Effects of calcium and temperature on tension in isolated canine coronary artery

The effects of calcium and temperature on the tension of isolated canine coronary arterial strips were studied.In 20mEq·l ^–1 K solution, the tension was significantly increased from 0mg with 0mEq·l ^–1 Ca to 33 ± 18mg with 0.2mEq·l ^–1 Ca at 37°C, from –40 ± 18mg with 0mEq·l ^–1 Ca to –17 ± 11mg with 0.2mEq·l ^–1 Ca at 30°C, from –77 ± 19mg with 0mEq·l ^–1 Ca to –52 ± 17mEq·l ^–1 with 1mEq·l ^–1 Ca at 25°C, from –88 ± 13mg with 0mEq·l ^–1 Ca to –41 ± 18mg with 2mEq·l ^–1 Ca at 20°C, from –125 ± 16mg with 0mEq·l ^–1 Ca to –116 ± 13mg with 2mEq·l ^–1 Ca at 15°C. Ca higher than 0.2mEq·l ^–1 produced a dose-dependent increase in tension between 37°C and 15°C. In spite of the presence of 4mEq·l ^–1 Ca, the development of tension was strongly supressed by lowering the temperature below 20°C, and completely inhibited at 10°C. The rate of a decrease in tension caused by cooling was about 5.5mg·°C^–1.This study demonstrated that Ca²⁺ produced a dose-dependent increase in tension in high-K solution, which was suppressed as the temperature was lowered.(Yoshida K, Fujii Y, Ina H, et al.: Effects of calcium and temperature on tension in isolated canine coronary artery. J Anesth 5: 172–176, 1991)     

Breathing pattern and respiratory mechanics in sevoflurane-anesthetized humans

In order to determine the respiratory effects of sevoflurane in humans, breathing pattern and mechanical behavior of respiratory system were investigated in ten subjects at anesthetic depth of 1MAC (minimum alveolar concentration). Average tidal volume and breathing frequency amounted to 275ml and 20.9 breaths per minute. Arterial carbon dioxide tension amounted to 45.6mmHg. Duration of inspiration was 1.06s and that of expiration was 1.92s. Mean inspiratory flow rate amounted to 259ml·s^–1. Average value of passive respiratory elastance determined by the method of Zin et al. amounted to 21.8cmH₂O·l ^–1, while those of active respiratory elastance and resistance obtained by the method of Behrakis et al. were 28.0cmH₂O·l ^–1 and 3.15cmH₂O·l ^–1·s^–1, respectively.Values of these variables were compared to those reported in halothane and enflurane anesthesia and possible explanations of the differences between the anesthetics are discussed.(Izumi Y, Kochi T, Isono S, et al.: Breathing pattern and respiratory mechanics in sevoflurane-anesthetized humans. J Anesth 4: 343–349, 1990)     

Respiration by tracheal insufflation of oxygen (TRIO) at high flow rates in apneic dogs

Tracheal insufflation of oxygen (TRIO) is a technique in which oxygen is introduced into the trachea at a constant flow rate via a catheter advanced to the level of the carina. We studied the effects of flow rates (0.5, 1.0, 1.5 and 2.0l·kg^–1·min^–1) on arterial blood gases during TRIO in 6 apneic dogs. The constant flow was administered through the tip of a catheter (I.D. 2.0mm) advanced to a site of 1cm above the carina. After 30min of TRIO, the mean Pa_{CO 2} at the flow rates of 0.5, 1.0, 1.5 and 2.0l·kg^–1·min^–1 were 88 ± 20, 76 ± 20, 64 ± 23 and 52 ± 18mmHg, respectively. CO₂ elimination increased as the flow rates increased from 0.5 to 2.0l·kg^–1·min^–1.Based on the above study, we examined the effects of TRIO at a flow rate of 3l·kg^–1·min^–1 in another 5 apneic dogs. TRIO, at a flow rate of 3l·kg^–1·min^–1, was able to maintain normocarbia over 4hr. The mean Pa_{O 2} and Pa_{CO 2} at 4.0hr were 465 ± 77 and 41 ± 4mmHg. Although the mechanism of pulmonary gas exchange during TRIO is unclear, our study is the first to document that normocarbia can be maintained by high-flow TRIO in apneic dots.(Urata K, Okamoto K and Morioka T.: Respiration by tracheal insufflation of oxygen (TRIO) at high flow rates in apneic dogs. J Anesth 5: 153–159, 1991)     

The effects of sevoflurane on lidocaine-induced convulsions

The influence of sevoflurane on lidocaine-induced convulsions was studied in cats. The convulsive threshold (mean ± SD) was 41.4 ± 6.5mg·l ^–1 with lidocaine infusion (6mg·kg^–1·min^–1), increasing significantly to 66.6 ± 10.9mg·l ^–1 when the end-tidal concentration of sevoflurane was 0.8%. However, the threshold (61.6 ± 8.7mg·l ^–1) during 1.6% sevoflurane was not significant from that during 0.8% sevoflurane, indicating a celling effect. There was no significant difference in the convulsive threshold between sevoflurane and enflurane. The rise in blood pressure became less marked when higher concentrations of sevoflurane or enflurane were administered and the blood pressure at convulsions decreased significantly in 1.6% sevoflurane, and in 0.8% and 1.6% enflurane. However, there was no significant difference in the lidocaine concentrations measured when the systolic blood pressure became 70mmHg. Apamin, a selective blocker of calcium-dependent potassium channels, was administered intracerebroventricularly in rats anesthetized with 0.8% sevoflurane to investigate the mechanism of the anticonvulsive effects. Apamin (10ng) had a tendency to decrease the convulsive threshold (21.6 ± 2.2 to 19.9 ± 2.5mg·l ^–1) but this was not statistically significant. It is suggested that sevoflurane reduces the convulsive effect of lidocaine toxicity but carries some risk due to circulatory depression.(Karasawa F: The effects of sevoflurane on lidocaine-induced convulsions. J Anesth 5: 60–67, 1991)     

KB-R9032, newly developed Na<Superscript>+</Superscript>/H<Superscript>+</Superscript> exchange inhibitor,attenuates reperfusion-induced arrhythmias in isolated perfused rat heart

Purpose This study was conducted to elucidate the effects of KB-R9032, a newly developed Na⁺-H⁺ exchange inhibitor, on reperfusion-induced ventricular arrhythmia in the isolated perfused rat heart.Methods Male Wistar rat hearts (n = 48; 12 for each group) were perfused with modified Krebs-Ringers solution equilibrated with 5% carbon dioxide in oxygen by means of the Langendorff technique. An occluder was placed around the left anterior descending coronary artery (LAD). Heart rate, coronary flow, and ECG were monitored. Drug-free perfusate was used for 10min before switching to a perfusate containing various concentrations of KB-R9032. The added concentrations of KB-R9032 varied in the range of 0 (control) to 1 × 10^–5mol·l^–1. Each heart was subjected to regional ischemia (occlusion of LAD for 11min) and to 3min of reperfusion (release of the ligation).Results In the control group, reperfusion-induced ventricular fibrillation (VF) occurred in 91.7%, and the duration was 158.2 ± 14.4s (mean ± SEM); however, 1 × 10^–7, 1 × 10^–6, and 1 × 10^–5mol·l^–1 KB-R9032 reduced the incidence of VF to 75.0%, 42.9%, and 6.7%, respectively (P < 0.05 at 1 × 10^–5mol·l^–1 of KB-R9032) and reduced the duration of VF to 64.8 ± 22.1, 16.8 ± 10.1, and 1.2 ± 1.2s, respectively (P < 0.05 at 1 × 10^–6 and 1 × 10^–5mol·l^–1 of KB-R9032).Conclusion It was shown in this study that the Na⁺/H⁺ exchange inhibitor KB-R9032 suppresses reperfusion arrhythmias in the ischemia-reperfusion model of isolated rat heart.     

Dose-finding study of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam

Purpose We investigated the effective and safe dose of intravenous midazolam for sedation and amnesia during spinal anesthesia in patients premedicated with intramuscular midazolam.Methods One hundred and eighty patients aged 20–50 years scheduled for spinal anesthesia received midazolam 0.06mg·kg^–1 and atropine 0.01mg·kg^–1 intramuscularly 15min before entering the operating room. Spinal anesthesia was performed with 0.5% hyperbaric tetracaine. Five minutes after starting surgery, midazolam 0 (control group), 0.01, 0.02, 0.03, 0.04, or 0.05mg·kg^–1 was intravenously administered (30 patients each). Blood pressure, heart rate, respiratory rate, percutaneous oxygen saturation (S_{p O 2}), verbal response, eyelash reflex, and involuntary body movement were measured every 5min for 30min. Memory during surgery was also investigated.Results The number of the patients with loss of verbal response, with loss of eyelash reflex, and with no memory during surgery were significantly larger in the groups receiving midazolam 0.03mg·kg^–1, 0.04mg·kg^–1, and 0.02mg·kg^–1, respectively. The decrease in blood pressure or increase in respiratory rate with decrease in S_{p O 2} was significantly larger in the groups receiving midazolam 0.03mg·kg^–1 or 0.05mg·kg^–1, respectively.Conclusion For sedation and amnesia of the patients aged 20–50 years in spinal anesthesia with about 1h duration receiving intramuscular midazolam 0.06mg·kg^–1 as a premedication, intravenous midazolam 0.02mg·kg^–1 might be effective and safe.     

Decreased beta-adrenergic receptor

We investigated alterations in the number and affinity of cardiac beta-adrenergic receptors during hemorrhagic shock. Forty male Wistar rats were divided into two groups: (1) a shock group (n = 20), in which mean arterial blood pressure was decreased to 40–50mmHg by bleeding and kept constant for 6h; and (2) a control group (n = 20), which underwent a sham operation. We used (–)[³H]dihydroalprenolol for the determination of the number and affinity of beta-adrenergic receptors in myocardial membranes. An additional 25 rats were used for determination of plasma epinephrine and norepinephrine concentrations. Scatchard analysis showed a 20% reduction (P < 0.05) in beta-adrenergic receptor density in the shock group (70.3 ± 3.5fmol·mg^–1 protein) compared to the control group (90.0 ± 4.8fmol·mg^–1 protein) but no significant change in the affinity (2.52 ± 0.06 vs. 2.31 ± 0.09nmol·l ^–1, control vs. shock). Plasma catecholamine concentrations were increased significantly at 1, 2, 4 and 6h after the start of hypotension. These data suggest that increased levels of plasma catecholamines in hemorrhagic shock may be correlated a significant loss of beta-adrenergic receptors in rat myocardium.(Mizumachi K, Yahagi M, Kawabata H, et al.: Decreased beta-adrenergic receptor density in rat myocardium during hemorrhagic shock. J Anesth 5: 404–411, 1991)     

Propofol inhibits lidocaine metabolism in human and rat liver microsomes

Purpose.When two drugs are metabolized by similar P450 isoforms, one drug inhibits the metabolism of the other when both the present. The metabolism of lidocaine and propofol can be mediated by similar P450 isoforms. Therefore, we investigated the relationship in the metabolism between lidocaine and propofol in both rat and human liver microsomal P450 (CYP) systems in vitro. Methods.(1) Propofol, 4µg·ml^–1, as the substrate and lidocaine (between 0.5 and 8µg·ml^–1) and (2) lidocaine, 4.7µg·ml^–1, as the substrate and propofol (between 0.5 and 40µg·ml^–1) were reacted separately with human and rat microsomes. The concentrations of lidocaine, its major metabolite (monoethylglycinexylidide, MEGX) and propofol were measured using high-pressure liquid chromatography. The metabolism of lidocaine was presented as a reaction activity (MEGX/lidocaine). Results.The dose-dependent inhibitory effects of propofol on lidocaine metabolism were observed in both the human and rat groups. The IC50 (the concentration producing 50% maximal inhibition) of propofol was 5.0µg·ml^–1 and 0.70µg·ml^–1 in the human and the rat groups, respectively. The propofol concentration of 5.0µg·ml^–1 is within the range of clinical doses for humans. On the other hand, lidocaine did not change propofol metabolism. Conclusion.Propofol possesses a dose-dependent inhibitory effect on the metabolism of lidocaine in both human and rat CYP systems in vitro.     

Vascular responses to hypercapnia in anesthetized dogs

To evaluate the vascular responses to systemic acute mild hypercapnia (Pa_{CO 2} = 65mmHg), we determined the vascular compliance with the relation between the change in circulating blood volume and the change in central venous pressure during and after fluid infusion in dogs anesthetized with halothane in normocapnia and hypercapnia. Circulating blood volume was measured continuously by ⁵¹Cr-labeled erythrocyte dilution method together with hemodynamic variables. Small reduction in vascular compliance (8.1 ± 1.0ml·mmHg^–1·kg^–1 in normocapnia, 5.8 ± 0.5ml·mmHg^–1·kg^–1 in hypercapnia), large reduction in delayed compliance, which were quantitated by computer simulation using Maxwells viscoelastic model, and significant increase in blood volume in central circulation were observed in hypercapnia. The essential change in hypercapnia was concluded as the vasoconstriction in capacitance vessels. Simultaneously, the reduction of total peripheral resistance (1.09 ± 0.08mmHg·min·kg·ml^–1 in normocapnia, 0.98 ± 0.07mmHg·min·kg·ml^–1 in hypercapnia) with no change in transvascular filtration coefficient (0.14 ± 0.02ml·mmHg^–1·min^–1·kg^–1) suggests the increase in shunt flow in peripheral circulation.(Shigemi K: Vascular responses to hypercapnia in anesthetized dogs. J Anesth 2: 1–7, 1988)     

Cyclic alteration in the anticonvulsant effect of nitrous oxide in rats

The anticonvulsant action of nitrous oxide and its time course were studied in rats. Bicuculline, a GABA-receptor antagonist, was administered intravenously at a rate of 0.2mg·kg^–1·min^–1 during exposure to air (n = 60) or 75% nitrous oxide in oxygen (n = 80). The convulsant dose of bicuculline was determined. The rats were divided into subgroups according to the duration of exposure to air or nitrous oxide, from 0 to 120min at 15min intervals. Although the convulsant dose of bicuculline was consistent in the air group (1.03 ± 0.06mg·kg^–1, mean ± SEM), it showed two peaks at 30- and 90min exposures to nitrous oxide. The threshold dose in the nitrous oxide group was significantly higher than in the air group at only 15- and 30min exposures (1.50 ± 0.16, 2.15 ± 0.25mg·kg^–1, respectively, P 0.05). We conclude that nitrous oxide has an anticonvulsant action against bicuculline-induced seizure, and that a cyclic nature exists in its action.(Shingu K, Osawa M, Mori K: Cyclic alteration in the anticonvulsant effect of nitrous oxide in rats. J Anesth 4: 309–312, 1990)     

Comparison of adjuvant anesthetics for propofol induction

Purpose.Fentanyl was compared with nitrous oxide/sevoflurane as an adjuvant anesthesia to propofol during induction.Methods.Two-hundred sixty-three patients of American Society of Anesthesiologists physical status 1 or 2 undergoing minor surgery were randomly divided into two groups. Group F patients (n = 125) received 2g·kg^–1 fentanyl and 1.8mg·kg^–1 propofol, and were ventilated by mask with oxygen. Group S patients (n = 138) received 1.8mg·kg^–1 propofol, followed by inhalation of 4% sevoflurane in N₂O (4l·min^–1) and oxygen (2l·min^–1) by mask. The trachea was intubated exactly 2, 3, 4, or 5min after injection of 0.1mg·kg^–1 vecuronium, and the conditions of endotracheal intubation were scored according to the patients' responses to laryngoscopy and endotracheal intubation. Systolic blood pressure (SBP) and heart rate (HR) were measured before and after endotracheal intubation. The cost of anesthetics was also calculated.Results.No significant differences in SBP were observed between the groups throughout the induction period. HR did not change from preanesthetic values in group F. In contrast, HR in group S patients increased by 9–18 beats·min^–1 (bpm) after inhalation of N₂O/sevoflurane and further increased by 17–21bpm following endotracheal intubation. Significant differences in HR were noticed between the groups (P 0.001). The conditions of endotracheal intubation were similar in the two groups and were satisfactory when mask ventilation exceeded 3min. Fentanyl was less expensive than sevoflurane/N₂O anesthesia when mask ventilation exceeded 3min.Conclusion.From the standpoints of hemodynamics and drug cost, fentanyl is preferable to N₂O/sevoflurane inhalation as an adjuvant to propofol during induction, because mask ventilation for more than 3min was required for satisfactory endotracheal intubation.     

Temperature and humidity of the DrÄger Cato anesthetic machine circuit

Purpose.The DrÄger Cato anesthetic machine (DrÄger, LÜbeck, Germany) effectively humidifies and warms anesthetic gases, because it has a built-in hotplate to heat the breathing system, and expired gas passes through the CO₂ absorbent three times during one breath. In the present study, we measured the temperature and absolute humidity (AH) of the anesthetic circuit in the DrÄger Cato machine with and without heat moisture exchangers (HME), and compared them with those in another anesthetic machine, the Aestiva/5 (Datex-Ohmeda, Helsinki, Finland).Methods.Forty-eight adult patients were randomly assigned to one of eight groups according to the anesthetic machine, fresh gas flow (FGF), and the use of HME (n = 6 each): Cato 0.5l·min^–1 without HME (group 1), Cato 1.0l·min^–1 without HME (group 2), Cato 0.5l·min^–1 with HME (group 3), Cato 1.0l·min^–1 with HME (group 4), Aestiva 0.5l·min^–1 without HME (group 5), Aestiva 1.0l·min^–1 without HME (group 6), Aestiva 0.5l·min^–1 with HME (group 7), and Aestiva 1.0l·min^–1 with HME (group 8). The temperature and AH of the anesthetic gases were measured with a Moiscope (S.K.I. Net, Tokyo, Japan), which was placed between the endotracheal tube and the Y-piece of the anesthetic circuit. The HME was placed between the Moiscope and the Y-piece of the anesthetic circuit. The temperature and AH of the anesthetic gases were measured at 5, 10, and 15min and then every 15min up to 150min after tracheal intubation.Results.Among the groups without HME (groups 1, 2, 5, and 6), the inspired temperatures and AH in groups 1 and 2 were significantly higher than those in groups 5 and 6 at all times during the study period (P 0.01–0.001). The inspired temperatures and AH of the groups with HME (groups 3, 4, 7, and 8), were significantly higher than those in groups 2, 5, and 6 (P 0.01–0.001). Among the groups with HME, the AH in group 3 was significantly higher than that in group 8 until the final study period.Conclusion.The present study indicates that the DrÄger Cato machine was more effective in warming and humidifying respiratory gas than the Aestiva/5, and that Aestiva/5 without HME does not reach the optimal temperature and humidity ranges, even if minimal flow anesthesia (0.5l·min^–1) is performed.     

Addition of epinephrine to intrathecal tetracaine augments depression of the bispectral index during intraoperative propofol sedation

Purpose Epinephrine added to local anesthetic agents for spinal anesthesia is frequently used to prolong the duration of anesthesia. Epinephrine stimulates the -adrenoceptor, and it is known that the 2-adrenoceptor agonists have a central inhibitory effect. We investigated the effect of intrathecal epinephrine during propofol sedation with spinal anesthesia, using a bispectral index (BIS) monitor.Methods Twenty adult patients, scheduled for spinal anesthesia, were allocated to the control group (n = 10) or epinephrine group (n = 10). Patients in the control group received 14mg of tetracaine, whereas the epinephrine group received 14mg of tetracaine and 0.2mg of epinephrine. Immediately after the pinprick test, propofol was administered at 0.5mg·kg^–1 by infusion for the initial dose, then continuously at 2mg·kg^–1·h^–1 in both groups. BIS scores were recorded before subarachnoid block, and then every 5min for 90min after subarachnoid block.Results There were significant differences in the BIS score between the two groups at 45–55min and at 60–70min after subarachnoid block.Conclusion Intrathecal epinephrine augments the sedative effect of propofol during spinal anesthesia.     

The neuromuscular effects of sevoflurane and isoflurane alone and in combination with vecuronium or atracurium in the rat

Sevoflurane was compared to isoflurane anesthesia alone and in combination with atracurium or vecuronium in 84 rats using the sciatic nerve—anterior tibialis muscle preparation. Both bolus injection and infusion rate techniques were used to evaluate these drug interactions. The ED₅₀ (dose which produced a 50% depression of twitch tension) of atracurium was 311 ± 31 and 360 ± 32µg·kg^–1 during 1.25MAC sevoflurane and isoflurane anesthesia respectively. The ED₅₀ of vecuronium was 190 ± 27 and 149 ± 14µg·kg^–1 during 1.25MAC sevoflurane and isoflurane anesthesia respectively. The mean infusion rates of atracurium and vecuronium required to maintain a 50% depression of twitch tension were 5.04 ± 0.7 and 2.02 ± 0.3mg·kg^–1·hr^–1. These infusion rates were 5.04 ± 0.7 and 2.02 ± 0.3mg·kg^–1·hr^–1 during 1.25MAC sevoflurane and 3.73 ± 0.3 and 1.81 ± 0.4mg·kg^–1·hr^–1 during 1.25MAC isoflurane anesthesia respectively. With both atracurium and vecuronium, the infusion rate required to maintain a 50% depression twitch of tension was inversely related to the concentrations of isoflurane and sevoflurane. The authors conclude that sevoflurane is similar in potency to that of isoflurane in augmenting a vecuronium or atracurium induced neuromuscular blockade in a dose-dependent manner.(Shin YS, Miller RD, Caldwell JE, et al.: The neuromuscular effects of sevoflurane and isoflurane alone and in combination with vecuronium or atracurium in the rat. J Anesth 6: 1–8, 1992)     

Analysis of oxygen transport to the brain when two or more parameters are affected simultaneously

We composed a model, combining oxygen transport system from blood to tissue with the oxygen consumption system at the tissue. The aim of this study is to apply it to the brain tissue under conditions when two or more oxygen transport parameters are affected simultaneously. The following values were assumed. Critical tissue P_{O 2} (Pcrit_{O 2}) 2mmHg; oxygen consumption above this level 3ml·min^–1·100g^–1; diffusion coefficient from blood vessel to tissue (Dvt) 0.2ml·min^–1·mmHg^–1·100g^–1; cerebral bloow flow (CBF) 50ml·min^–1·100g^–1; hemoglobin 15g·100ml^–1. The Hill equation was used for oxygen dissociation curve with n of 2.7 and P₅₀ of 27.0mmHg.The changes of oxygen consumption of the brain (V¨_{O 2}) were analyzed when 2 or more of 5 parameters, Pa_{O 2}, CBF, Dvt, P₅₀ and hemoglobin decreased simultaneously from their respective normal values.As the number of parameters affected increased, the level at which oxygen consumption begins to be affected became higher. With all five parameters combined, a reduction down to 78 per cent of normal resulted in tissue hypoxia. We conclude that the oxygen consumption of the brain is fairly resistant when only one parameter is affected, but it becomes increasingly vulnerable when several parameters are affected simultaneously. A clinically important finding is that the brain is particularly vulnerable to a combination of hypocapnia and a decreased level of 2,3DPG.(Suwa K: Analysis of oxygen transport to the brain when two or more parameters are affected simultaneously. J Anesth 6: 297–304, 1992)     

Functional and metabolic effects of propafenone in the rat heart-lung preparation

The effects of propafenone on cardiac function and myocardial metabolism were assessed in the isolated rat heart-lung preparation. Propafenone 0.3, 3 or 30µg·ml^–1 was administered 5min after the start of perfusion. Heart rate decreased in the 30µg·ml^–1 group significantly following the drug administration. The highest dose of propafenone (30µg·ml^–1) reduced cardiac output significantly, and this dose was associated with a higher incidence of arrhythmias than the other groups. Although there were no significant differences in myocardial lactate and glycogen concentrations among groups, ATP content in the 30µg·ml^–1 group was significantly less than that in the control group. As therapeutic plasma concentration of propafenone is about 0.6 (range 0.06 to 1.0) µg·ml^–1, 30µg·ml^–1 is 50 times greater than its concentration. These results suggest that the negative inotropic and chronotropic effects of propafenone are almost same with those of lidocaine which we have previously reported.(Kashimoto S, Oguchi T, Nakamura T, et al.: Functional and metabolic effects of propafenone in the rat heart-lung preparation. J Anesth 5: 392–395, 1991)     

Plasma concentration for optimal sedation and total body clearance of propofol in patients after esophagectomy

The present study investigated plasma propofol concentration for optimal sedation and total body clearance in patients who required sedation for mechanical ventilation after esophagectomy. Seven patients after esophagectomy were enrolled in this study. Plasma propofol concentrations were measured with high performance liquid chromatography. Total body clearance was calculated from the steady-state concentration. The infusion rate of propofol for achieving the sedation score of level 3 (drowsy, responds to verbal stimulation) was 1.74 ± 0.82mgkg^–1h^–1 (mean ± SD, n = 7) when the plasma propofol concentration and the total body clearance were 0.85 ± 0.24µgml^–1 and 1.83 ± 0.54lmin^–1 (mean ± SD, n =7), respectively.     

Sustained effects of plasma norepinephrine levels on femoral-radial pressure gradient after cardiopulmonary bypass

In order to determine the influence of the sympathetic nervous system upon the femoral-radial artery pressure gradient after cardiopulmonary bypass (CPB), we examined plasma norepinephrine levels in 34 adult male patients undergoing coronary artery bypass grafting. Cardiovascular parameters, including systolic arterial pressure, mean arterial pressure, cardiac index (CI), systemic vascular resistance index (SVRI), pulmonary artery pressure (PAP), hemoglobin (Hb) and peak dP/dt of radial and femoral artery pressures were measured after sternotomy, and immediately after the discontinuation of CPB and 90min after CPB. Plasma norepinephrine levels were measured after sternotomy, after aortic declamping and 90min after CPB.The patients were divided into two groups. Group A consisted of 17 patients whose femoral minus radial systolic pressure difference was 15mmHg or more at 90min after CPB, while Group B consisted of 17 patients with the difference less than 15mmHg. Group A patients had significantly longer time values in the duration of both CPB (Group A 175 ± 10min; Group B 115 ± 12min, P 0.001) and aortic cross clamping (Group A 116 ± 7min, Group B 71 ± 9min, P 0.001).Although there was no significant difference in Hb or PAP of 90min after CPB in Groups A and B, the following values, listed in the order of A to B, were obtained; CI, 2.79 ± 0.10 versus 3.46 ± 0.16l·min^–1·m^–2 (P 0.01); mean radial artery pressure (MRP), 58.7 ± 2.4 versus 65.1 ± 1.8mmHg (P 0.05); peak dP/dt of radial artery pressure, 568 ± 64 versus 1026 ± 61mmHg·sec^–1 (P 0.001); and plasma norepinephrine concentration, 1.81 ± 0.25 versus 0.98 ± 0.10ng·ml^–1 (P 0.01), which were statistically significant.The higher femoral-radial artery pressure gradient after CPB was observed in patients with both a longer CPB time and a higher plasma norepinephrine concentration. These results suggest that a marked constriction of peripheral arteries might have produced a damped transmission of the pressure pulse to the radial artery.(Nakayama R, Goto T, Kukita I, et al.: Sustained effects of plasma norepinephrine levels on femoral-radial pressure gradient after cardiopulmonary bypass. J Anesth 7: 8–15, 1993)     

Difference in the effect of pancuronium and vecuronium on baroreflex control of heart rate in humans

The effects of pancuronium and vecuronium, each in doses of 0.05 and 0.08mg·kg^–1, on the baroreflex control of the heart rate were studied in 40 adult patients of either sex (21 men and 19 women) during stable nitrous oxide-oxygen-fentanyl anesthesia. The blood pressure was elevated by intravenous infusion of phenylephrine (4µg·kg^–1·min^–1) for the pressor test, and lowered by a bolus injection of nitroglycerin (0.3–0.5mg) for the depressor test. Baroreflex sensitivity was judged from the slope of the regression of the systolic blood pressure on the succeeding R-R intervals on the ECG. There was no significant difference between the baseline blood pressure at which both tests were carried out. Nitrous oxide-oxygen-fentanyl anesthesia alone suppressed the baroreflex sensitivity to a level which was at the lower limit of the physiological and non-anesthetized state. The 0.08mg·kg^–1 dose of pancuronium significantly suppressed the reflex sensitivity in both the pressor and depressor tests. However, the 0.05mg·kg^–1 dose of pancuronium and both doses of vecuronium did not cause any significant change in the test results.(Tsuchida H, Seki S, Nakae Y, et al.: Difference in the effect of pancuronium and vecuronium on baroreflex control of heart rate in humans. J Anesth 5: 255–259, 1991)     

Prevention of succinylcholine-induced myalgia with lidocaine pretreatment

We studied the effects of 3mg·kg^–1 lidocaine iv on the succinylcholine (SCh)-induced myalgia in 94 unpremedicated ambulant patients undergoing dilatation and curettage of the uterus. The post-SCh myalgia was confirmed through interview by telephone. The data were correlated with the degree of fasciculation and changes in the serum electrolytes and creatine kinase (CK) levels following SCh administration. Pretreatment with lidocaine, 3mg·kg^–1 iv, significantly reduced the incidence of myalgia from 40.4% of control group to 12.8% lidocaine-treated group, but not the CK levels. The severity of myalgia was not related to the intensity of fasciculation assessed by visual observation. The pretreatment with lidocaine had no untoward effect on the circulation, although the peak arterial and peak venous lidocaine levels achieved were 29.6 ± 23µg·ml^–1 and 10.1 ± 3.3µg·ml^–1 respectively. These finding indicated that the pretreatment with lidocaine, 3mg·kg^–1 iv, was effective in prevention of SCh-induced myalgia.(Tat-Leang Lee, Tar-Choon Aw: Prevention of succinylcholine-induced myalgia with lidocaine. J Anesth 5: 239–246, 1991)