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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isoflurane was selected as the main agent for induction and maintenance of anesthesia in two patients scheduled for resection of pheochromocytoma. The inspired concentration was calculated with a pocket computer (Sharp PC 1401) and adjusted to maintain an alveolar concentration of 1.5 to 1 MAC. With this technique, a stable heart rate was observed, without arrhythmias. The blood pressure stabilised at normal levels before surgery and only moderate hypertension was seen during tumor manipulation. No specific antihypertensive medication was needed. Transient hypotension after tumor resection was treated with ephedrine and volume replacement. Recovery of anesthesia was rapid and uneventful.
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PMID:Isoflurane anesthesia for resection of pheochromocytoma. A report of two cases. 652 86

MAC BAR, the minimum end-tidal alveolar anesthetic concentration that inhibits adrenergic response to a noxious stimulus in 50% of subjects, is a quantifiable physiological parameter that can be used to determine potency and therapeutic indices of volatile anesthetics. We wished to determine whether there is a minimal intraarterial plasma concentration (MIC BAR) of an opiate such as fentanyl that will prevent a hypertensive response to noxious stimuli in 50% of patients undergoing aortocoronary bypass surgery (ACBP). Forty-three patients with good left ventricular function were studied. All patients were premedicated with diazepam, morphine, and scopolamine. Five groups of patients were anesthetized with different fentanyl anesthesia protocols, each designed to produce different plasma fentanyl concentrations (PFC). A 20% increase in systolic blood pressure compared to control was considered an adrenergic response that related to the plasma fentanyl concentration inferred from each patient's PFC time-concentration curve. Only four patients became hypertensive with a PFC greater than 20 ng/ml. One patient became hypertensive at intubation with a PFC of 12.3 ng/ml. There was no statistically significant difference in the mean PFC in patients who became hypertensive at each event. During aortic dissection, when significantly more patients became hypertensive, there was no difference in the incidence of hypertension in patients with a PFC above or below 20 ng/ml. Two patients became hypertensive at skin incision with a PFC over 30 ng/ml. A MIC BAR could not be identified because of the great variability in the PFC of patients who became hypertensive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Narcotic requirements for intravenous anesthesia. 660 97

This study explored the effectiveness of oral clonidine premedication in attenuating sympathetic activation, tachycardia, and hypertension triggered by desflurane. After institutional review board approval, informed consent was obtained from 15 young, healthy male volunteers. Heart rate (HR, electrocardiogram), mean arterial pressure (MAP, radial artery catheter), and central venous pressure (CVP, jugular vein) were monitored. Recordings of sympathetic nerve activity (SNA) were obtained from the peroneal nerve via percutaneously placed tungsten needles. After baseline recordings, subjects were randomized to receive either a placebo (n = 10) or 0.3 mg of clonidine (n = 9) per os (PO). One hour later, repeat recordings were obtained. Propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg) were given intravenously. Ventilation via a mask (100% O2) was used to maintain normocarbia. Two minutes after propofol administration, the desflurane vaporizer was set at 3.6% (0.5 minimum alveolar anesthetic concentration [MAC]) and increased at 1-min intervals to 7.2% and 11% (1.0 and 1.5 MAC). After 10 min, the trachea was intubated and 20 min later steady-state neurocirculatory recordings were obtained at 5.4%, during the first 5 min after advancing the vaporizer from 5.4% to 11% ("transition"), and at 11%. Resting HR, MAP, and SNA were similar between the two groups. PO clonidine reduced SNA, CVP, and MAP but did not change HR. In both groups propofol decreased SNA and MAP, and increased HR. The administration of desflurane via a mask resulted in significant increases in SNA, HR, and MAP. Clonidine reduced the HR and MAP responses by approximately 30%-40% during induction and transition periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine on desflurane-mediated sympathoexcitation in humans. 789 34

Tachycardia and hypertension usually accompany laryngoscopy and tracheal intubation. This response is undesirable, especially in patients with cardiovascular or intracranial diseases. Esmolol is a cardioselective, ultrashort-acting beta adrenergic blocking agent with a very short half-life. The efficacy of bolus dose of esmolol in blunting hemodynamic responses during laryngoscopy and tracheal intubation was evaluated. 45 patients (15 in each group) of ASA physical status I and II scheduled for elective non-cardiac surgery were included in this randomized, placebo-controlled study. At time zero, the study preparation (placebo, 100 or 200 mg of esmolol) was administered intravenously, followed by thiopentone 5 mg/kg and succinylcholine 1.5 mg/kg for induction. Tracheal intubation was performed 2 minutes after time zero. Anesthesia was maintained with 50% nitrous oxide and 1.0 MAC halothane in oxygen, and vecuronium 0.08 mg/kg. Heart rate (HR) and systolic blood pressure (SBP) were recorded every minute for 10 minutes. To compare with the placebo group, there was a significant decrease in either HR or SBP in 200 mg group in the 8 minutes course after intubation (p < 0.05). There was a significant decrease in HR in the 100 mg group at the 3rd, 4th, and 5th minutes when compared with the placebo group (p < 0.05). The differences in SBP between the 100 mg group and placebo group were significant at the 3rd and 4th minutes (p < 0.05). Both bolus dosages of esmolol could effectively attenuate the tachycardia and hypertension produced by laryngoscopy and tracheal intubation. Furthermore, esmolol 200 mg presented a better hemodynamic stability than esmolol 100 mg during induction of anesthesia.
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PMID:The effect of single bolus dose of esmolol for controlling the tachycardia and hypertension during laryngoscopy and tracheal intubation. 792 58

Carbon black is a commercial product manufactured under controlled conditions. It is not considered as a carcinogenic substance. It is even assumed that it reduces considerably carcinogenesis of substances adsorbed on its surface. The aim of the study was to present the condition of the circulatory system of workers involved in the carbon black production. The study covered the group of exposed persons (n = 118) and the control group (n = 241). The results of environmental studies indicated excess of dust MAC values at work posts. It was concluded that exposure to carbon black was harmful to health of workers employed in its production, especially in the case of a long-term exposure to dust concentrations exceeding MACs. Hypertension occurs more frequently in persons exposed, and smoking proved to be an additional pathogenic factor affecting health of this group of workers. Pathogenesis of hypertension is unknown and investigations should be continued.
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PMID:[The circulatory system in workers involved in carbon black production]. 799 49

Ohmeda PPD is counting on desflurane's decreased solubility, which provides improved control of anesthetic level and allows faster recovery, and its reduced toxicity to the liver and kidney to sufficiently differentiate it from its competitor, isoflurane, to make it the inhalation anesthetic of choice in the future. However, even though initial interest has been high, resistance has arisen for several reasons: Desflurane's high MAC requires reduced fresh-gas flows to keep its rate of consumption down. It may not be suitable for certain applications (e.g., for induction of pediatric patients, for use with patients with tachycardia or hypertension). It is usually necessary to supplement it with an injectable agent for induction. Even though it is superior to other agents with respect to speed of initial recovery, no striking advantage relative to time of discharge from the hospital has been demonstrated. Agent monitors will need to be upgraded or new monitors will need to be purchased if the drug is to be measured. The future prices of the drug and its vaporizer are not certain. All of these factors must be considered before committing to this new technology.
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PMID:Desflurane (Suprane). Considerations for introducing the new inhalation anesthetic agent into clinical practice. 803 14

Ornipressin (OR), a synthetic derivative of natural vasopressin, is widely used in combination with local anaesthetics in order to reduce surgical bleeding and systemic absorption of the local anaesthetic. As shown previously in experimental studies, OR causes severe coronary vasoconstriction. The myocardial oxygen balance is compromised by an increase in myocardial oxygen demand due to hypertension and impaired oxygen delivery following coronary vasoconstriction. We describe the case of a 19-year-old male who was admitted to the hospital for elective tonsillectomy. There was no evidence of systemic or cardiovascular disease (ASA I). Following the induction of anaesthesia with thiopentone 4 mg/kg and ventilation with N2O/O2 (FiO2:0.25), vecuronium was administered to facilitate orotracheal intubation. Anaesthesia was maintained with N2O/O2 (FiO2:0.33) and 2 MAC isoflurane. After reaching an anaesthetic steady state with stable haemodynamic conditions, peritonsillar infiltration with a prilocaine solution containing a total of 0.8 IU OR (0.1 IU/ml) produced marked tachycardia and hypertension. Concomitantly, distinct ST-segment-depression was observed in a lead II ECG. Hypertension and tachycardia occurred within 3 min after the local infiltration with prilocaine/OR. Maximum ST-segment depression and haemodynamic changes were recorded 11 min after infiltration, with an increase in heart rate from 58 to 136 min and a rise in blood pressure from 115/50 to 217/130 mmHg. Considering experimental results, the ECG changes in this case show clear evidence that even in healthy humans OR-induced systemic haemodynamic changes may be complicated by severe myocardial ischaemia due to coronary vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Signs of a severe myocardial ischemia following peritonsillar infiltration with ornipressin (POR 8)]. 831 91

We have studied the effects of magnesium on atrioventricular (AV) conduction times and surface electrocardiogram during both sinus rhythm and atrial pacing in seven dogs anaesthetized with 1 MAC of sevoflurane. A bolus dose of magnesium sulphate (MgSO4) 30, 60 and 90 mg kg-1 significantly increased plasma magnesium concentrations from 1.3 (SEM 0.1) to 15.3 (1.3) mg dl-1. MgSO4 significantly prolonged A-H (AV nodal conduction time during sinus rhythm), St-H (intra-atrial and AV nodal conduction time during atrial pacing) and H-S (total ventricular conduction time) intervals at doses > or = 30 mg kg-1 ; H-V interval (His-Purkinje conduction time) at doses > or = 60 mg kg-1; RR and PR intervals and QRS duration at doses > or = 30 mg kg-1 in a dose-related manner during both sinus rhythm and atrial pacing. QTc interval remained unchanged during sinus rhythm. The doses of MgSO4 used did not have deleterious effects on AV conduction times and surface electrocardiogram during 1 MAC of sevoflurane anaesthesia. This finding suggests that MgSO4 in high doses was safe and may be indicated for cardiac arrhythmia and hypertension during sevoflurane anaesthesia. However, further study is required to apply these findings to clinical anaesthesia.
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PMID:Effects of magnesium sulphate on atrioventricular conduction times and surface electrocardiogram in dogs anaesthetized with sevoflurane. 905 8

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

Barbiturates, etomidate and propofol decrease cerebral blood flow (CBF), mediated by a decrease in cerebral metabolism, thus decreasing intracranial pressure (ICP). As the reduction in CBF is secondary to a decrease in cerebral metabolism, these agents will have little effect on CBF or ICP in patients without active cerebral metabolic activity. Ketamine is usually not administered for the anaesthetic management of patients at risk of intracranial hypertension because of the reported increases in cerebral metabolism, CBF and ICP. The increase in CBF, however, may be partly mediated by a sympathetically induced increase in blood pressure and partly by a simultaneous increase in PaCO2 in spontaneously breathing patients. More recent studies report no increase in ICP or flow when ventilation is controlled or when other agents are associated. There is renewed interest in ketamine because it blocks excitatory amino acid receptors in the brain. Synthetic opioids including fentanyl, sufentanil, and alfentanil have been reported to cause an increase in ICP in patients with various intracranial lesions. When blood pressure was supported, no clinically relevant increase in ICP or flow velocity with alfentanil or sufentanil was observed. Thus, the increase in ICP reported with these agents may be related to the compensatory autoregulation-mediated vasodilation, underscoring the importance of administering these agents carefully to avoid systemic hypotension. Halothane consistently increases CBF and should not be used in patients with increased ICP. In contrast, isoflurane does not cause increase in CBF at concentrations below 1 to 1.5 MAC, although the effects on cerebral blood volume are less clear. Desflurane and sevoflurane have similar effects. CO2 reactivity is preserved with all inhaled agents. In patients with increased ICP however, it would be preferable to avoid these agents or to administer very low doses.
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PMID:[Effects of anesthetic agents on intracranial pressure]. 975 May 96


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