Naoyuki Fujimura

Effect of hemidiaphragmatic paresis caused by interscalene brachial plexus block on breathing pattern, chest wall mechanics, and arterial blood gases.

We investigated the effects of hemidiaphragmatic paresis caused by interscalene brachial plexus block on breathing patterns, chest wall mechanics, and arterial blood gas tensions using respiratory inductive plethysmography.Ten healthy patients received interscalene block with 20-40 mL 1.5% lidocaine with epinephrine. Rib cage contribution to tidal volume (%RC) increased from 28.9% +/- 9.7% to 50.0% +/- 8.3% (P <0.01), respiratory frequency (f) increased from 14.6 +/- 3.2/min to 16.3 +/- 2.4/min (P <0.05), and PaO2 decreased from 84.7 +/- 7.3 mm Hg to 78.0 +/- 9.5 mm Hg (P <0.05). No significant changes were observed in tidal volume (VT), minute volume (VE), or PaCO2. These results indicated that VT, VE, and PaCO2 were maintained after interscalene block, apparently by increases in f and %RC to compensate for hemidiaphragmatic paresis caused by interscalene block. Nevertheless, PaO2 was reduced, presumably due to increased ventilation-perfusion mismatching. Recognizing that we studied healthy patients, the decrease in PaO2 may be more in patients with cardiopulmonary disease. (Anesth Analg 1995;81:962-6)

Alteration in diaphragmatic contractility during septic peritonitis in rats: effect of polyethylene glycol-absorbed superoxide dismutase.

Objectives To assess the alterations in diaphragmatic contractility measured in vitro during experimental septic peritonitis and to evaluate the effect of polyethylene glycol-absorbed superoxide dismutase (PEG-SOD) on the alterations in contractility. Design Prospective, randomized, controlled animal trial. Setting Research laboratory. Subjects A total of 321 male Wistar rats, weighing 250–300 g. Interventions Rats were treated with cecal ligation and puncture (CLP). In the first experiment, diaphragmatic contractility was measured at 4, 10, 12, and 16 hrs after CLP. In the second experiment, PEG-SOD (4000 units/kg) was administered intraperitoneally, and then diaphragmatic contractility was measured at 10 and 16 hrs after CLP. Levels of lipid peroxides and antioxidant enzymes in the diaphragm tissue were measured at 10 and 16 hrs after CLP. Measurements and Main Results In experiment 1, diaphragmatic twitch characteristics and force-frequency relationships were determined at 4, 10, 12, and 16 hrs after CLP. In experiment 2, the effects of administration of PEG-SOD on twitch characteristics and force-frequency relationships were determined at 10 and 16 hrs after CLP. The levels of diaphragmatic thiobarbituric acid reactive substances and superoxide dismutase (SOD) and glutathione peroxidase activities were measured at 10 and 16 hrs after CLP. Twitch tension and force-frequency curves were significantly lower in the CLP groups than in the sham-operated group. Administration of PEG-SOD attenuated the reduction in twitch tension and the downward shift of force-frequency curves after CLP. Diaphragmatic levels of thiobarbituric acid reactive substances increased after CLP. However, the administration of PEG-SOD prevented increases in levels of diaphragmatic thiobarbituric acid reactive substances after CLP. Diaphragmatic SOD activity, but not glutathione peroxidase activity, was increased after CLP. Conclusions Intra-abdominal sepsis (CLP) induced a marked reduction in diaphragmatic contractility, but PEG-SOD attenuated this reduction. Therefore, we conclude that oxygen-derived free radicals play an important role in the alterations in diaphragmatic contractility during intra-abdominal sepsis.

Geranylgeranylacetone attenuates septic diaphragm dysfunction by induction of heat shock protein 70.

ObjectiveThe purposes of the present study were to evaluate the induction of heat shock protein (HSP) 70 expression in the diaphragm by geranylgeranylacetone (GGA) administration and to determine the effect of HSP70 induction on diaphragm contractility measured in vitro and the production of oxygen-derived free radicals during experimental septic peritonitis. DesignProspective laboratory study. SettingUniversity laboratory. SubjectsOne-hundred sixty male Wistar rats. InterventionsIn experiment 1, rats received GGA intragastrically, and time-dependent induction of HSP70 expression in the diaphragm was determined at 0, 12, 24, and 36 hrs after GGA administration. To evaluate dose-dependent inhibition of GGA-induced HSP70 expression by quercetin, rats were pretreated with progressive doses of quercetin before GGA administration. In experiment 2, rats received gum arabic solution (vehicle), 100, 200, or 400 mg/kg of GGA. In experiment 3, rats were pretreated with quercetin or glycerol before GGA or vehicle administration. Intra-abdominal sepsis was induced by cecal ligation and perforation (CLP) under inhalation anesthesia after GGA or vehicle administration in experiments 2 and 3. Measurements and Main ResultsWestern blot analysis using diaphragm homogenates obtained from normal rats showed that HSP70 expression peaked at 24 or 36 hrs after GGA administration and that pretreatment with >10 mg/kg of quercetin blocked the induction of HSP70 expression by GGA. CLP induced diaphragmatic dysfunction and increased diaphragmatic malondialdehyde concentrations and superoxide dismutase and glutathione peroxidase activities. GGA attenuated CLP-induced diaphragm dysfunction and increased malondialdehyde concentrations in a dose-dependent manner but did not affect superoxide dismutase and glutathione peroxidase activities after CLP. Diaphragm dysfunction and increased diaphragmatic malondialdehyde concentrations after CLP were maintained on quercetin pretreatment despite GGA administration. ConclusionsGGA induces HSP70 expression in the diaphragm, and this induction attenuates septic diaphragm impairment by inhibiting the production of oxygen-derived free radicals.

Sepsis attenuates the intensity of the neuromuscular blocking effect of d-tubocurarine and the antagonistic actions of neostigmine and edrophonium accompanying depression of muscle contractility of the diaphragm.

Background: Prolonged effects of non‐depolarizing muscle relaxants in septic patients have been reported, although the influence of sepsis on neuromuscular transmission has not yet been clarified satisfactorily. These studies were intended to elucidate the influence of sepsis on neuromuscular transmission and on the action of drugs being utilized for regulation of muscle tone (a neuromuscular blocker and anti‐cholinesterase (anti‐ChE) drugs).

NMDA receptor-mediated mechanism of ketamine-induced facilitation of glutamatergic excitatory synaptic transmission.

The effect of ketamine on CA1-field EPSPs (fEPSPs) in rat hippocampal slices was investigated. Ketamine (100 microM) facilitated fEPSPs at 0.05 Hz. The fEPSP facilitation was suppressed completely by AP-5 and partially by propranolol, and also by an increase in stimulation frequency. These results indicate that ketamine facilitates excitatory synaptic transmission by activating NMDA receptors via beta-adrenoceptors under conditions in which NMDA receptor channel block is slight.

Bronchospasm Induced by Propofol in a Patient with Sick House Syndrome

IMPLICATIONS Propofol is often used in patients with asthma, but it can induce bronchospasm. We report a patient with sick house syndrome (nonspecific complaints of mucosal irritation, headache, nausea, and chest symptoms) who suffered bronchospasm. This case suggests that propofol is not always a safe anesthetic for patients with asthma, especially drug-induced asthma.

Propofol enhances a d-tubocurarine-induced twitch depression in septic rat diaphragm.

We estimated the effect of d-tubocurarine (dTc) on neuromuscular transmission and the action of propofol on dTc-induced twitch depression by using sham control and septic rat nerve-hemidiaphragm preparations in vitro. Isometric twitch tension elicited by indirect (phrenic nerve) or direct (muscle) stimulation at 0.1 Hz was evaluated. Sepsis induced by panperitonitis attenuated the twitch tension elicited by indirect and direct stimulation (P < 0.01 in each group) in the absence of significant morphological inflammatory damage to the diaphragm. dTc (1 &mgr;M) decreased the twitch tension elicited by indirect stimulation (P < 0.01) less intensely in the septic group than in the sham group (P < 0.01). Propofol accentuated dTc-induced depressed twitch more intensely in the septic group (P < 0.01 or 0.05). These results demonstrate that sepsis attenuates both muscle contractile force and the effect of a neuromuscular blocker and that propofol more intensely enhances dTc-induced twitch depression during sepsis. Implications Propofol and nondepolarizing muscle relaxants are widely used for various clinical cases, including sepsis. Interactions between nondepolarizing muscle relaxants and propofol during sepsis are interesting from a clinical point of view. We demonstrated that propofol significantly enhances d-tubocurarine-induced twitch depression in vitro in the septic rat model compared with that in the nonseptic rat model.

Preferable inotropic action of procaterol, a potent bronchodilator, on impaired diaphragmatic contractility in an intraabdominal septic model

Intraabdominal sepsis can lead to acute respiratory failure, and concomitant diaphragmatic dysfunction may be aggravated by sepsis-induced airway hyperreactivity. We previously reported that isoproterenol, a nonselective β-adrenoceptor agonist, increased diaphragmatic contractility and accelerated recovery from fatigue during sepsis. The purpose of this study was to demonstrate the direct inotropic effect of a potent bronchodilator and β2-selective adrenoceptor agonist, procaterol, on fatigued diaphragmatic contractility in an intraabdominal septic model. Rats were divided into two groups: a cecal ligation and perforation (CLP) group and a sham group. CLP was performed in the CLP group whereas laparotomy alone was performed in the sham group. The left hemidiaphragm was removed at 16 h after the operation. The diaphragmatic tissues were exposed to procaterol (10−8–10−6 M), and muscle contractility was assessed. Intracellular cyclic AMP levels were also measured in the CLP model. Procaterol caused an upward shift in the force–frequency curves in the CLP group whereas it had no effect on the curves in the sham group. Procaterol significantly increased cyclic AMP levels in the CLP model. We conclude that the potent bronchodilator procaterol had a direct and positive inotropic effect on the diaphragm in an intraabdominal septic model.

Anesthetic management of a patient with acute fatty liver of pregnancy

A 35-year-old woman was admitted to our hospital at 23 weeks of gestation. She had a 5-day of history of general fatigue, appetite loss, nausea, vomiting, and abdominal pain. On physical examination, she appeared jaundiced. Her consciousness was alert. Blood pressure (BP) was 100/50mmHg, heart rate (HR) was 86bpm, temperature was 37.1~ and respiration was 20 breaths per minute. Abdominal examination revealed a 23-weekpregnant uterus. Continuous cardiotocography (CTG) monitoring revealed poor fetal HR variability with a late deceleration pattern. Laboratory data demonstrated acute hepatic impairment and coagulopathy (Table 1). Her previous pregnancy had required cesarean section for cephalopelvic disproportion at 40 weeks but was otherwise uneventful. Since becoming pregnant, she had been checked by an obstetrician regularly

Effect of severe cardiac valve regurgitation on the onset of the neuromuscular blocking action of pancuronium

Monitoring the onset of neuromuscular block produced by nondepolarizing relaxants provides useful and important information on muscle relaxation and the timing of endotracheal intubation. Goat and her colleagues [1] initially reported that the onset and intensity of paralysis produced by gallamine were directly related to muscle blood flow. We also reported that the onset of neuromuscular blockade in the adductor pollicis muscles occurred more rapidly in patients given vecuronium via the pulmonary artery than in patients given the drug via a peripheral vein on the hand [2]. Furthermore, the onset time of a neuromuscular relaxant is governed by noncirculatory factors, such as the concentration gradient between plasma and receptor sites, the potency, and the administered dose [3,4]. It has also been reported that the onset of action of pancuronium is slower in children with congenital heart disease (CHD) than in children without CHD [5]. We examined the influence of severe cardiac valve disease on the time of onset of action of pancuronioum in adult patients. With approval from our institutions human research committee and the informed consent of the patients, 47 patients scheduled for elective cardiac surgery (coronary artery bypass graft, n = 22; valve replacement, n = 25) aged 17-78 years (mean, 55) and weighing 40-75 kg (mean, 58) were included. The severity of mitral or aortic regurgitation in 25 patients with cardiac