Diurnal variation in baseline heart rate of anencephalic fetuses

Abstract The diurnal change in baseline fetal heart rate (FHR) of four anencephalic fetuses at 20, 23, 24 and 30 weeks of gestation were examined. The mean baseline FHR in 00.00–06.00 h, 06.00–12.00 h, 12.00–18.00 h and 18.00–24.00 h were compared by one-factor ANOVA and Scheffe's test in each case. The diurnal variations in baseline FHR were recognized in all subjects ( P < 0.01). In 3/4 subjects, the lowest values were at 00.00–06.00 h. The diurnal variation in baseline FHR might be caused by maternal factors because it was present even in the anencephalic fetuses that had no central nervous system having the oscillators of the circadian rhythm.     

Exercise-induced ventricular tachycardia without demonstrable heart disease in childhood

Exercise-induced ventricular tachycardia (VT) without demonstrable heart disease was studied in pediatric patients. The study population consisted of 17 patients aged 5–14 years (average 9.1 years), who demonstrated reproducible VT during or immediately after exercise testing using a treadmill. The main reasons for the exercise testing were episodes of exercise-related syncope in two patients, exercise-related palpitation in seven and evaluation of sporadic ventricular premature contraction (VPC) in eight. Of the eight patients in the asymptomatic group, two developed sustained VT and the other six had non-sustained VT. Of the nine patients in the symptomatic group, six developed sustained VT. Verapamil produced a good response in seven of 14 patients, and propranolol in six. None of the patients died during the follow-up period, an average of 59.6 months. In four patients, both VT and VPC disappeared, not only on exercise testing, but also on Holter electro-cardiograms, so the anti-arrhythmic agents were discontinued. One patient had syncope and convulsion caused by rapid bidirectional VT in the follow-up period. It was concluded that the prognosis of exercise-induced VT without demonstrable heart disease in children is relatively benign, but careful follow-up is required.     

Echographic Detection of Latent Severe Thrombotic Stenosis of the Superior Vena Cava and Innominate Vein in Patients with a Pacemaker: Integrated Diagnosis Using Sonography, Pulse Doppler, and Color Flow

Thrombosis of the innominate vein and SVC is a serious complication in patients with pacemakers, inducing puhnonary embolism or SVC syndrome. Venography is the definitive method for its diagnosis; however, it is too invasive for related studies. The purpose of this study was to validate sonography, pulse Doppler, and color flow in detecting noninvasively innominate vein or SVC thrombosis in patients with pacemakers. In 53 patients with pacemakers, the 1 severe SVC stenosis and 18 severe innominate vein stenoses due to thrombosis were diagnosed by digital subtraction angiography. Sonography accurately showed the severe SVC stenosis due to thrombosis, but had limitations on the innominate vein thrombosis. Color flow demonstrated mosaic flow, indicating poststenotic turbulence due to stenosis of the innominate vein and SVC caused by thrombosis in 15 of 16 patients, and pulse Doppler disclosed absence of flow due to complete occlusion of the innominate vein in 2 of 2 patients. Sensitivity and specificity for detecting severe innominate vein stenosis due to thrombosis using combined color flow and pulse Doppler was 94% and 100%, respectively. In conclusion, sonography, pulse Doppler, and color flow allow accurate detection of severe innominate vein or SVC stenosis due to thrombosis, and are therefore useful for the follow-up of patients with a pacemaker.     

Transabdominal vesical sonography of urethral syndrome and stress incontinence

BACKGROUND: Transabdominal ultrasonography was used to study the bladder neck morphology in women with urethral syndrome or stress urinary incontinence, in order to determine the ultrasonographic findings of these conditions. METHODS: A total of 210 female patients with a normal bladder, asymptomatic trigonitis, urethral syndrome, and stress incontinence were studied. The mucosal thickness around the bladder neck, the length of the anterior base plate of the bladder, and the anteroposterior vesical wall angle (APVA) at the bladder neck were measured on sagittal transabdominal vesical ultrasonograms with the patient in the supine position. RESULTS: Patients with asymptomatic trigonitis or urethral syndrome had thicker mucosa around the bladder neck than the subjects with a normal bladder, and the subjects with stress incontinence had normal mucosa. The APVA was 158 +/- 17 (mean +/- SD) degrees in the subjects with a normal bladder. It was smaller in symptomatic patients and decreased to 109 +/- 10 degrees in those with conservative therapy-resistant incontinence. The anterior edge of the vesical base plate was visible approximately 2 cm from the bladder neck in subjects without incontinence, while it tended to be absent in patients with incontinence and an APVA of less than 126 degrees. CONCLUSION: A small APVA appears to reflect bladder neck descent, while a small APVA without a visible anterior base plate edge may reflect hypotonia of the vesical base plate. Transabdominal vesical ultrasonography with the patient in the supine position provides useful information and can be carried out as a routine examination in female patients with micturition disorders.     

Prediction of Optimal Atrioventricular Delay in Patients with Implanted DDD Pacemakers

In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3+/-12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155+/-26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16+/-5, 39+/-6, 65+/-4 and 88+/-5 ms, respectively (r = 0.97, P<0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166+/-23 ms) and the optimal AV delay (CO: 161+/-26 msec, r = 0.93, P<0.0001, PCWP: 161+/-28 msec, r = 0.95, P<0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.     

Renoprotective effects of asialoerythropoietin in diabetic mice against ischaemia–reperfusion-induced acute kidney injury

Aim: Diabetic patients are at higher risk of failure to recover after acute kidney injury, however, the mechanism and therapeutic strategies remain unclear. Erythropoietin is cytoprotective in a variety of non‐haematopoietic cells. The aim of the present study was to clarify the mechanism of diabetes‐related acceleration of renal damage after ischaemia–reperfusion injury and to examine the therapeutic potential of asialoerythropoietin, a non‐haematopoietic erythropoietin derivative, against ischaemia–reperfusion‐induced acute kidney injury in diabetic mice. Methods: C57BL/6J mice with and without streptozotocin‐induced diabetes were subjected to 30 min unilateral renal ischaemia–reperfusion injury at 1 week after induction of diabetes. They were divided into four group: (i) non‐diabetic plus ischaemia–reperfusion injury; (ii) non‐diabetic plus ischaemia–reperfusion injury plus asialoerythropoietin (3000 IU/kg bodyweight); (iii) diabetic plus ischaemia–reperfusion injury; and (iv) diabetic plus ischemia–reperfusion injury plus asialoerythropoietin. Experiments were conducted at the indicated time periods after ischaemia–reperfusion injury. Results: Ischaemia–reperfusion injury of diabetic kidney resulted in significantly low protein expression levels of bcl‐2, an anti‐apoptotic molecule, and bone morphogenetic protein‐7 (BMP‐7), an anti‐fibrotic and pro‐regenerative factor, compared with non‐diabetic kidneys. Diabetic kidney subsequently showed severe damage including increased tubular cell apoptosis, tubulointerstitial fibrosis and decreased tubular proliferation, compared with non‐diabetic kidney. Treatment with asialoerythropoietin induced bcl‐2 and BMP‐7 expression in diabetic kidney and decreased tubular cell apoptosis, tubulointerstitial fibrosis and accelerated tubular proliferation. Conclusion: Reduced induction bcl‐2 and BMP‐7 may play a role in the acceleration of renal damage after ischaemia–reperfusion injury in diabetic kidney. The renoprotective effects of asialoerythropoietin on acute kidney injury may be mediated through the induction of bcl‐2 and BMP‐7.     

Absorption of unconjugated bile acids and tauroursodeoxycholate in the rat intestine

The absorption of ursodeoxycholate and its tauro-conjugate by the jejunum and the terminal ileum of rat intestine was compared with that of other unconjugated bile acids and taurocholate. In the ligated jejunum, the efficacy of absorption of unconjugated bile acids was in the following order: ursodeoxycholate = deoxycholate > chenodeoxycholate = cholate > lithocholate. This order cannot be explained by the theory that the passive diffusion of bile acids is faster the less hydroxyl bonds in the molecule. These findings on the unconjugated bile acids in the ligated jejunum were further confirmed by perfusion experiments. In the ligated terminal ileum, ursodeoxycholate, cholate and deoxycholate were absorbed as fast as taurocholate or tauroursodeoxycholate, whereas absorption of chenodeoxycholate was significantly slower. The Na⁺-dependency of the absorption of ursodeoxycholate and cholate in the terminal ileum was confirmed by perfusion studies. In conclusion, intestinal absorption of ursodeoxycholate was efficient in both the jejunum and ileum and these results may contribute to the high availability of ursodeoxycholate in various hepatobiliary diseases.