improvements in technology have advanced the monitoring capabilities for patients with TBI. The primary goal of monitoring the patient with TBI is to prevent secondary insults to the brain, primarily cerebral ischemia. Cerebral ischemia may occur early and without clinical correlation and portends a poor outcome. Measurement of ICP is the cornerstone of monitoring in the patient with TBI. Monitoring of ICP provides a measurement of CPP and a rough estimation of CBF. However, with alterations in pressure autoregulation, measurement of CPP does not always allow for determination of CBF. To circumvent this problem, direct measurements of CBF can be performed using clearance techniques (133Xe, N2O, Xe-CT) or invasive monitoring techniques (LDF, TDF, NIRS). Although direct and quantitative, clearance techniques do not allow for continuous monitoring. Invasive CBF monitoring techniques are new, and artifactual results can be problematic. The techniques of jugular venous saturation monitoring and TCD are well established and are powerful adjuncts to ICP monitoring. They allow the clinician to monitor cerebral oxygen extraction and blood flow velocity, respectively, for any given CPP. Use of TCD may predict posttraumatic vasospasm before clinical sequelae. Jugular venous saturation monitoring may detect clinically occult episodes of cerebral ischemia and increased oxygen extraction. Jugular venous saturation monitoring optimizes the use of hyperventilation in the treatment of intracranial hypertension. Although PET and SPECT scanning allow direct measurement of CMRO2, these techniques have limited application currently. Similarly, microdialysis is in its infancy but has demonstrated great promise for metabolic monitoring. EEG and SEP are excellent adjuncts to the monitoring arsenal and provide immediate information on current brain function. With improvements in electronic telemetry, functional monitoring by EEG or SEP may become an important part of routine monitoring in TBI.
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PMID:Monitoring in traumatic brain injury. 1008 12

The postoperative pain treatment is one of important factors of a successful outcome after kidney transplantation. Improperly controlled pain leads to agitation, tachycardia, hypertension and increases risk of respiratory complications. Many studies have demonstrated good analgetic effect of morphine delivered by the method of patient controlled analgesia (PCA). Because the intensity of postoperative pain in end-stage kidney insufficiency patients can be modified by the type of received anaesthesia, it was decided to analyze the influence of standardized general anaesthesia on postoperative morphine consumption. 140 (ASA III) patients scheduled for kidney transplantation were included. Patients were divided into four groups; group K (control)--anaesthetised with fentanyl and N2O, group 1--fentanyl, N2O plus halothane, group 2--fentanyl, N2O plus propofol, group 3--fentanyl, N2O plus isoflurane. After operation and initial loading dose, PCA infusion of morphine was started. Bolus doses were set to 30 ug/kg, and lockout interval 10 min. Our results suggest that observed greater morphine consumption after GA with the use of propofol is connected with better psychomotor functions. In that group patients were better oriented and more efficiently controlled the PCA pump and pain.
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PMID:The influence of the type of anaesthesia on postoperative pain after kidney transplantation. 1085 Jun 7

An 83-yr-old, 44-kg woman with a 2-month history of abdominal distension received diagnostic laparoscopy. Except for chronic treated hypertension, she was healthy. The preoperative chest X-ray demonstrated small pleural effusion occupying the lower left hemithorax, but she did not present with dyspnea or chest pain. After premedication with intravenous ranitidine 50 mg, anesthesia was induced with thiopental 150 mg, vecuronium 7 mg and maintained by 1-2% sevoflurane in 50% N2O/O2. SpO2 decreased after insufflation of CO2, but breath sound was audible on both lungs. At completion of operation, chest X-ray revealed the left hemilateral hydrothorax and 650 ml of pleural fluid was suctioned. Blood gas improved and the tracheal tube was removed. The diagnosis of tuberculous peritonitis was established by the demonstration of granulomas of the peritoneum. We speculated on four reasons for the increased pleural effusion on the left thorax: 1) Increase of systemic and capillary pressure caused by CO2 insufflation. 2) Increase of capillary permeability by tuberculous pleuritis. 3) Decrease of colloid osmotic pressure by hypoalbuminemia. 4) Decreased pleural fluid removal because of venous compression caused by increased intrathoracic pressure. Peritoneal insufflation of CO2 to create the pneumoperitoneum may induce hydrothorax in patients with tuberculous pleuritis.
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PMID:[Hydrothorax during diagnostic laparoscopy]. 1121 54

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.
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PMID:Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors. 1142 92

The main objective for anaesthesia in patients with intracranial hypertension (ICH) is to maintain the cerebral perfusion pressure (CPP). Before the operation, the assessment of the level of intracranial pressure relies on the Glasgow coma score and the signs of ICH on the CT-scan. In the perioperative period, repeated transcranial Doppler examinations may help in determining the adequate CPP. Haemodynamic and respiratory complications are common after subarachnoid haemorrhage or head injury. Careful preoperative screening of the cardiovascular and respiratory system is mandatory before anaesthesia. There is no recommended anaesthetic technique for patients with ICH. Nitrous oxide should be avoided in patients with severe ICH or during emergency surgery. Theoretically, intravenous anaesthesia is a better choice than inhalation anesthesia because of the cerebral vasodilatation induced by inhalation agents. In the most severe cases thiopental is the only anaesthetic agent to consider. Treatment of hypovolaemia with fluid loading and the early use of vasoactive agents can be recommended to maintain CPP. Before intracranial surgery, large doses of mannitol have been demonstrated to improve neurological recovery in brain injured patients. The urinary losses due to the infusion of mannitol should be replaced with isotonic saline. Emergence and extubation are best performed in the intensive care unit under close systemic and cerebral haemodynamic control.
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PMID:[Anaesthesia for patients with intracranial hypertension due to cerebral oedema]. 1274 91

In order to evaluate the safety of the new synthetic opioids, alfentanil and sufentanil, in neurosurgical patients, we administered sufentanil 1 microg/kg i.v., alfentanil 50 microg/kg i.v. followed by an infusion of 1 microg/kg/min, or fentanyl 5 microg/kg i.v. to 30 patients with supratentorial tumors anesthetized with nitrous oxide (N2O), 60% in O2. Lumbar cerebrospinal fluid pressure (CSFP) and mean arterial pressure (MAP) responses were recorded for 10 min thereafter, while ventilation was held constant [mean PaCO2 = 36.1 +/- 1.0 mm Hg (SEM)]. There was no change in CSFP after fentanyl. In contrast, both sufentanil and alfentanil caused increases in CSFP, equal to 89 +/- 31 % SE (p < 0.05) and 22 +/- 5% (p < 0.05), respectively. MAP decreased after administration of each opioid. Peak decreases in cerebral perfusion pressure (MAP - CSFP) were 14 +/- 3% after fentanyl, 25 +/- 5% after sufentanil, and 37 +/- 3% after alfentanil. It is concluded that because sufentanil increased CSFP in patients who have brain tumors, it also may be contraindicated in other neurosurgical patients at risk for intracranial hypertension. Alfentanil may share this propensity, since CSFP increased despite a profound reduction in MAP. Among the three opioids evaluated, only fentanyl appears to be appropriate for supplementing N2O-2 anesthesia in patients who have compromised intracranial compliance.
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PMID:Sufentanil, alfentanil, and fentanyl: impact on cerebrospinal fluid pressure in patients with brain tumors. 1581 32

Cerebral blood flow measurements using a thermal diffusion technique were made in conjunction with an extensive cardiovascular evaluation, during and after administration of intravenous labetalol given for blood pressure control in craniotomy patients. Eighteen patients, ages 30-65 years, ASAII and III, scheduled for elective craniotomy, became hypertensive during emergence and recovery from a pentothal/fentanyl/vecuronium/N2O/isoflurane general anesthesia. Labetalol was administered in a stepwise manner every 10 minutes during an average period of 1 h. After this titration period, an 8-h maintenance period followed. During titration and maintenance periods, comprehensive systemic hemodynamic parameters were collected through intra-arterial and flow-directed pulmonary artery catheters. Cerebral cortical blood flow (CBF) was continuously recorded using a thermal diffusion cortical blood flow probe (Saber System). Data were analyzed using variance F tests to evaluate changes from baseline over time. Labetalol controlled postoperative hypertension in all cases with a total dose range of 0.4-6.8 mg/kg. During titration, statistically significant decreases in blood pressure were obtained, accompanied by a small decrease in systemic vascular resistance (SVR) and slight increase in cardiac index (CI). Heart rate decreased in a manner directly proportional to the dose of labetalol administered. In the maintenance period, further decreases in blood pressure and heart rate were observed, with significant decreases in central venous pressure, pulmonary capillary wedge pressure, and SVR and an increase in CI. All values remained within normal ranges and no adverse effects were observed. CBF decreased slightly during the study period, although not significantly (from 67 +/- 8 to 57 +/- 7 ml 100 g min). Blood pressure control achieved with labetalol in postoperative neurosurgical patients seems to be the result of mild alpha-adrenoceptor blocking effects (i.e., reduced SVR) and beta-adrenoceptor blocking effects (i.e., reduced heart rate) at higher doses. The 6-8 h duration of effect of labetalol was enough to control postoperative hypertension in all patients with no additional therapy. Compared with alternative drugs available for blood pressure control in similar clinical conditions, labetalol appears to be reliable, safe, and effective, by providing a lasting effect with no evidence of rebound hypertension, increased CBF, or cardiac dysfunction.
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PMID:Cerebral blood flow measurements during blood pressure control with intravenous labetalol following craniotomy. 1581 60


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