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Biomedical subjects

Hiroyuki Kobayashi

Publications and source records attributed to Hiroyuki Kobayashi.

At least 91 records · Page 5Linked to original sources
PubMed2005

Optimal puncture site of the right internal jugular vein after laryngeal mask airway placement.

BACKGROUND: Puncturing of the internal jugular vein (IJV) after placement of a laryngeal mask airway (LMA) is difficult. Overlapping of the right internal jugular vein (IJV) and common carotid artery (CCA) after placement of an LMA-Classic (Laryngeal Mask Company, Henley-on-Thames, United Kingdom) was investigated using an ultrasound scanner. A study was conducted to determine the optimal puncture site in the case of puncturing the right IJV after LMA-Classic placement. METHODS: The subjects in this study consisted of 114 patients (60 men and 54 women) scheduled to undergo LMA-Classic placement (size 4 for men and size 3 for women). Overlapping between the IJV and CCA was investigated at three points (high, middle, and low points) on the right side of the neck after LMA-Classic placement. A test puncture was also made at the right low (supraclavicular) point after LMA-Classic placement. RESULTS: (1) The degree of overlapping of the right IJV and CCA after LMA-Classic placement was clearly greater than before LMA placement. (2) With the exception of some measurements, there were many cases in which the right IJV and CCA were completely overlapping after LMA-Classic placement. Furthermore, the CCA was not observed in the vicinity of the right IJV at the right low point. (3) There were no complications (including pneumothorax and accidental arterial puncture) during supraclavicular IJV puncture after LMA-Classic placement. CONCLUSION: After placement of the LMA-Classic, overlapping of the IJV and CCA increased at the high and middle puncture points of the IJV; however, at the lower puncture point, the position of the vessels remained unaffected. Therefore, during IJV puncture at high or middle points, ultrasound guidance is advisable to avoid CCA puncture.

Adult↗
PubMed2005

Identification of human P450 isoforms involved in the metabolism of the antiallergic drug, oxatomide, and its kinetic parameters and inhibition constants.

Oxatomide is an antiallergic drug used for the treatment of diseases mediated by type I allergy. Recently, terfenadine and astemizole, which have antiallergic actions similar to those of oxatomide, showed side effects on the cardiovascular system. This might be because concomitant drugs such as itraconazole inhibit cytochrome P450 3A4 (CYP3A4), the enzyme responsible for the degradation of terfenadine and astemizole, and thus the blood concentrations of the drugs are abnormally increased. In another article of this issue, we have reported that oxatomide is metabolized by CYP2D6-Val and CYP3A4, and simultaneously inhibits the metabolism of the model substrates for these enzymes. In this study, we performed the kinetic analysis of oxatomide metabolism using microsomes prepared from human liver, and found that the Km and Vmax values were 26.1 microM and 1254.4 pmol/mg protein/min, respectively. Ketoconazole, one of the representative inhibitors for CYP3A4, potently inhibited the metabolism of oxatomide, but other well-known CYP inhibitors did not show significant inhibition. These results suggest that the metabolism of oxatomide is principally catalyzed by CYP3A4. Furthermore, oxatomide inhibited the metabolism of (+/-) bufuralol and testosterone, model substrates for CYP2D6 and CYP3A4, respectively, in a dose-dependent manner with the Ki values of 57.4 and 24.3 microM, respectively. These observations, together with the finding that the putative highest concentration of oxatomide in blood was congruent with 40 ng/ml ( congruent with 93 nM) at 4 h after each dosage during consecutive 6-d administration, encouraged us to conclude that oxatomide won't inhibit CYP2D6 or CYP3A4 at clinical doses.

Anti-Allergic Agents↗
PubMed2005

A case of Henoch-Schönlein purpura with rare complications: necrosis of the small intestine, neurological symptoms, and pericardial tamponade.

A case of Henoch-Schönlein purpura (HSP) with necrosis of the small intestine, neurological symptoms, and pericardial tamponade after frequent recurrence is described. Neurological symptoms were controlled well with steroid pulse therapy, and pericardial tamponade was treated successfully with pericardiocentesis and steroid pulse therapy. To treat necrosis of the small intestine, the necrotic tissue was excised and artificial anuses were constructed. Five months later, the small intestine was anastomosed in a curative operation. Periodic administration of coagulation factor XIII was required from the onset of symptoms until curative surgery, but the activity of this factor returned to normal levels after surgery operation. We report a case of Henoch-Schönlein purpura with extremely rare complications: necrosis of the small intestine, neurological symptoms, and pericardial tamponade.

Abdominal Pain↗
PubMed2005

Cilnidipine, an N+L-type dihydropyridine Ca channel blocker, suppresses the occurrence of ischemia/reperfusion arrhythmia in a rabbit model of myocardial infarction.

Dihydropyridine Ca channel blockers are widely prescribed for the treatment of hypertension and coronary artery diseases, but it remains unknown whether these agents protect against arrhythmias. We investigated whether cilnidipine, an N+L-type Ca channel blocker, reduces the incidences of ventricular premature beats (VPBs) and, if so, via what mechanisms. Japanese white rabbits underwent 30 min of ischemia and 48 h of reperfusion. Cilnidipine (0.5 or 1.0 microg/kg/min, i.v.) or saline (i.v.) was administered from 30 min before ischemia to 30 min after reperfusion. Electrocardiogram and blood pressure were monitored and the incidences of VPBs were measured. At 48 h after reperfusion, myocardial infarct was measured. Myocardial interstitial noradrenaline levels were determined before, during and after 30 min of ischemia with cilnidipine (0.5 and 1.0 microg/kg/min) or saline. The incidences of VPBs during ischemia and reperfusion were significantly attenuated in the cilnidipine 0.5 group (15.6 +/- 3.1 and 6.8 +/- 1.9 beats/30 min) and in the cilnidipine 1.0 group (10.4 +/- 4.9 and 3.5 +/- 1.0 beats/30 min) compared to the control group (27.2 +/- 4.5 and 24.2 +/- 3.1 beats/30 min), respectively. Myocardial interstitial noradrenaline levels were significantly reduced in the cilnidipine 0.5 and 1.0 groups compared to the control group during ischemia and reperfusion. The antiarrhythmic effect of cilnidipine may be related to the attenuation of cardiac sympathetic nerve activity. This finding may provide new insight into therapeutic strategies for hypertensive patients with ventricular arrhythmias.

Animals↗
PubMed2005

Airway biofilms: implications for pathogenesis and therapy of respiratory tract infections.

The differentiation of bacterial biofilms in the airway environment, the pathogenesis of airway biofilm, and possible therapeutic methods are discussed. Biofilm diseases that characteristically involve the respiratory system include cystic fibrosis (CF), diffuse panbronchiolitis (DPB), and bronchiectasia with Pseudomonas aeruginosa (P. aeruginosa) infection. There is evidence to suggest that almost all strains of P. aeruginosa have the genetic capacity to synthesize alginate, a main matrix of biofilms, when ecological conditions are unfavorable for their survival. The bacteria inside the mature biofilm show increased resistance to both antibacterials and phagocytic cells, express fewer virulence factors because of their stationary state of growth, and are less stimulatory to the mucosa because of the 'sandwich binding'. These factors facilitate both the colonization of bacteria and their extended survival even under unfavorable conditions. Since the biofilm limits colonization to a latent form, the clinical symptoms in this situation are unremarkable. However, the clinical progression of both CF and DPB proceeds in two characteristic directions. The first is an acute exacerbation caused by planktonic bacteria that have germinated from the biofilm. The second is a slow progression of disease that is induced by harmful immune reactions. The harmful reactions are mediated by alginate, which induces antigen antibody reactions around the airways, as well as formation of circulating immune complexes that are deposited on lung tissue. Furthermore, the highest titer of bacterial permeability increasing anti-neutrophil cytoplasmic autoantibodies (BPI-ANCA) is observed in association with highly impaired pulmonary function in patients with CF and DPB, as well as in patients with a lengthy period of colonization with P. aeruginosa. BPI-ANCA subsequently makes chronic airway infection even more intractable. The long-term use of 14- or 15-ring membered macrolides results in a favorable clinical outcome for patients with DPB and in some patients with CF. In the last 10 years, an increasing number of studies have reported secondary actions of macrolides that include effects on both airway and phagocytic cells, as well as an anti-biofilm activity. The 14- or 15-ring membered macrolides inhibit: (i) the alginate production from P. aeruginosa; (ii) the antibody reaction to alginate, which leads to a decrease in the immune complex formation; and (iii) the activation of the autoinducer 3-O-C12-homoserine lactone and subsequent expression of lasI and rhlI in quorum sensing systems in P. aeruginosa. These anti-biofilm actions of macrolides may represent their basic mechanisms of action on airway biofilm disease.

Anti-Bacterial Agents↗
PubMed2004

INK4a/Arf is required for suppression of EGFR/DeltaEGFR(2-7)-dependent ERK activation in mouse astrocytes and glioma.

Amplification of the epidermal growth factor receptor (EGFR) or expression of its constitutively activated mutant, DeltaEGFR(2-7), in association with the inactivation of the INK4a/Arf gene locus is a frequent alteration in human glioblastoma. The notion of a cooperative effect between these two alterations has been demonstrated in respective mouse brain tumor models including our own. Here, we investigated underlying molecular mechanisms in early passage cortical astrocytes deficient for p16(INK4a)/p19(Arf) or p53, respectively, with or without ectopic expression of DeltaEGFR(2-7). Targeting these cells with the specific EGFR inhibitor tyrphostin AG1478 revealed that phosphorylation of ERK was only abrogated in the presence of an intact INK4a/Arf gene locus. The sensitivity to inhibit ERK phosphorylation was independent of ectopic expression of DeltaEGFR(2-7) and independent of the TP53 status. This resistance to downregulate the MAPK pathway in the absence of INK4a/Arf was confirmed in cell lines derived from our mouse glioma models with the respective initial genetic alterations. Thus, deletion of INK4a/Arf appears to keep ERK in its active, phosphorylated state insensitive to an upstream inhibitor specifically targeting EGFR/DeltaEGFR(2-7). This resistance may contribute to the cooperative tumorigenic effect selected for in human glioblastoma that may be of crucial clinical relevance for treatments specifically targeting EGFR/DeltaEGFR(2-7) in glioblastoma patients.

Animals↗
PubMed2004

Association between cardiovascular autonomic neuropathy and left ventricular hypertrophy in diabetic haemodialysis patients.

BACKGROUND: Patients with diabetic nephropathy are likely to have neurological complications including cardiovascular autonomic dysfunction, which is related to increased risk of mortality. We investigated whether cardiovascular autonomic neuropathy is associated with left ventricular hypertrophy (LVH) in diabetic haemodialysis patients. METHODS: Holter electrocardiography was carried out for 24 h with time and frequency domain analyses of heart rate variability in 154 diabetic (age 62+/-11 years) and 63 non-diabetic haemodialysis patients (62+/-10 years). The left ventricular mass index (LVMI) was determined by echocardiography. We used the percentage of differences exceeding 50 ms between adjacent normal RR intervals (pNN50) in time domain analysis and the power in the high-frequency range (HF: 0.15-0.40 Hz) in frequency domain analysis as indicators of parasympathetic activity. RESULTS: The mean LVMI was greater in diabetic than in non-diabetic patients (168+/-63 vs 144+/-54 g/m(2), P<0.01). LVMI inversely correlated with pNN50 (r = -0.270, P = 0.0007, n = 154) and HF (r = -0.277, P = 0.0005, n = 154) in diabetic patients, but not in non-diabetic patients. By multiple logistic analysis, LVH was strongly associated with pNN50 (odds ratio 0.088; 0, <2%; 1, >/=2%) and HF (odds ratio 0.058; 0, <500 ms(2); 1, >/=500 ms(2)) in diabetic patients. CONCLUSIONS: Impaired parasympathetic activity, which indicates cardiovascular autonomic neuropathy, was associated with the presence of LVH in diabetic haemodialysis patients. The co-existence of cardiovascular autonomic neuropathy and LVH may be one of the key factors for the high incidence of cardiovascular events in diabetic haemodialysis patients.

Aged↗