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Biomedical subjects

Hitoshi Yamaguchi

Publications and source records attributed to Hitoshi Yamaguchi.

5 recordsLinked to original sources
PubMed2006

Coronary flow reserve by contrast enhanced transesophageal coronary sinus Doppler measurements can evaluate diabetic microvascular dysfunction.

BACKGROUND: This study was undertaken to investigate whether coronary flow reserve (CFR) using coronary sinus flow (CSF), which can be measured by transesophageal Doppler echocardiography (TEDE), especially when contrast enhanced, is useful in evaluating microvascular dysfunction in patients with diabetes mellitus (DM). METHODS AND RESULTS: CSF recordings using contrast enhanced TEDE were performed before and after adenosine triphosphate infusion (0.15 mg x kg(-1) x min(-1)) in 16 patients with type 2 DM and diabetic retinopathy and in 13 non-DM patients (control). Coronary angiography revealed normal epicardial coronary arteries. CFR was defined as the ratio of the antegrade flow velocity time integral in hyperemic conditions and basal levels. Clear envelopes of CSF were obtained in all DM patients using contrast-enhanced TEDE. CFR using CSF in the DM group was significantly decreased compared with the control group (1.4+/-0.4 vs 2.1+/-0.5, p<0.01), but there were no significant differences of age, ejection fraction, rate of hypertension and hypercholesterolemia between the 2 groups. Using 1.7 of CFR as the cut-off value, diabetic microvascular dysfunction could be detected with 82% sensitivity and 83% specificity. CONCLUSIONS: CFR calculated by CSF using contrast-enhanced TEDE may be useful for evaluating diabetic microvascular dysfunction.

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PubMed2004

Elevation of plasma brain natriuretic peptide is a hallmark of diastolic heart failure independent of ventricular hypertrophy.

OBJECTIVES: We tested a hypothesis that elevation of the plasma level of brain natriuretic peptide (BNP) is one of the characteristics of patients with diastolic heart failure (DHF) independent of left ventricular (LV) hypertrophy. BACKGROUND: The clinical characteristics of DHF are not well acknowledged, although DHF has become a great social burden. Such a lack of clinical information leads to inaccuracy in the diagnosis of DHF. We have demonstrated enhancement of ventricular production of BNP with progression of maladaptive ventricular hypertrophy, but not with development of compensatory hypertrophy in an animal DHF model. METHODS: Of 372 patients who presented to the emergency department because of acute pulmonary congestion without acute coronary syndrome between January 1996 and May 2002, those with an ejection fraction > or =45% upon admission, who were stably controlled at least for a year in our outpatient clinics, comprised the DHF group (n = 19). A control group consisted of 22 hypertensive patients with a LV mass index greater than or equal to its minimum value of the DHF group and an ejection fraction > or =45%, in whom cardiac symptoms had not occurred. RESULTS: Despite a similar distribution of LV mass index, the BNP level was higher in the DHF group than in the control group (149 +/- 38 vs. 31 +/- 5 pg/ml, p < 0.01). There was no difference in LV cavity size or parameters derived from pulsed Doppler transmitral flow velocity curves. CONCLUSIONS: An elevation of BNP may be a hallmark of patients with or at risk of DHF among subjects with preserved systolic function independent of LV hypertrophy.

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PubMed2003

Autonomic mechanisms of bradycardia during nitrox exposure at 3 atmospheres absolute in humans.

BACKGROUND: This experiment was designed to examine the involvement of the autonomic nervous systems and intrinsic component in the occurrence of hyperbaric bradycardia. METHODS: Eight male divers were exposed to a N2-O2 (Nitrox) environment at 3 atmospheres absolute (ATA) for 7 d. The heart rate (HR), plasma norepinephrine (NE), and a spectral power of the variability of cardiac interval were measured during a 4-d predive control period, a 7-d saturation period at 3 ATA, and a 4-d postdive period. In each dive period, atropine and propranolol were administered intravenously for cholinergic blockade and beta-adrenergic blockade, respectively. RESULTS: Basal HR decreased by -10% (p < 0.05) during the saturation period compared with that of the predive control. The HR after an administration of atropine was attenuated by 5.5 +/- 2.4% (p < 0.05) during hyperbaric exposure. The HR after a simultaneous administration of atropine and propranolol, the intrinsic HR, was similar throughout the dive periods. Plasma NE decreased at 3 ATA (p < 0.05). The basal level of high-frequency power of cardiac interval variability, an index of cardiac parasympathetic modulation, remained unchanged throughout the dive period, whereas this power was eliminated by atropine administration. CONCLUSIONS: These results suggest that reduced sympathetic activity plays a primary role in the reduction of HR in the present hyperbaric environment.

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PubMed2002

Myocardial dysfunction after electrical defibrillation.

We hypothesized that electrical shocks that defibrillate hearts successfully also produce myocardial injury, but only in settings in which the myocardium is underperfused. Myocardial function was measured in isolated, conventionally perfused or underperfused rat hearts during sinus rhythm and conventionally perfused or underperfused hearts during ventricular fibrillation (VF) after delivery of a sham, a 0.4 J, or a 0.7 J shock. In underperfused hearts, the dP/dt, negative dP/dt, left ventricular diastolic pressure and left ventricular pressure-volume relationships demonstrated significant impairment in myocardial function. Impairment increased with the higher energy shocks. This contrasted with normally perfused hearts, whether in sinus rhythm or during VF, in which shocks resulted in no significant impairment. Electrical shocks therefore produce myocardial injury but only when myocardial perfusion is reduced.

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