PubMed Health⌕ Search

Biomedical subjects

Noriaki Kanaya

Publications and source records attributed to Noriaki Kanaya.

At least 19 recordsLinked to original sources
PubMed2007

Propofol increases pulmonary vascular resistance during alpha-adrenoreceptor activation in normal and monocrotaline-induced pulmonary hypertensive rats.

BACKGROUND: Using isolated perfused lungs of normal or monocrotaline (MCT: 50 mg/kg)-induced pulmonary hypertensive rats, we tested the hypothesis that the pulmonary vascular effects of propofol depend on activation of the alpha-adrenoreceptor. METHODS: Changes in pulmonary perfusion pressure induced by propofol (10(-5) to 10(-4) M) were measured with or without phenylephrine (10(-6) M) pretreatment. Before phenylephrine administration, we assessed the effects of inhibitors of nitric oxide synthase (N(omega)-nitro-l-arginine methylester: 10(-4) M), cyclooxygenase (indomethacin: 10(-5) M), and protein kinase C inhibitor, bisindolylmaleimide I (10(-6) M) or calphostin C (10(-6) M). RESULTS: Changes in pulmonary perfusion pressure by phenylephrine after pretreatment of nitric oxide synthase inhibitor and indomethacin in normal rats were significant (5 +/- 3 and 7 +/- 2 mm Hg), whereas that after pretreatment of bisindolylmaleimide I were small in MCT-rats (2 +/- 1 mm Hg). Propofol caused pulmonary vasoconstriction after phenylephrine pretreatment both in normal and MCT-treated rats. In normal rats, the propofol-induced increase in pulmonary perfusion pressure after indomethacin pretreatment was slightly smaller than that in the non-pretreated lungs (P < 0.05). In MCT-treated rats, the propofol-induced increases in pulmonary perfusion pressure after both protein kinase C inhibitors were smaller than that in the non-pretreated lungs (P < 0.05). CONCLUSIONS: Propofol may increase pulmonary vascular resistance during alpha-adrenoreceptor activation.

Animals↗
PubMed2006

Effects of L-type Ca2+ channel modulation on direct myocardial effects of diazepam and midazolam in adult rat ventricular myocytes.

PURPOSE: Our objective was to determine whether an L-type Ca2+ channel modulation could alter myocardial depression induced by midazolam or diazepam in adult rat ventricular myocytes. METHODS: Freshly isolated rat ventricular myocytes were loaded with fura-2/AM and field-stimulated (0.3 Hz) at 28 degrees C. Amplitude and timing of intracellular Ca2+ concentration ([Ca2+]i) and myocyte shortening were simultaneously monitored in individual cells. RESULTS: Midazolam (3-100 microM) caused a decrease in both peak [Ca2+]i and shortening. Diazepam (30, 100 microM) increased myocyte shortening and peak [Ca2+]i; however, higher concentration of diazepam (300 microM) decreased shortening and peak [Ca2+]i. Bay K 8644 (0.01-10 microM), an L-type Ca2+ channel agonist, caused dose-dependent increases in peak [Ca2+]i and shortening. In contrast, verapamil (0.1-50 microM), an L-type Ca(2+) channel antagonist, caused dose-dependent decreases in peak [Ca2+]i and shortening. Dose-response curves to benzodiazepines on peak [Ca2+]i and shortening were not affected by pretreatment with Bay K 8644 (0.1 microM) or verapamil (1 microM). Diazepam (30, 100 microM), but not midazolam (3-30 microM), increased shortening and [Ca2+]i in the presence or absence of L-type Ca2+ channel modulators. Diazepam (30 microM) and midazolam (10 microM) had no effect on peak [Ca2+]i of a caffeine-induced [Ca2+]i transient, which was used as a measure of SR Ca2+ content. CONCLUSION: Midazolam and diazepam have differential effects on cardiac E-C coupling. Diazepam, but not midazolam, enhances cardiac E-C coupling independent of L-type Ca2+ channel modulation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2006

Effects of ulinastatin on pulmonary artery pressure during abdominal aortic aneurysmectomy.

STUDY OBJECTIVE: Abdominal aortic aneurysmectomy (AAAectomy) results in a general ischemia-reperfusion syndrome accompanied by an acute rise in pulmonary artery pressure (PAP). We examined whether ulinastatin, a urinary trypsin inhibitor, prevents ischemia-reperfusion injury and increase in PAP after aortic unclamping (XU) during AAAectomy. DESIGN: Prospective study. SETTING: Public, university-affiliated hospital. PATIENTS: Sixteen patients (11 males and 5 females) scheduled for AAAectomy. INTERVENTIONS AND MEASUREMENTS: The patients received 300000 IU of ulinastatin intravenously before XU (n = 8) or no additional treatment (n = 8) (control). Heart rate, central venous pressure, PAP, pulmonary arterial wedge pressure, arterial pressure, mixed venous oxygen saturation (Sv(O2)), and cardiac output were monitored. Arterial and mixed venous blood samples were analyzed for pH, Pa(CO2), Pa(O2), hemoglobin, and oxygen saturation, and the physiological shunt function (Qs/Qt) were calculated. Plasma concentrations of malondialdehyde, myeloperoxidase, granulocyte elastase, alpha1-antitrypsine, and thromboxane B2 and the stable hydrolysis products of thromboxane A2 were measured. Measurements were conducted before aortic crossclamping (XC) (baseline) and at 10, 30, and 60 minutes after XU. MAIN RESULTS: A significant increase in PAP was observed 10 minutes after XU in the control group but not in the ulinastatin group. At 60 minutes after XU, Qs/Qt values had increased in the control group but had decreased in the ulinastatin group. There were no significant changes in malondialdehyde, thromboxane B2, granulocyte elastase, and alpha1-antitrypsine levels after XU in either group. A significant decrease in the plasma level of myeloperoxidase after XU was found in both groups. CONCLUSIONS: The present study demonstrated that ulinastatin prevents increase in PAP and shunting after XU during AAAectomy.

Aged↗
PubMed2006

[Case of papillary muscle rupture diagnosed by preoperative transesophageal echocardiography].

A 46-year-old man with severe mitral regurgitation (MR) was scheduled for emergency surgery for chordae tendae repairment. Preoperative transesophageal echocardiography (TEE) revealed massive MR due to a rupture in the antero-lateral papillary muscle. We changed the operation procedure to mitral valve replacement. It is difficult to diagnose papillary muscle rupture. Therefore, we should perform TEE on the patient with acute MR of unknown origin.

Echocardiography, Transesophageal↗
PubMed2005

Experimental conditions are important determinants of cardiac inotropic effects of propofol.

BACKGROUND: The rationale for this study is that the depressant effect of propofol on cardiac function in vitro is highly variable but may be explained by differences in the temperature and stimulation frequency used for the study. Both temperature and stimulation frequency are known to modulate cellular mechanisms that regulate intracellular free Ca2+ concentration ([Ca2+]i) and myofilament Ca2+ sensitivity in cardiac muscle. The authors hypothesized that temperature and stimulation frequency play a major role in determining propofol-induced alterations in [Ca2+]i and contraction in individual, electrically stimulated cardiomyocytes and the function of isolated perfused hearts. METHODS: Freshly isolated myocytes were obtained from adult rat hearts, loaded with fura-2, and placed on the stage of an inverted fluorescence microscope in a temperature-regulated bath. [Ca2+]i and myocyte shortening were simultaneously measured in individual cells at 28 degrees or 37 degrees C at various stimulation frequencies (0.3, 0.5, 1, 2, and 3 Hz) with and without propofol. Langendorff perfused hearts paced at 180 or 330 beats/min were used to assess the effects of propofol on overall cardiac function. RESULTS: At 28 degrees C (hypothermic) and, to a lesser extent, at 37 degrees C (normothermic), increasing stimulation frequency increased peak shortening and [Ca2+]i. Times to peak shortening and rate of relengthening were more prolonged at 28 degrees C compared with 37 degrees C at low stimulation frequencies (0.3 Hz), whereas the same conditions for [Ca2+]i were not altered by temperature. At 0.3 Hz and 28 degrees C, propofol caused a dose-dependent decrease in peak shortening and peak [Ca2+]i. These changes were greater at 28 degrees C compared with 37 degrees C and involved activation of protein kinase C. At a frequency of 2 Hz, there was a rightward shift in the dose-response relation for propofol on [Ca2+]i and shortening at both 37 degrees and 28 degrees C compared with that observed at 0.3 Hz. In Langendorff perfused hearts paced at 330 beats/min, clinically relevant concentrations of propofol decreased left ventricular developed pressure, with the effect being less at 28 degrees C compared with 37 degrees C. In contrast, only a supraclinical concentration of propofol decreased left ventricular developed pressure at 28 degrees C at either stimulation frequency. CONCLUSION: These results demonstrate that temperature and stimulation frequency alter the inhibitory effect of propofol on cardiomyocyte [Ca2+]i and contraction. In isolated cardiomyocytes, the inhibitory effects of propofol are more pronounced during hypothermia and at higher stimulation frequencies and involve activation of protein kinase C. In Langendorff perfused hearts at constant heart rate, the inhibitory effects of propofol at clinically relevant concentrations are more pronounced during normothermic conditions.

Anesthetics, Intravenous↗
PubMed2005

[Anesthetic management in a patient with Goldenhar's syndrome using a perilaryngeal airway and a videolaryngoscope].

A 5-year-old girl with Goldenhar's syndrome was scheduled for reconstruction of her left thumb. Because her preanesthetic X-p had revealed airway abnormality, difficult intubation was anticipated. After induction of anesthesia with thiamylal, the lungs were ventilated easily via a facemask. A perilaryngeal airway (PLA) was inserted after obtaining adequate depth of anesthesia with sevoflurane. Anesthesia was maintained with sevoflurane (2%) plus nitrous oxide (66%) under spontaneous ventilation. The operation was finished uneventfully. However, a re-operation was scheduled for postoperative hemorrhage on that day. In consideration of potential regurgitation of gastric content, endotracheal intubation was scheduled. Her vocal cord was confirmed with a videolaryngoscope, and she was intubated successfully. In conclusion, a PLA and a videolaryngoscope are useful for airway management of patients with Goldenhar's syndrome for whom difficulty in intubation is anticipated.

Anesthesia, General↗
PubMed2004

Forehead is as sensitive as finger pulse oximetry during general anesthesia.

PURPOSE: To compare the performance of a forehead probe to a conventional finger pulse oximetry probe in anesthetized patients. METHODS: Eighteen patients participated in the study. Each probe was connected to a Nellcor N-550 pulse oximeter. Anesthesia was induced and maintained with propofol. After intubation, the patients received air to achieve a steady-state of peripheral arterial oxygen saturation (SpO(2)). Ventilation was interrupted to induce a hypoxic state. As soon as one of the two SpO(2)'s decreased to 90%, the patients' lungs were ventilated with 100% oxygen. To evaluate the performance of the two pulse oximeters, time to the lowest (TL), time of recovery (TR) and lag times to beginning of SpO(2) decrease (Lag) were measured. RESULTS: There were no significant differences in TL and TR between forehead and finger pulse oximetry under normal perfusion conditions during general anesthesia. When the axillary artery was compressed to mimic reduced peripheral perfusion, SpO(2) in the forehead decreased sooner than in the finger during hypoxia. The forehead and finger TLs were similar, however, TR was significantly longer in the finger. CONCLUSION: The forehead SpO(2) sensor can be used as an alternative to the conventional finger sensor during general anesthesia.

Anesthesia, General↗
PubMed2004

Differential pressor response to intravenous ephedrine during recovery from deliberate hypotension.

STUDY OBJECTIVE: To determine whether nitroglycerin or trimethaphan alters pressor response to intravenous (i.v.) ephedrine. DESIGN: Prospective, randomized study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I female patients scheduled for mastectomy. INTERVENTIONS: Patients were assigned to one of six groups (n = 10 in each). Group 1: nitroglycerin + normal saline (NS) i.v., Group 2: nitroglycerin + ephedrine 0.1 mg/kg i.v., Group 3: nitroglycerin + ephedrine 0.15 mg/kg i.v., Group 4: trimethaphan + NS i.v., Group 5: trimethaphan + ephedrine 0.1 mg/kg i.v., and Group 6: trimethaphan + ephedrine 0.15 mg/kg i.v. MEASUREMENTS: Hemodynamic responses to ephedrine following withdrawal of vasodilators were observed for 15 minutes. MAIN RESULTS: Ephedrine increased heart rate and mean blood pressure. After ephedrine 0.1 mg/kg i.v., the maximum pressor response in the trimethaphan group was approximately twofold that of the nitroglycerin group (p = 0.038). CONCLUSIONS: Ephedrine restored BP more easily in those patients who had received trimethaphan compared with those who had received nitroglycerin for deliberate hypotension.

Blood Gas Analysis↗
PubMed2004

A comparison of the failure times of pulse oximeters during blood pressure cuff-induced hypoperfusion in volunteers.

Important information may not be obtained if the pulse oximetry signal is lost during inflation of a cuff for blood pressure measurement, particularly in patients with hemodynamic instability. In the present study, we compared the failure times of pulse oximeters during cuff-induced hypoperfusion in volunteers. A pulse oximeter sensor was attached to the index finger, and a blood pressure cuff was attached to the same arm of each volunteer. MasimoSET Radical (Masimo), Nellcor N-395 (N-395), Nellcor N-20PA, and Nellcor D-25 were tested. To evaluate the failure time of each pulse oximeter, time to peak of cuff pressure, time to loss of signal, time to recovery of signal, and failure interval were measured. All measurements were performed three times for each pulse oximeter and were averaged. There were no differences in hemodynamic measurements among the groups. Time to loss of signal was longer in Masimo than the other pulse oximeters. Masimo and N-395 showed significantly shorter times to recovery of signal than those of the other two pulse oximeters. Failure interval was in the order of Masimo << N-395 < Nellcor D-25 = Nellcor N-20PA. Masimo did not lose a signal as rapidly as the other oximeters studied. Masimo was similar in performance to the N-395 at providing useful data sooner than conventional technology after a loss of the signal. These observations suggest that data will be more available with fewer false-positive alarms when using the Masimo oximeter followed by the N-395 when compared with conventional oximeters.

Adult↗
PubMed2004

[The use of a Parker Flex-Tip tube in a case of large laryngeal polyps].

A 58-year-old man was scheduled for laryngomicrosurgery for treatment of large laryngeal polyps. Although awake induction was initially attempted to prevent airway obstruction, his vocal cords could not be visualized. We therefore tried intubation with a Parker Flex-Tip (PFT) tube under the guidance of a bronchial fiberscope (BF). After inserting the BF, his trachea was intubated easily. The operation was performed without any complications. We conclude that a PFT tube is useful for endotracheal intubation in a patient with large laryngeal polyps.

Anesthesia↗
PubMed2004

[The usefulness of intraoperative TEE monitoring in a patient with renal cell carcinoma].

A 55-year-old man was admitted to our hospital for treatment of renal cell carcinoma. Preoperative MRI showed infradiaphragmatic extension of the tumor thrombus. However, intraoperative transesophageal echocardiography (TEE) revealed intracardiac extension of the thrombus. Therefore, the tumor thrombus was extirpated under cardiopulmonary bypass. The patient recovered without any complications. Intraoperative TEE monitoring is useful not only for the evaluation of cardiac functions but also for intraoperative diagnosis of a tumor thrombus during the operation for renal cell carcinoma.

Carcinoma, Renal Cell↗
PubMed2004

[In vitro evaluation of lubrication properties of a suction catheter].

BACKGROUND: Lubrication is an important factor for passage of a suction catheter through a tracheal tube. This study was carried out to evaluate the effects of lubricants on resistance against removal of a suction catheter from a tracheal tube in an experimental setting. METHODS: A tracheal tube (I.D. of 7.5mm) was inserted into a mannequin, and the resistance against removal of a suction catheter from the tube was measured. RESULTS: Lubrication was improved by using a lubricant (lidocaine jelly or KY jelly), but there was no difference between the effects of the two lubricants. The use of water as lubricant markedly decreased lubrication. Differences in lubrication depending on the type of tracheal tube used, probably due to differences in coating, were also found. CONCLUSIONS: The use of water as a lubricant is not recommended for tracheal suction.

Catheterization↗
PubMed2003

Landiolol, esmolol and propranolol protect from ischemia/reperfusion injury in isolated guinea pig hearts.

PURPOSE: Beta blockers are thought to exert beneficial effects on the ischemic heart. The authors examined the effects of landiolol (ONO 1101), a highly selective beta1 antagonist, propranolol, a nonspecific beta blocker, and esmolol, a selective beta1 antagonist, on postischemic contractile recovery. Drugs were given prophylactically. METHODS: Ischemia-reperfusion in isolated guinea pig hearts was induced by stopping the perfusion for 45 min and reperfusing for 60 min. Hearts (n = 7 in each group) were treated with or without propranolol (1 or 10 microM), esmolol (5 or 50 microM), or landiolol (20, 100 or 500 microM) ten minutes before inducing ischemia. RESULTS: At the end of reperfusion, left ventricular pressure (LVP) recovered to 64 +/- 3% of the baseline value in the control group. With 1 and 10 microM propranolol, LVP recovered to 90 +/- 5% and 100 +/- 6% of the baseline value at 60 min after reperfusion, respectively. Fifty microM but not 5 microM of esmolol resulted in restoration of LVP to 97 +/- 17% of the pre-ischemic value at 60 min after reperfusion. In hearts pretreated with 100 and 500 microM landiolol, LVP was restored to 109 +/- 5% and 104 +/- 5% of the baseline value, respectively. Landiolol 100 microM did not depress LVP in the pre-ischemic period. CONCLUSIONS: The present study shows that landiolol, an ultra-short-acting cardioselective beta1 blocker, has cardioprotective effects on ischemia-reperfusion injury in isolated guinea pig hearts. All three beta blockers were equally protective but the intermediate dosage of landiolol preserved LVP during the pre-ischemic period.

Adrenergic beta-Antagonists↗
PubMed2003

Hemodynamic and bispectral index responses to tracheal intubation during isoflurane or sevoflurane anesthesia.

PURPOSE: The effects of volatile anesthetics on change in the bispectral index (BIS) due to tracheal intubation are unclear. We investigated hemodynamic and BIS responses to intubation during isoflurane or sevoflurane anesthesia. METHODS: After obtaining Institutional Review Board approval and informed consent, we randomly allocated 40 patients of American Society of Anesthesiologists (ASA) physical status I to receive either isoflurane (ISO group; n = 20) or sevoflurane (SEV group; n = 20). The patients were anesthetized with thiamylal and were ventilated with 100% oxygen, using a mask. The inspired concentrations of isoflurane and sevoflurane were gradually increased and maintained at end-tidal anesthetic concentrations of 2 minimum alveolar concentration (MAC) during the study period. Tracheal intubation was performed 15 min after the end-tidal anesthetic concentrations had reached 2 MAC. Mean arterial pressure (MAP), heart rate (HR), and BIS were recorded before induction, at the loss of consciousness, before laryngoscopy, and at 1, 3, and 5 min after intubation. RESULTS: Anesthesia with 2 MAC volatile anesthetics increased HR in the ISO group, and decreased MAP in the SEV group. The BIS value decreased from 95 +/- 3 and 96 +/- 2 before thiamylal to 39 +/- 9 and 38 +/- 10 before intubation in the ISO and SEV groups, respectively. MAP and HR were significantly increased in both groups 1 and 3 min after intubation, but BIS remained unchanged. CONCLUSION: Anesthesia with 2 MAC of isoflurane and sevoflurane was effective to suppress the change in BIS due to intubation but was not sufficient to prevent changes in hemodynamic responses.

Adult↗
PubMed2003

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.

Anesthesia, Intravenous↗
PubMed2003

Differential effects of propofol and sevoflurane on heart rate variability.

BACKGROUND: Propofol is reported to reduce both sympathetic and parasympathetic tone; however, it is not clear whether the changes in heart rate variability are associated with depth of anesthesia. The purposes of the present study were (1) to evaluate the changes in heart rate variability at different depths of hypnosis and (2) to compare the effects of propofol on heart rate variability with that of sevoflurane. METHODS: Thirty patients were randomly allocated into the propofol or sevoflurane for induction of anesthesia. The depth of hypnosis was monitored by the Bispectral Index (BIS). Spectral analysis of heart rate variability using a maximum-entropy method resulted in a characteristic power spectrum with two main regions, a high frequency (HF) and a low frequency (LF). Hemodynamics, entropy, LF, HF, and LF/HF were monitored when the patients were awake and after induction of anesthesia. RESULTS: Both propofol and sevoflurane decreased blood pressure in a BIS-dependent manner, whereas heart rate showed no significant changes during the study period. In the propofol group, entropy and HF decreased with a reduction in the BIS value. Although LF decreased after induction of anesthesia, propofol caused no further decrease in LF in spite of a reduction in the BIS value. In the sevoflurane group, LF decreased with a reduction in the BIS value. Entropy and HF decreased after induction of anesthesia (BIS at 80); however, no further decreases were observed in spite of a reduction in the BIS value. CONCLUSIONS: Induction of anesthesia with propofol decreased blood pressure, entropy, and HF in a BIS-dependent manner, indicating that propofol reduces cardiac parasympathetic tone depending on the depth of hypnosis. Conversely, sevoflurane did not show the BIS-dependent decreases in heart rate, blood pressure, HF, and entropy, indicating that sevoflurane has little or no effect on cardiac parasympathetic tone.

Adult↗
PubMed2003

Role of endothelium-derived hyperpolarizing factor in phenylephrine-induced oscillatory vasomotion in rat small mesenteric artery.

BACKGROUND: In small mesenteric arteries, endothelium-derived hyperpolarizing factor (EDHF) in addition to endothelium-derived relaxing factors (EDRFs) including NO plays an important role in acetylcholine-induced vasodilation. It has been reported that EDRFs play an important role in alpha(1)-adrenoceptor agonist-induced oscillatory vasomotion and in limiting vasoconstrictor response to the agonists; however, contribution of EDHF to the alpha(1)-agonist-induced oscillation is unknown. METHODS: Rat small mesenteric arteries were isolated and cannulated at each end with a glass micropipette. The vessels were immersed in a bath (37 degrees C) containing physiologic saline solution. Changes in vessel diameter were measured using an optical density video detection system. RESULTS: Denudation of the endothelium and inhibition of NO synthesis caused a leftward shift in the concentration-response relation for phenylephrine in the mesenteric arteries, whereas inhibition of cyclooxygenase by indomethacin had no effect. Blockade of Ca2+-activated K+ (K(Ca)) channels by charybdotoxin and apamin caused a further leftward shift in the concentration-response relation in the vessels pretreated with Nomega-nitro-l-arginine methylester and indomethacin. Phenylephrine at concentrations higher than 10(-6) m caused endothelium-dependent oscillatory vasomotion, which was reduced but not abolished after combined inhibition of the cyclooxygenase and NO synthase pathways. However, the K(Ca) channel blockers completely abolished the remaining component of oscillation. CONCLUSIONS: Endothelially-derived NO is an important modulator of sustained agonist-induced vasoconstriction. NO, as well as endothelially-derived cyclooxygenase products and EDHF, also contribute significantly to phenylephrine-induced oscillatory vasomotion.

Animals↗