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We present the case report of a patient who developed interventricular septal hematoma as a complication during perimembranous ventricular septal defect closure. Although cardiopulmonary bypass was re-established and the hematoma was aspirated, postoperative echocardiography revealed that the hematoma reaccumulated in the interventricular septum. She suffered from low-cardiac-output syndrome for 1 week requiring a large amount of inotropic agents. Postoperative echocardiography revealed that the interventricular septal hematoma gradually disappeared. At 1 year follow-up, 99mTc-tetrofosmin myocardial single-photon emission computed tomographic revealed myocardial ischemia in the inferior and septal walls. At 4 years follow-up, her cardiac function has gradually improved. She has no symptoms of heart failure with angiotensin-converting enzyme inhibitor and beta-blocker. [ABSTRACT FROM AUTHOR]

Birth trauma and pelvic injury have been implicated in the etiology of stress urinary incontinence (SUI). This study aimed to assess changes in the biomechanical properties and adrenergic-evoked contractile responses of the rat urethra after simulated birth trauma induced by vaginal distension (VD). Urethras were isolated 4 days after VD and evaluated in our established ex vivo urethral testing system that utilized a laser micrometer to measure the urethral outer diameter at proximal, middle, and distal positions. Segments were precontracted with phenylephrine (PE) and then exposed to intralumenal static pressures ranging from 0 to 20 mmHg to measure urethral compliance. After active assessment, the urethra was rendered passive with EDTA and assessed. Pressure and diameter measurements were recorded via computer. Urethral thickness was measured histologically to calculate circumferential stress-strain response and functional contraction ratio (FCR), a measure of smooth muscle activity. VD proximal urethras exhibited a significantly increased response to PE compared with that in controls. Conversely, proximal VD urethras had significantly decreased circumferential stress and FCR values in the presence of PE, suggesting that VD reduced the ability of the proximal segment to maintain smooth muscle tone at higher pressures and strains. Circumferential stress values for VD middle urethral segments were significantly higher than control values. Histological analyses using antibodies against general (protein gene product 9.5) and sympathetic (tyrosine hydroxylase) nerve markers showed a significant reduction in nerve density in VD proximal and middle urethral segments. These results strongly suggest that VD damages adrenergic nerves and alters adrenergic responses of proximal and middle urethral smooth muscle. Defects in urethral storage mechanisms, involving changes in adrenergic regulation, may contribute to stress urinary incontinence induced by simulated birth trauma. incontinence; innervation; biomechanics; smooth muscle; phenylephfine doi: 10.1152/ajprenal.00299.2009.

In this study, we investigated the effects of bladder outlet obstruction (BOO) on the expression and function of large conductance (BK) and small conductance (SK) [Ca.sup.2+]-activated [K.sup.+] channels in detrusor smooth muscle. The bladder from adult female Sprague-Dawley rats with 6-wk BOO were used. The mRNA expression of the BK channel [alpha]-subunit, [beta]1-, [beta]2-, and [beta]4-subnnits and SK1, SK2, and SK3 channels were investigated using real-time RT-PCR. All subunits except for the BK-[beta]2, SK2, and SK3 channels were predominantly expressed in the detrusor smooth muscle rather than in the mucosa. The mRNA expression of the BK channel [alpha]-subunit was not significantly changed in obstructed bladders. However, the expression of the BK channel [beta]1-subunit and the SK3 channel was remarkably increased in obstructed bladders. On the other hand, the expression of the BK channel [beta]4-subunit was decreased as the severity of BOO-induced bladder overactivity progressed. In detrusor smooth muscle strips from obstructed bladders, blockade of BK channels by iheriotoxin (IbTx) or charybdotoxin (CTx) and blockade of SK channels by apamin increased the amplitude of spontaneous contractions. These blockers also increased the contractility and affinity of these strips for carbachol during cumulative applications. The facilitatory effects elicited by these [K.sup.+] channel blockers were larger in the strips from obstructed bladders compared with control bladders. These results suggest that long-term exposure to BOO for 6 wk enhances the function of both BK and SK types of [Ca.sup.2+]-activated [K.sup.+] channels in the detrusor smooth muscle to induce an inhibition of bladder contractility, which might be a compensatory mechanism to reduce BOO-induced bladder overactivity. bladder outlet obstruction; [Ca.sup.2+]-activated [K.sup.+] channels; spontaneous contraction; muscarinic stimulation doi: 10.1152/ajpregu.00523.2009.