Hemodynamic effects of KRN2391 (potassium channel opener) in halothane-anesthetized dogs

The cardiovascular responses to an infusion of KRN2391, a potassium channel opener, was studied in halothane-anesthetized dogs. Intravenous administration of KRN2391 at 1.0 and 5.0 μg·kg⁻¹·min⁻¹ for 60 min produced dose-dependent decreases in mean arterial pressure (MAP) and systemic vascular resistance (SVR) associated with dose-dependent increases in the cardiac index (CI) and stroke volume index (SVI) but was not accompanied by an increase in heart rate (HR). The maximum decrease in MAP during the infusion of KRN2391 at 1.0 and 5.0 μg·kg⁻¹·min⁻¹ was −13±7% (P<0.01) and −37±10% (P<0.01), respectively. The maximum reduction in SVR after 1.0 and 5.0 μg·kg⁻¹·min⁻¹ was −20±11% (P<0.01) and −60±16% (P<0.01), respectively. A KRN2391 infusion of 1.0 and 5.0 μg·kg⁻¹·min⁻¹ increased Cl a maximum of 11±13% (P<0.05) and 65±33% (P<0.01), respectively. KRN2391 1.0 μg·kg⁻¹·min⁻¹ showed a tendency to increase SVI but this change was not significant, KRN2391 5.0 μg·kg⁻¹·min⁻¹, however, produced a significant increase in SVI. The present results demonstrate that the decrease in MAP and the increases in CI and SVI caused by KRN2391 are due to a reduction in the afterload. Therefore, we conclude that these cardiovascular profiles of KRN2391 may be benificial in perioperative uses including the control of systemic blood pressure and the treatment of hypertension during halothane anesthesia in clinical practice.     

Effect of phenylephrine on histamine-induced bronchoconstriction in dogs

Purpose Although an α-adrenoceptor has been suggested to be involved in the mechanism of asthma, the effect of α₁-agonist on the airway is still unclear. In this study we evaluated the effect of phenylephrine on the airway with a direct visualization method using a superfine fiberoptic bronchoscope (SFB). Methods Seven mongrel dogs were anesthetized with pentobarbital (30 mg·kg⁻¹ IV) and paralyzed by pancuronium (0.2mg·kg⁻¹·h⁻¹). The trachea was intubated with an endotracheal tube (ID 7 mm) that has a second lumen for insertion of a SFB (OD 2.2 mm) to monitor the bronchial cross-sectional area (BCA) continuously. The tip of a SFB was placed at the level between the second and third bronchial bifurcation. To assess hemodynamics, the direct arterial blood pressure (ABP) and pulmonary arterial pressure (PAP) were monitored via a femoral arterial catheter and Swan-Granz catheter. Bronchoconstriction was elicited by histamine (10 μg·kg⁻¹+ 500 μg·kg⁻¹·h⁻¹_. At 30 min after the histamine was started, saline or phenylephrine (1, 10, and 100μg·kg⁻¹) was given intravenously. The BCA and hemodynamic variables were assessed before (basal) and 30 min after the histamine was started and 5 min after saline and each phenylephrine dose. Results Histamine reduced BCA by 40.3±6.3%. Phenylephrine at 10 and 100 μg·kg⁻¹ significantly increased the ABP and PAP; and it significantly decreased the BCA, by 6.5±6.9% and 14.2±7.9%, respectively. Plasma epinephrine and norepinephrine were also significantly reduced following phenylephrine 100 μg·kg⁻¹ IV. Conclusion The dose of phenylephrine that produced vasopressive actions worsened the histamine-induced bronchoconstriction slightly but significantly. Therefore, phenylephrine should be used with caution in asthmatic patients.     

Effects of fentanyl on cardiovascular and plasma catecholamine responses in surgical patients

Purpose. Whether opioids administered before skin incision, under inhalational anesthesia, improve cardiovascular and plasma catecholamine responses to surgical stimulation compared with those administered after skin incision remains unclear. We compared the effects of fentanyl injected before and after skin incision on these responses. Methods. We studied 50 healthy female patients [American Society of Anesthesiologist (ASA) physical status 1] who underwent elective total abdominal hysterectomy through an infraumbilical incision (midline incision) under nitrous oxide (60%)–oxygen–isoflurane (1.2%) anesthesia. Fentanyl (2.0 or 4.0 μg·kg⁻¹) was administered IV 5 min before (pretreatment group) or 5 min after (posttreatment group) skin incision. Control patients received a saline injection. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded 1 min before incicsion and serially for 30 min afterward. Plasma levels of norepinephrine (Nor) and epinephrine (Epi) were determined 1 min before incision and serially up to 20 min after skin incision. Results. The MAP response to incision had decreased after 10 min in posttreatment fentanyl (2 μg·kg⁻¹) (P < 0.05) and after 8, 10, 15, and 20 min in posttreatment fentanyl (4 μg·kg⁻¹) (P < 0.05). At the same doses, fentanyl administered before skin incision attenuated MAP response to incision after 1 min with the smaller dose (P < 0.05) and after 1, 3, 5, 6, 8, 10, 15, and 20 min with the higher dose (P < 0.05). Fentanyl suppressed Epi response to surgery 8 and 20 min after skin incision (P < 0.05) at both doses, except for 8 min after incision in pretreatment fentanyl (2 μg·kg⁻¹). Overall, the hemodynamic and sympathoadrenergic responses after skin incision were attenuated, with the exception of plasma Nor after fentanyl irrespective of time and dose. Conclusions. Our results indicated that fentanyl depressed cardiovascular and plasma catecholamine responses irrespective of the time of administration, and that the higher dose of fentanyl produced a greater suppression of MAP and HR responses. In addition, the depressant effects on MAP of high-dose fentanyl administered 5 min before skin incision lasted longer than when injected 5 min after incision. At both doses, the opioid attenuated the rise in plasma Epi, but not Nor. Received: November 9, 2001 / Accepted: March 18, 2002     

Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats

Purpose  Dexmedetomidine has been used for purposes of anesthesia and sedation, and experimental studies have demonstrated its neuroprotective effects. However, it has also been shown that the constriction of cerebral vessels in response to high doses of dexmedetomidine decreases cerebral blood flow. We tested the hypothesis that dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic cerebral injury. Methods  The effects of dexmedetomidine on cerebral blood flow and mean arterial blood pressure were studied first. Six rats received intravenous infusions of dexmedetomidine in doses ranging from 0.01 to 10 μg·kg⁻¹·min⁻¹. At the end of this phase of treatment, the alpha-2 adrenergic antagonist yohimbine was administered (3 mg·kg⁻¹ ip). Cerebral blood flow and mean arterial blood pressure were recorded continuously. A second series of experiments was then performed using a rat model of transient middle cerebral artery occlusion. Forty-two rats received 1μg·kg⁻¹·min⁻¹ or 10 μg·kg⁻¹·min⁻¹ dexmedetomidine with or without pretreatment with either of the alpha-2 adrenergic antagonists yohimbine or rauwolscine. Five days after middle cerebral artery occlusion and reperfusion, the rat brains were removed and the infarct volumes were measured. Results  In the first protocol, increasing the dose of dexmedetomidine significantly decreased cerebral blood flow. Mean arterial blood pressure decreased to 79.9% relative to baseline with a dose of 0.01 μg·kg⁻¹·min⁻¹ dexmedetomidine, and increased to 119.9% relative to baseline with a dose of 10 μg·kg⁻¹·min⁻¹ dexmedetomidine. In the second protocol, the infarct volume in the control group was 9.5% of the total brain volume; the infarct volume increased to 11.3% in rats treated with 1 μg·kg⁻¹·min⁻¹ dexmedetomidine and the volume increased to 24.5% in rats treated with 10 μg·kg⁻¹·min⁻¹ dexmedetomidine. Pretreatment with an alpha-2 adrenergic antagonist, either yohimbine or rauwolscine, reduced the size of these high-dose dexmedetomidine-induced infarct volumes. Conclusion  Hypertension following the administration of high-dose dexmedetomidine is associated with cerebral hypoperfusion and the exacerbation of ischemic brain injury, possibly through alpha-2-induced cerebral vasoconstriction.     

Oral clonidine reduces thiamylal requirement for induction of anesthesia in adult patients

Although preanesthetic clonidine, an α-2 agonist, is known to reduce anesthetic requirements, the effect of preanesthetic oral clonidine medication per se on the requirement of thiamylal in adult humans has not yet been examined. One hundred and sixty-one adult patients (14–78 years of age) were randomly assigned to groups that received oral clonidine (5μg·kg⁻¹ (n=51), 2.5μg·kg⁻¹ (n=55), or none (n=55)) in addition to 20mg oral famotidine 90min before anesthesia induction. Thiamylal was injected at the rate of 25mg every 15 s until the eyelash reflex disappeared, while blood pressure and heart rate were recorded at 30-s intervals from the start of the induction. Thiamylal requirements were significantly less in both clonidine groups (2.95±0.09 and 3.14±0.10 mg·kg⁻¹ (mean±SE) for patients receiving 5μg·kg⁻¹ and 2.5μg·kg⁻¹ clonidine, respectively) than in the control group (3.81±0.11 mg·kg⁻¹,P<0.05); however, no difference was found between the two clonidine groups. Although mean blood pressure and heart rate during the study period were significantly lower in both clonidine groups than in the control group, no profound hypotension or marked bradycardia were noted in the clonidine groups.     

Comparative hemodynamic effects of hypotension induced by CGRP and PGE1 in dogs

Calcitonin gene-related peptide (CGRP) produces vasodilation, hypotension, and tachycardia. We compared the hemodynamic effects of CGRP-induced hypotension with the effects of prostaglandin E₁ (PGE₁), which is currently used as a hypotensive agent during anesthesia. Eighteen mongrel dogs were anesthetized with pentobarbital (25 mg·kg⁻¹), and 0.87% halothane in oxygen (1MAC). Measurements of hemodynamic variables were made before, during, and after induced hypotension. The mean arterial pressure (MAP) was lowered to 60 mmHg by the infusion of either CGRP (n=10) or PGE₁ (n=8). This decrease in MAP was appoximately 50% of the baseline value. The CGRP- and PGE₁-induced hypotension resulted in 61% and 51% maximum reductions (P<0.01, respectively) in systemic vascular resistance associated with a significant increase in stroke volume index; the two treatments, however produced inconsistent changes in cardiac index (CI). With CGRP, a maximum increase of 144% (P< 0.01) in CI was observed during induced hypotension. In contrast, PGE₁-induced hypotension caused no significant changes in CI throughout the observation period. Left ventricular maximum dP/dt decreased (P<0.01) during the hypotensive period with PGE₁, whereas it remained un-changes during CGRP-induced hypotension. The different results for changes in CI and cardiac contractility during the CGRP- and PGE₁-induced hypotension were probably due to differences in ventricular filling pressure. Hypotension induced by PGE₁ was associated with a significant decrease in heart rate (HR), whereas CGRP did not affect HR. This study shows that both CGRP and PGE₁ are effective in decreasing afterload and in inducing hypotension; the results suggest that CGRP is a useful vasodilator for inducing hypotension during halothane anesthesia. This study was presented, in part, at the Annual Meeting of the American Society of Anesthesiologists, October, 1993, Washington DC, and at the 41st Annual Meeting of the Japan Society of Anesthesiology, April, 1994, Tokyo This study was supported by a Grant-in-Aid (No 04807115) for Scientific Research (C) from the Ministry of Education, Science, Sports, and Culture, Japan     

What is the optimal dose of glucose administration during minor surgery under sevoflurane anesthesia?

Purpose. We attempted to identify the optimal infusion rate of glucose to maintain an appropriate usage of energy sources during minor surgery after an overnight fast. Methods. Forty patients scheduled for tympanoplasty or skin grafting under sevoflurane anesthesia were assigned to four groups. The patients received a 2-h infusion of either saline or glucose at a rate of 0.1, 0.2, or 0.3 g·kg⁻¹·h⁻¹. Blood samples were collected before the induction of anesthesia, and at 1 and 2 h after the start of the saline or glucose infusion. Plasma glucose, free fatty acid, β-hydroxybutyrate, acetoacetate, and immunoreactive insulin were measured. Results. Plasma glucose concentration increased dose-dependently. Immunoreactive insulin levels increased in the groups receiving 0.2 or 0.3 g·kg⁻¹·h⁻¹ of glucose infusion. Free fatty acid and ketone bodies did not increase in any glucose infusion groups. The arterial ketone body ratio increased to over 1.00 in the groups receiving 0.2 or 0.3 g·kg⁻¹·h⁻¹ of glucose infusion. Glycorrhea was observed only in the group receiving 0.3 g·kg⁻¹·h⁻¹ of glucose. Conclusion. The smaller doses of glucose (0.1–0.2 g·kg⁻¹·h⁻¹) prevented lipolysis and hyperglycemia during minor surgery. Received for publication on March 17, 1999; accepted on September 22, 1999     

Optimum priming dose of vecuronium for tracheal intubation

To determine the optimum priming dose of vecuronium, we divided 173 surgical patients into five groups according to priming dose (0, 2.5, 5.0, 7.5, and 10 μg·kg⁻¹). For endotracheal intubation, we administered a priming dose of vecuronium, and then after 4 min, the remainder was injected for a total dosage of 0.15 mg·kg⁻¹. Onset time was determined by a 95% depression of twitch height as shown by electromyography (EMG) of the hypothenar muscles. This was measured by repeating the train-of-four (TOF) stimulation. An increased priming dose shortened the onset time; however, this shortening rate diminished when the dosage was above 7.5 μg·kg⁻¹. In the zero priming dose group there was a significant correlation between onset time and age, and between onset time and body mass index (BMI) in women (r=0.62 and −0.45, respectively); however, this correlation was not observed in men. A priming dose of 10 μg·kg⁻¹ showed a decrease of TOF ratio to 95% or less in 1 out of 25 cases. Although one-third of the patients in the 5 and 7.5 μg·kg⁻¹ groups complained of clinical symptoms such as ptosis, this was clinically allowable. We conclude that the optimum priming dose of vecuronium is 7.5 μg·kg⁻¹; however, in obese patients, a smaller dosage would be recommended.     

Respiratory and cardiovascular effects of fentanyl during propofol-induced sedation under spinal anesthesia

Purpose To determine whether fentanyl augments respiratory and cardiovascular problems during propofol-induced sedation, we investigated the effects of propofol and fentanyl on respiratory and hemodynamic profiles in 30 female patients under spinal anesthesia, administering oxygen via face mask. Methods After spinal anesthesia, 20 patients were sedated with propofol (0.5 mg·kg⁻¹ bolus, 3 mg·kg⁻¹·h⁻¹), followed by administration of either 2 μg·kg⁻¹ fentanyl in group PF or normal saline in group P, whereas another 10 patients (group F) received 2 μg·kg⁻¹ fentanyl without propofol. We measured heart rate, mean arterial pressure, end-tidal carbon dioxide tension, and respiratory rate before and after treatment. We also evaluated apnea, arterial oxygen desaturation, and airway obstruction. Results Mean arterial pressure was significantly lower in group P and PF than in group F. However, there were comparable changes in heart rate in the three groups. The combination of fentanyl and propofol decreased respiratory rate and increased end-tidal carbon dioxide tension more than fentanyl or propofol alone. Although apnea occurred in groups F and PF, arterial oxygen desaturation did not occur in any of the groups. Conclusion The combination of fentanyl and propofol augmented the risks of respiratory depression and apnea compared with the use of fentanyl or propofol alone.     

Flumazenil reduces the hypnotic dose of propofol in male patients under spinal anesthesia

Purpose. Flumazenil has been reported to produce a partial benzodiazepine-agonist-like effect in some psychopharmacological examinations. This study investigated the effect of flumazenil on the hypnotic activity of propofol in 60 men scheduled for minor surgical procedures done under spinal anesthesia. Methods. After a steady state of spinal anesthesia had been reached, patients were pretreated with saline or flumazenil, 5 μg·kg⁻¹, followed by the administration of saline or midazolam, 10 μg·kg⁻¹. Then, 250 μg·kg⁻¹·min⁻¹ of propofol was infused until hypnosis was achieved. Loss of response to a simple command with a slight stimulus, served as the end-point for hypnosis. Immediately after achievement of the end-point, propofol infusion was discontinued, and a 2-ml venous blood sample was obtained from the dorsal pedis vein to determine plasma propofol concentration. Results. Flumazenil significantly decreased the dose of propofol required and the time required to achieve hypnosis compared with values in the control group (55 ± 10 [mean ± SD] vs 71 ± 14 mg and 212 ± 42 vs 268 ± 48 s, respectively; P < 0.05), whereas flumazenil attenuated the effect of midazolam in reducing the plasma concentration of propofol at hypnosis (2.9 ± 0.5 and 2.5 ± 0.6 μg·ml⁻¹, respectively; P < 0.05). Conclusion. These results suggested that flumazenil may potentiate the hypnotic properties of propofol, despite flumazenil having an antagonistic effect on the enhanced hypnotic activity of propofol induced by the coadministration of midazolam. Received: January 11, 2001 / Accepted: July 25, 2001     

RETRACTED ARTICLE: Prophylactic antiemetic therapy with droperidol in patients undergoing laparoscopic cholecystectomy

Purpose. The incidence of postoperative nausea and vomiting (PONV) following laparoscopic cholecystectomy (LC) is relatively high when no prophylactic antiemetic is given. We have studied the efficacy of a commonly used and well-established antiemetic, droperidol, for the prevention of PONV in patients undergoing LC. Methods. In a randomized, double-blind, placebo-controlled study, 60 patients received placebo (saline) or droperidol 50 μg·kg⁻¹ (maximum dose, 2.5 mg) intravenously immediately before the induction of anesthesia (n = 30 of each). A standard general anesthetic technique was employed throughout. Results. A complete response, defined as no PONV and no need for another rescue antiemetic medication during the first 24 h after anesthesia, was 57% and 83% in patients who had received placebo and droperidol 50 μg·kg⁻¹, respectively (P < 0.05). No clinically serious adverse events were observed in any of the groups. Conclusion. Prophylactic antiemetic therapy with droperidol 50 μg·kg⁻¹ (maximum dose, 2.5 mg) is highly effective for preventing PONV after LC. Received for publication on August 3, 1998; accepted on February 23, 1999     

RETRACTED ARTICLE: Nicardipine inhibits amrinone-enhanced contractility in fatigued diaphragm

The purpose of this study was to examine the effect of amrinone, a bipyridine derivative, with and without nicardipine, a calcium channel blocker, on the contractility of fatigued diaphragm in dogs. Twenty dogs were divided into two groups of ten each: amrinone group (group A) and combined amrinone and nicardipine group (group AN). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (P_di). In group A, after producing fatigue, amrinone (0.75 mg·kg⁻¹ loading dose plus 10 μg·kg⁻¹·min⁻¹ maintenance dose) was administered iv. In group AN, nicardipine 5 μg·kg⁻¹·min⁻¹ was infused iv simultaneously with amrinone during this period. After diaphragmatic fatigue, P_di at low-frequency (10–30 Hz) stimulation decreased compared with the prefatigue values (P<0.05), whereas no change in P_di was observed at high-frequency (50–100 Hz), stimulation. The P_di at each stimulus were increased compared with the fatigued values (P<0.05) by administering amrinone, and returned to these values after this agent was discontinued. The P_di values at any frequency of stimulation did not change when amrinone was administered with nicardipine. Our results suggest that amirinone may enhance contractility in fatigued diaphragm via its effect on transmembrane calcium movement.     

Hemodynamic effects of oral clonidine premedication in lumbar epidural anesthesia

Clonidine, an α₂-adrenergic agonist, has a potent sympatholytic effect and augments the pressor effect of ephedrine during general anesthesia. We evaluated whether oral clonidine premedication would alter the hemodynamic changes and enhance the pressor response to intravenous ephedrine during epidural anesthesia in 35 adult patients. They were randomly administered either premedication with clonidine approximately 5 μg·kg⁻¹ po (n=17) or no clonidine medication (n=18). After establishment of epidural anesthesia, the hemodynamic response to ephedrine iv was measured in the awake state at 1-min intervals for 10 min. Then, the same hemodynamic measurement was repeated in the asleep state induced with midazolam iv. There were no differences in blood pressure (BP) and heart rate values between groups during the onset of epidural anesthesia, except that BP before epidural anesthesia was lower in the clonidine group than the control group (P<0.05). The magnitude and duration of pressor responses to ephedrine were comparable between groups in awake and asleep states. In conclusion oral clonidine premedication 5 μg·kg⁻¹ alters neither the hemodynamic changes nor the pressor response to intravenous ephedrine during epidural anesthesia. Presented at the Annual Meeting of the Japan Society for Clinical Anesthesia, Oita City, Oita, November, 1994     

A comparison of sympathetic adrenal nerve responses to intravenous high-dose morphine and fentanyl administration in rats

We compared the effects of intravenous morphine (5 mg·kg⁻¹) and fentanyl, (50μg·kg⁻¹) on systolic blood pressure (SBP), heart rate (HR), and efferent sympathetic adrenal nerve action potentials (SANA) in rats. We also determined the extent of the reflex responses of these parameters of 9% carbon dioxide (CO₂) challenge during the above narcotic anesthesia. In the morphine group, SBP was elevated and the elevated levels were maintained, while changes in SBP in the fentanyl group were not significant. In the morphine group, SANA showed initial stimulation and subsequent depression, while in the fentanyl group, SANA showed sustained depression. CO₂ challenge induced only very small changes in SBP and HR, suggesting that during high-dose narcotic anesthesia the hypercapnic stimulus may not be reflected in circulatory parameters. In both groups, hypercapnia increased SANA to 30% of the baseline values from the pre-challenge level. However, these values were only 91% and 56% of the baseline value in the morphine and the fentanyl, groups, respectively.     

Intravenous famotidine does not always change core temperature during general anesthesia

It has been reported that oral premedication with the H₂ receptor antagonist famotidine augmented intraoperative hypothermia. We again investigated whether the H₂ receptor antagonist famotidine significantly affected body temperature during open abdominal surgery under general anesthesia. We studied 20 female patients undergoing elective gynecological surgery. Participating patients were assigned randomly to one of two regimens: (1) 10 ml saline given intravenously just before induction of general anesthesia or (2) 20 mg famotidine in 10 ml saline given just before induction of general anesthesia. General anesthesia was induced by 2 mg·kg⁻¹ propofol and 0.1 mg·kg⁻¹ vecuronium. After tracheal intubation, anesthesia was maintained with sevoflurane (1%–2%) in nitrous oxide (2 l·min⁻¹) and oxygen (1 l·min⁻¹) along with 1–2 μg·kg⁻¹ fentanyl as needed. Tympanic temperature (T_Tym) was measured as the core temperature, and arteriovenous perfusion of the fingertip was evaluated using the forearmminus-fingertip skin-surface temperature gradient (Grad_a–f). T_Tym gradually and significantly decreased in both groups during anesthesia, and no significant differences in these values were observed between the two groups. Grad_a–f did not differ significantly between the two groups during anesthesia. We conclude that intravenous famotidine does not always change the core temperature during general anesthesia.     

Experimental study of efficacy and optimal dose of intraoperative glucose in rabbits under general anesthesia

This experimental study was designed to investigate the efficacy of glucose loading during surgery. Rabbits, fasted overnight, received 20 ml·kg⁻¹·h⁻¹ fluid infusion containing glucose at various concentration (0,0.5, 1.0, 1.5, 2.0% w/v) for 3 h intraoperatively. Plasma glucose level increased after the beginning of operation, but the increase was slight in groups given 0.2 g·kg⁻¹·h⁻¹ or lower doses of glucose. Glucose at higher doses caused marked hyperglycemia. These higher doses also promoted urinary glucose excretion, and in the group given the maximum glucose dose (0.4 g·kg⁻¹·h⁻¹), this parameter was significantly elevated compared with findings in the 0.2 g·kg⁻¹·h⁻¹ group (P<0.05), whereas it showed no significant difference among groups given 0–0.2g·kg⁻¹·h⁻¹. The liver glycogen content in animals that received no glucose was significantly lower than that of the 0.2 g·kg⁻¹·h⁻¹ group (P <0.01). However, there was no correlation between glycogen level and glucose dose among groups receiving glucose. These results suggest that intraoperative glucose supplementation is effective in preventing glycogen depletion, and indicate that, to avoid glucose overloading, the optimal dose is 0.1–0.2 g·kg⁻¹·h⁻¹.     

Effects of combined intravenous nicardipine and diltiazem administration on the circulatory response to laryngoscopy and tracheal intubation

To evaluate the effect of combined intravenous administration of the calcium antagonists, nicardipine and diltiazem, on the circulatory responses to tracheal intubation, the mean arterial pressure (MAP) and rate pressure product (RPP) in response to laryngoscopy following tracheal intubation were compared in patients receiving saline placebo or nicardipine 10 μg·kg⁻¹ and diltiazem 0.1 mg·kg⁻¹ 60 s before the initiation of laryngoscopy. Each group was comprised of ten patients undergoing elective surgery. The patients receiving saline showed a significant increase in MAP and RPP associated with tracheal intubation. However, these increases were significantly attenuated (P<0.05) in the patients to whom nicardipine and diltiazem were administered concurrently.     

Effect of fentanyl on heart rate variability during mechanical ventilation

Purpose This study was performed to investigate the effect of fentanyl alone on heart rate variability (HRV) during mechanical ventilation using power spectral analysis. Arterial baroreceptor reflex was also tested with pharmacological manipulation to assess the contribution of vagal baroreceptor reflex modulation of HRV during fentanyl anesthesia. Method Ten patients participated in this study. Electrocardiograms and arterial pressure were recorded prior to and during fentanyl (10 μg·kg⁻¹) and vecuronium (0.2 mg·kg⁻¹) anesthesia, with respiratory rate and tidal volume controlled ventilation. R-R intervals were analyzed by fast Fourier transformation, and changes in low-frequency (LF) and high-frequency (HF) power were compared. Arterial baroreceptor reflex regulation was also tested with administration of nitroglycerin (250 μg) or phenylephrine (250 μg). Results HF power was significantly reduced during anesthesia from 3.20±2.93 to 0.46±0.48 ms²·Hz⁻¹·10³ (mean±SD,P<0.05). However, LF power did not change despite increases in plasma catecholamine concentrations. The response to phenylephrine was reduced during fentanyl anesthesia from 16.6±5.7 to 9.5±5.4 ms·mmHg⁻¹ (P<0.05), whereas the response to nitroglycerin was not affected. Conclusion Our data indicate that fentanyl modulates the respiratory frequency fluctuation of HRV. This is partly caused by the effects of fentanyl on arterial baroreflex sensitivity.     

Comparison of heart rate changes after neostigmine-atropine administration during recovery from propofol-N2O and isoflurane-2O anesthesia

Purpose. Propofol augments the reduction of heart rate (HR) in combination with cholinergic agents and attenuates the HR response to atropine. We examined whether propofol anesthesia was associated with an increased incidence and extent of bradycardia after neostigmine-atropine administration compared with the effects of isoflurane anesthesia. Methods. Thirty-six adult patients were randomly assigned to two groups (n = 18 each): the propofol group patients were anesthetized with propofol (5–10 mg·kg⁻¹·h⁻¹)-₂O-fentanyl, and the isoflurane group patients were anesthetized with isoflurane (0.5%–1.0%)-₂O-fentanyl. When surgery was completed, anesthetics were discontinued, and then a mixture of neostigmine 0.05 mg·kg⁻¹ and atropine 0.02 mg·kg⁻¹ was injected intravenously over 20 s. Blood pressure (BP) and HR were measured noninvasively at 1-min intervals for 10 min. Results. At the completion of the surgery, the average infusion rate of propofol was 6.2 ± 1.7 mg·kg⁻¹·h⁻¹, and the average inspired concentration of isoflurane was 0.73 ± 0.15%. Immediately before the neostigmine-atropine injections, HR and mean BP were similar in the two groups. The maximum increase in HR after the neostigmine-atropine injections was significantly less in the propofol group than in the isoflurane group (16 ± 9 and 34 ± 6 beats·min⁻¹, respectively, P < 0.01). The subsequent maximum decrease in HR was greater in the propofol group than in the isoflurane group (−9 ± 4 and −5 ± 4 beats·min⁻¹, respectively; P < 0.01). The incidence of bradycardia (HR < 50 beats·min⁻¹) after neostigmine-atropine injection was greater in the propofol group than in the isoflurane group (61% and 28%, respectively; P < 0.01). Conclusion. We conclude that propofol anesthesia attenuates the initial increases in HR, enhances the subsequent decreases in HR, and increases the incidence of bradycardia after neostigmine-atropine injections compared with the effects of isoflurane anesthesia. Received: May 21, 2001 / Accepted: August 29, 2001     

Effects of bupivacaine and lidocaine on cardiac function in awake and pentobarbital-anesthetized rats

Using an implanted Doppler crystal, we evaluated emodynamic changes induced by subconvulsive doses of bupivacaine and lidocaine in awake and pentobarbitalanesthetized rats. Low doses of lidocaine (2.0 mg·kg⁻¹) and bupivacaine (0.5 mg·kg⁻¹) changed hemodynamics minimally. However, a high dose of lidocaine (8.0 mg·kg⁻¹) reduced heart rate, cardiac output, and regional myocardial wall thickening for a short period with or without anesthesia. In contrast, a high dose of bupivacaine (2.0 mg·kg⁻¹) increased mean arterial pressure and did not change heart rate or regional myocardial wall thickening in the awake state. Under pentobarbital anesthesia, a high dose of lidocaine reduced mean arterial pressure significantly shortly after the injection, but bupivacaine did not. Thus, it is unlikely that bupivacaine has more potent cardiotoxicity than lidocaine in subconvulsive doses.