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The mechanism of slow muscarinic excitation in bullfrog sympathetic ganglia was studied using a single-electrode voltage clamp technique. The membrane current induced by muscarine (0.01-30 microM: Imus) consisted of a voltage-dependent component (dIM) induced by the inhibition of K+-current (known as IM), a voltage-independent cation-selective current (ID), or both. In the last case, the magnitude of either component varied in different cells. Generation of both dIM and ID were equally suppressed by pirenzepine with a dissociation constant (Ki) of 30 nM, while they were inhibited less by AF-DX116 with a Ki of 600 nM. Kd values for muscarinic induction of dIM and ID were 0.35 and 5 microM respectively. This difference was also seen even after reducing the receptor population by pretreatment with propylbenzilylcholine mustard. ID was enhanced after blockade of dIM by Ba2+ (4 mM), with a little change in Kd. This effect was larger when the control ID was smaller. These results suggest that a single subtype (M1) of muscarinic receptor generates both the dIM and ID with different efficacies and that Ba2+, known as a blocker of IM (accordingly of a high-efficacy current, dIM), potentiates a low-efficacy current (ID).

oronary arteriovenous fistula (CAVF) is an abnormal communication between a coronary artery and a cardiac chamber, great vessel, or other vascular structure. Most of them are found incidentally during coronary angiography (CAG), and are identified as a cause of a continuous murmur, myocardial ischemia, congestive heart failure or, rarely, bacterial endocarditis. [1][2][3] However, cases with pericardial effusion (PE) caused by rupture of the aneurysmal coronary artery are quite rare; only 3 cases of cardiac tamponade caused by rupture of the CAVF have been previously reported. [4][5][6] We report a case of chronic PE caused by a CAVF. The PE was observed for 6 months, and finally developed into cardiac tamponade. Case ReportA 75-year-old woman was referred to hospital for investigation of recurrent PE. She had a history of pulmonary tuberculosis 50 years ago. In August 1998, she had been admitted to another hospital for further investigation of cardiomegaly (cardiothoracic ratio (CTR) 63%) and was the PE was diagnosed for the first time. However, she was free of symptoms and the laboratory examinations were normal, including thyroid function and tuberculin reaction. Chest computed tomography (CT) did not show any abnormal findings except for the PE and a scar from the pulmonary tuberculosis. She was treated with diuretics and the PE disappeared within 6 months. The CTR decreased Circulation Journal Vol.66, August 2002from 63% to 54% on the chest X-ray. In February 1999, she developed shortness of breath and general fatigue, and echocardiographic examination revealed that the PE had recurred.On the admission to hospital in February 1999, her vital signs were: blood pressure 148/70 mmHg, heart rate 92 beats/min, respiratory rate 20 breaths/min, and body temperature 36.5°C. Pulsus paradoxus was not detected. Chest auscultation revealed bilaterally normal respiratory sounds and a soft continuous murmur at the left sternal border of the 4th intercostal space. She had hepatomegaly, bilateral leg edema and a markedly expanded external jugular vein.Laboratory tests were as follows: leukocytes 7.2×10 3 / l; C-reactive protein 0.5 mg/dl; erythrocyte sedimentation rate of 24 mm/h; TSH 1.86 IU/ml; free T3 1.77 pg/ml; free T4 0.83 ng/ml; tuberculin reaction 10×10 mm. A chest Xray revealed cardiomegaly (CTR = 67%) without pulmonary infiltration. The electrocardiogram (ECG) on admission was normal except for flat T waves in leads V4-6 (Fig 1A). An enhanced CT scan revealed a dilated right coronary artery (RCA) and a dilated coronary sinus (CS) vein, an expanded inferior vena cava and a large, circumferential PE (Fig 2). However, leakage of contrast media into the pericardial space was not seen. A diagnostic pericardiocentesis yielded 20 ml of bloody fluid (Hct = 22%) that contained 5.7 mg/dl of protein, 56 mg/dl of glucose and 23.2 IU/L of adenosine deaminase. The culture for bacteria in the pericardial fluid was negative, and a polymerase chain reaction for the tuberculosis bacillus was not detected. There was no evidence of ...

Hypertrophic cardiomyopathy (HCM) is a rare cardiac complication in patients with Klinefelter syndrome. We report the case of a 67-year-old Japanese man with Klinefelter syndrome, HCM, sick sinus syndrome, and coronary arteriovenous fistula, in whom the 47XXY/46XY mosaic pattern was revealed by chromosomal study. Echocardiography revealed HCM with an interventricular septum thickness of 17 mm and a left ventricular posterior wall thickness of 10 mm. Sick sinus syndrome type III was diagnosed by paroxysmal atrial fibrillation (longest sinus arrest 9.0 sec) on 24-h Holter ECG recording. Coronary arteriovenous fistula was detected from the left anterior descending artery to the right ventricle by coronary arteriography. To our knowledge, this is the first case report of Klinefelter syndrome with HCM. As there have been a few reports of patients with Klinefelter syndrome in association with skeletal muscular diseases such as Becker-type muscular dystrophy or myotonic dystrophy, the gene mutation that causes Klinefelter syndrome may occur in the cardiac muscle. HCM may represent another variable expression of this chromosomal abnormality.

Noninvasive estimation of pulmonary arterial pressure is important for hemodynamic monitoring of patients with heart disease. In patients with tricuspid regurgitation (TR), the peak velocity of TR on continuous-wave (CW) Doppler can be used to estimate the systolic pulmonary arterial pressure (PAPs) using the simplified Bernoulli equation. We evaluated a new technique of contrast-enhanced CW Doppler for calculating PAPs in patients with trivial TR. Forty-one patients without visible TR detected by color Doppler, pulsed Doppler or CW Doppler were evaluated. Age ranged from 19 to 73 (55 +/- 12) years old. Tricuspid flow signals were recorded on CW Doppler after intravenous administration of indocyanin green (ICG) or Albunex. PAPs was calculated as; PAPs = 4 x VTR2 + 10 mmHg, where VTR is the peak velocity of TR. PAPs calculated using contrast-enhanced CW Doppler was compared with PAPs measured by the following cardiac catheterization. 1) TR signals were recorded using the contrast-enhanced CW Doppler technique in 39 of 41 patients (95%) after intravenous administration of contrast agents. 2) The error of estimate of PAPs using the contrast-enhanced CW Doppler technique was -2.4 +/- 7.5 mmHg, and the percent error was -10.7 +/- 32.4% in all patients. In 20 of 39 patients (51%), the error of estimate was within +/- 5 mmHg. 3) PAPs was overestimated by 12.2 +/- 6.1 mmHg in patients with good contrast enhancement of TR signals. The contrast-enhanced CW Doppler technique is useful for estimating PAPs noninvasively in patients with trivial TR. It is better to assume the right atrial pressure as 3-5 mmHg, not 10 mmHg, in patients with good enhancement of trivial TR. Physiological TR may be enhanced by contrast agents in these patients.

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Nisoldipine improved LV diastolic dysfunction and exercise tolerance in patients with HCM. These effects were similar to the first generation calcium antagonists. LV diastolic dysfunction may be improved due to the reduction of intracellular calcium concentration and the relief of myocardial ischemia by strong coronary artery dilating effect. However, nisoldipine did not affect the LV systolic function because of its less negative inotropic effect.