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Biomedical subjects

K Nagase

Publications and source records attributed to K Nagase.

At least 19 recordsLinked to original sources
PubMed2001

Ketamine, not propofol, attenuates cerebrovascular response to carbon dioxide in humans with isoflurane anesthesia.

STUDY OBJECTIVES: To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO(2)) in humans during isoflurane anesthesia. DESIGN: Randomized clinical investigation. SETTINGS: University hospital of a medical school. PATIENTS: 30 ASA physical status I and II adult, elective surgical patients. INTERVENTIONS AND MEASUREMENTS: With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artery (Vmca) and pulsatility index were measured using the transcranial Doppler method under hypocapnic [arterial CO(2)tension (PaCO(2)) 28-32 mmHg], normocapnic (PaCO(2) 38-42 mmHg), and hypercapnic conditions (PaCO(2) 48-52 mmHg). PaCO(2) was altered by supplementing the inspired gas with CO(2) without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg. kg(-1) or propofol (2 mg. kg(-1)followed by an infusion of 6-10 mg. kg(-1). hr(-1)) (n = 15 for each drug), and the measurements were repeated. MAIN RESULTS: Ketamine reduced both absolute and relative cerebrovascular reactivity to CO(2) significantly [2.9 +/- 0.8 (control) vs. 2.6 +/- 1.0 (ketamine) cm. sec(-1). mmHg(-1): p < 0.05; and 3.5 +/- 0.7 (control) vs. 2.8 +/- 0.9 (ketamine) %. mmHg(-1): p < 0.01, respectively]. However, ketamine did not reduce Vmca during hypercapnic conditions (117 +/- 29 cm. sec(-1)) compared with controls (120 +/- 28 cm. sec(-1)). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO(2) reactivity [2.5 +/- 0.8 (control) vs. 2.5 +/- 1.0 (propofol) cm. sec(-1). mmHg(-1), and 3.3 +/- 1.3 (control) vs. 4.1 +/- 1.0 (propofol) %. mmHg(-1), respectively]. CONCLUSIONS: In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO(2), but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO(2).

Adult↗
PubMed2001

The effects of topical and intravenous ketamine on cerebral arterioles in dogs receiving pentobarbital or isoflurane anesthesia.

To evaluate the effects of ketamine on cerebral arterioles, we used a closed cranial window technique in mechanically ventilated, anesthetized dogs. Fourteen dogs were assigned to one of the following two basal-anesthesia groups: pentobarbital 2 mg. kg(-1). h(-1) or isoflurane 0.5 MAC (n = 7 each). We administered three different concentrations of ketamine (10(-7), 10(-5), and 10(-3) M) under the window and measured arteriolar diameters. For comparison, in another 14 dogs we examined the effect of systemic (IV) ketamine (1 mg/kg and 5 mg/kg) using the same two basal anesthetics. We measured diameters before and after ketamine administration, and we evaluated the effect of ketamine on CO(2) reactivity of the cerebral arterioles. Neither topical nor systemic ketamine dilated pial arterioles in either basal-anesthesia group. CO(2) reactivity of pial arterioles was reduced under systemic ketamine in both basal-anesthesia groups. The results indicate that although ketamine does not dilate pial arteriolar diameters when topically or IV administered, IV ketamine does attenuate hypercapnic vasodilation in dogs under basal pentobarbital or isoflurane anesthesia. These results provide some insight that ketamine is suitable for supplementary neurosurgical anesthesia.

Adjuvants, Anesthesia↗
PubMed2001

The anxiolytic effects of the 5-hydroxytryptamine-1A agonist tandospirone before otolaryngologic surgery.

UNLABELLED: We studied 160 ASA I or II patients undergoing elective otolaryngologic surgery in order to compare the anxiolytic effects of a novel 5-hydroxytryptamine-1A agonist, tandospirone, with diazepam. To monitor preoperative anxiety, the following variables were used: systolic and diastolic arterial pressure, heart rate, and the state anxiety score yielded by the Spielberger State-Trait Anxiety Inventory. We performed pretreatment evaluation on the day before surgery and posttreatment examination immediately after entry into the operating room. In a double-blinded, randomized design, four groups of 40 patients each received one of the following oral medications 90 min before entry into the operating room: 1) tandospirone 10 mg (T10 group); 2) tandospirone 30 mg (T30 group); 3) diazepam 10 mg (D group); or 4) placebo (P group). After premedication, the State-Trait Anxiety Inventory state anxiety decreased in the T10 (P < 0.02), T30 (P < 0.02), and D groups (P < 0.001), but it increased in the P group (P < 0.001). Tandospirone, 10 and 30 mg, safely reduced preoperative anxiety to a similar extent as oral diazepam 10 mg in patients undergoing elective otolaryngologic surgery. IMPLICATIONS: Oral tandospirone reduces preoperative anxiety to a similar extent as oral diazepam in patients undergoing elective otolaryngologic surgery. This finding implies that tandospirone can be used as an oral premedicant drug for relieving anxiety before surgery.

Adolescent↗
PubMed2001

The differential effects of stereoisomers of ropivacaine and bupivacaine on cerebral pial arterioles in dogs.

UNLABELLED: We investigated whether the stereoisomers of ropivacaine and bupivacaine exert differential effects on the cerebral microcirculation. Pentobarbital-anesthetized dogs (n = 16) were prepared for measurement of cerebral pial vessel diameters by using a closed cranial window preparation. We administered three different concentrations (10(-7), 10(-5), and 10(-3) M) of each of three drug solutions [R(+), racemic, and S(-) forms of ropivacaine (n = 8) or bupivacaine (n = 8)] under the window in a randomized manner and measured cerebral pial arteriolar diameters. Various physiologic data were obtained before and after topical application of each test solution. All three forms of ropivacaine constricted cerebral pial arterioles, each in a concentration-dependent manner. The rank order for degree of vasoconstriction was S(-) ropivacaine > racemic ropivacaine > R(+) ropivacaine. In contrast, R(+) and racemic bupivacaine dilated, but S(-) bupivacaine constricted, cerebral pial arterioles, each in a concentration-dependent manner. We could find no difference in vascular reactivity to these drugs between large (> or = microm) and small (<100 microm) arterioles. Topical application of these drugs induced no changes in mean blood pressure or heart rate. The observed differences in the microvascular alterations induced by the stereoisomers of ropivacaine and bupivacaine suggest that the vasoactive effects of these drugs on cerebral arterioles could, at least in part, depend on their chirality. IMPLICATIONS: The differential effects of the stereoisomers of ropivacaine and bupivacaine on cerebral pial vessels could, at least in part, depend on their chirality.

Amides↗
PubMed2001

Spontaneous normalization of negative T waves in infarct-related leads reflects improvement in left ventricular wall motion even in patients with persistent abnormal Q waves after anterior wall acute myocardial infarction.

This study aimed to clarify whether spontaneous T-wave normalization (TWN) in infarct-related leads reflects improvement in left ventricular (LV) wall motion even in patients with persistent abnormal Q waves after acute myocardial infarction (AMI). Eighty-five patients were classified into the following 3 groups: patients with Q-wave regression (group A, n = 21), those with persistent abnormal Q waves and TWN (group B, n = 36), and those with persistent abnormal Q waves and absence of TWN (group C, n = 28). Groups A and B had greater improvement in LV ejection fraction and regional wall motion between 1 and 6 months after AMI than group C. In conclusion, spontaneous TWN in the healing stage of anterior AMI reflects functional recovery of viable myocardium in the infarct region even in patients with persistent abnormal Q waves.

Aged↗
PubMed2001

Relationship between terminal QRS distortion on the admission electrocardiogram and the time course of left ventricular wall motion in anterior wall acute myocardial infarction.

In order to clarify the time course of left ventricular (LV) wall motion in patients with anterior acute myocardial infarction (AMI) showing terminal QRS distortion on the admission electrocardiogram (ECG), the present study examined 106 patients with their first anterior AMI (< or =6 h) who underwent emergency coronary arteriography and cardiac cathetherization at 1 and 6 months after the infarction. The patients were classified into 2 groups according to the presence (group A, n=23) or absence (group B, n=83) of terminal QRS distortion (emergence of the J point at > or =50% of the R-wave amplitude in leads with QR configuration and/or absence of S waves in leads with RS configuration) on the admission ECG. Group A had a lower LV ejection fraction and more reduced regional wall motion (RWM) in the infarct region at both 1 and 6 months after AMI than group B. The degree of improvement in RWM between 1 and 6 months after AMI was less in group A than in group B (-0.1+/-0.5 vs 0.4+/-0.6 SD/chord, p<0.01). This study indicates that patients with anterior AMI showing terminal QRS distortion on the admission ECG have more severely depressed LV wall motion and less improvement in RWM in the infarct region in the healing stage, suggesting that this sign is an indicator of severe myocardial damage.

Aged↗
PubMed2000

Isolation of antigen from the circulating immune complex in mice infected with Plasmodium berghei.

Circulating immune complex (CIC) is known to play a role in pathological glomerular alterations in malaria. However, the nature of the antigens comprising the CIC is still not fully understood. We report here the isolation of the antigen in CIC and its localisation in mice infected with Plasmodium berghei NK65. The antigen was successfully isolated from CIC extracted from the blood of mice infected with P. berghei, by using C1q-coated microplates. The molecular mass of the antigen separated from CIC bound to C1q was found to be 78 kDa. Furthermore, localisation of the antigen was examined by the fluorescent antibody technique and immunoelectron microscopy. The antigen was detected in the parasitised erythrocyte and the mesangial matrix by both methods. These results suggest that the 78 kDa protein might be associated with the glomerular alterations in malaria infection.

Animals↗
PubMed2000

Conditionally immortalized brain capillary endothelial cell lines established from a transgenic mouse harboring temperature-sensitive simian virus 40 large T-antigen gene.

Five immortalized brain capillary endothelial cell lines (TM-BBB1-5) were established from 3 transgenic mice harboring temperature-sensitive simian virus 40 large T-antigen gene (Tg mouse). These cell lines expressed active large T-antigen and grew well at 33 degrees C with a doubling time of about 20 to 30 hours. TM-BBBs also grew at 37 degrees C but not at 39 degrees C. However, growth was restored when the temperature of the culture was lowered to 33 degrees C. Although significant amounts of large T-antigen were shown to be present in the cell culture at 33 degrees C, there was less of this complex at 37 degrees C and 39 degrees C. TM-BBBs expressed the typical endothelial marker, von Willebrand factor, and exhibited acetylated low-density lipoprotein uptake activity. The alkaline phosphatase and gamma-glutamyltranspeptidase activity in TM-BBBs were -10% and 50% to 80% of brain capillary fraction of normal mice, respectively. D-mannitol transport in the both apical-to-basal and basal-to-apical directions across the TM-BBB was 2-fold greater than for inulin. TM-BBBs were found to express GLUT-1 but not GLUT-3, and exhibited concentration-dependent 3-O-methyl-D-glucose (3-OMG) uptake activity with a Michaelis-Menten constant of 6.59 +/- 1.16 mmol/l. Moreover, P-glycoprotein (P-gp) with a molecular weight of -170 kDa was expressed in all TM-BBBs. Both mdr1a and mdr1b mRNA were detected in TM-BBB4 using reverse transcription-polymerase chain reaction (RT-PCR) analysis. [3H]-Cyclosporin A uptake by TM-BBB was significantly increased in the presence of 100 micromol/l verapamil and vincristine, suggesting that TM-BBB exhibits efflux transport activity via P-gp. In conclusion, conditional brain capillary endothelial cell lines were established from Tg mice. This cell line expresses endothelial markers and transporters at the BBB and is able to regulate cell growth, due to the amount of active large T-antigen in the cell, by changing the culture temperature.

3-O-Methylglucose↗
PubMed1999

Significance of spontaneous normalization of negative T waves in infarct-related leads during healing of anterior wall acute myocardial infarction.

This study was conducted to elucidate the significance of spontaneous normalization of negative T waves in infarct-related leads during the chronic phase of anterior wall acute myocardial infarction. Results of this study indicate that patients with spontaneous normalization of negative T waves in infarct-related leads between 1 and 6 months after anterior wall acute myocardial infarction have smaller infarct size, decreased left ventricular dysfunction, and greater improvement in left ventricular wall motion in the infarct area, suggesting that T-wave normalization represents functional recovery of viable myocardium in the infarct area.

Biomarkers↗
PubMed1999

Relation between negative U waves in precordial leads on the admission electrocardiogram and time course of left ventricular wall motion in anterior wall acute myocardial infarction.

This study indicates that patients with anterior wall acute myocardial infarction showing negative U waves in the precordial leads on the admission electrocardiogram have greater improvement in left ventricular wall motion in the infarct region between 1 and 6 months after acute myocardial infarction. This suggests that these patients have a larger amount of stunned myocardium in the infarct region.

Aged↗
PubMed1999

Relation of QT dispersion to infarct size and left ventricular wall motion in anterior wall acute myocardial infarction.

Previous studies have shown that QT dispersion increases during acute myocardial infarction (AMI). However, the relation of QT dispersion to infarct size and left ventricular (LV) function in AMI has not yet been fully clarified. Accordingly, this study was conducted to elucidate this relation at 1 month after anterior wall AMI. We examined 94 patients with first anterior wall AMI (< or = 6 hours) who underwent coronary arteriography at admission, 1 month, and 6 months after AMI, and left ventriculography at 1 and 6 months after AMI. Mean QT dispersion on the chronic phase (about 1 month after AMI) electrocardiogram was 79 +/- 33 ms. There were no significant correlations between QT dispersion and peak creatine phosphokinase levels, LV ejection fraction, and regional wall motion in the infarct region at 1 month after AMI (r = 0.06, p = 0.57; r = 0.11, p = 0.29; r = -0.05, p = 0.63, respectively). In conclusion, the findings of this study suggest that QT dispersion on the resting electrocardiogram at 1 month after anterior wall AMI is unrelated to infarct size estimated by the peak creatine phosphokinase level and the degree of LV dysfunction.

Aged↗
PubMed1999

Attenuated additional hypocapnic constriction, but not hypercapnic dilation, of spinal pial arterioles during spinal ropivacaine.

UNLABELLED: Ropivacaine constricts spinal vessels. Because the CO2 response of spinal vessels is similar to that of cerebral vessels, we tested to see if hypocapnia would cause further spinal vasoconstriction during ropivacaine administration. In 12 pentobarbital-anesthetized dogs, spinal pial arteriolar diameter was measured using a closed spinal window preparation. Either ropivacaine solution (0.1%; n = 6) or artificial cerebrospinal fluid (n = 6) was infused continuously into the spinal window. After a period of hypocapnia (Paco2, 20-25 mm Hg) had been induced, inspired CO2 levels were adjusted to produce normocapnia (35-40 mm Hg) followed by hypercapnia (55-60 mm Hg). When the desired Paco2 was reached, measurements were made of the arteriolar diameter and physiological variables. During normocapnia, ropivacaine infusion produced a significant constriction of pial arterioles, whereas artificial cerebrospinal fluid caused no change. Hypocapnia induced a much smaller (almost nonexistent) additional vasoconstriction in the ropivacaine group than in the control group (P < 0.01). The final hypercapnic vasodilation was somewhat greater during ropivacaine (P < 0.05 versus control group). Topical ropivacaine induced no change in hemodynamic variables. We conclude that hypocapnia of the magnitude tested did not cause further constriction in spinal vessels during spinal ropivacaine. IMPLICATIONS: During topical application of the local anesthetic ropivacaine in dogs, hypocapnia (Paco2, 20-25 mm Hg) induced almost no additional constriction of spinal arterioles, and the hypercapnic vasodilation was maintained. These data suggest that an additional constriction in spinal vessels is unlikely when hypocapnia occurs during spinal ropivacaine.

Administration, Topical↗
PubMed1999

Angiographic and clinical significance of 'transient' ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction.

This study aimed to clarify the significance of ST-segment depression in the lateral chest leads in anterior wall acute myocardial infarction (AMI) with ST-segment elevation. A total of 196 patients with their first anterior wall AMI (< or =6h) were divided into 2 groups according to the presence (group A, n=39) or absence (group B, n=157) of ST-segment depression > or =0.1 mV in V5 and/or V6 on the admission electrocardiogram. Patients with electrocardiographic confounding factors were excluded. No patients had persistent ST-segment depression in the lateral chest leads. Emergency coronary angiography revealed that group A had higher incidences of occlusion of the left anterior descending coronary artery (LAD) proximal to its first septal branch (77% vs 51%, p<0.01) and good collateral circulation than group B (46% vs 25%, p<0.05). Peak creatine kinase levels were significantly lower in group A than in group B (2060+/-1099 vs 2873+/-2077 IU/L, p<0.01). Left ventricular ejection fraction in the chronic phase was significantly greater in group A than in group B. Regional wall motion in the infarct region in the chronic phase was better in group A than in group B. These results indicate that patients with 'transient' ST-segment depression in the lateral chest leads in anterior wall AMI had a relatively smaller infarct size, despite their higher incidence of occlusion of the LAD proximal to its first septal branch, because of their higher incidence of good collateral circulation.

Aged↗