Recordings were made in a number of innovative preparations including in-line cultured cells, bladder-urethra sheets and cross-sections, spinal cord slices and

the cerebral cortex. Results: The animal models and methods used allow for the study of peripheral and central mechanisms of neurogenic AP24534 mw overactivity. While colonic irradiation results in solely neurogenic dysfunction, spinal cord lesions also induce non-neural changes resulting in increased spontaneous detrusor contractions that can directly stimulate afferent nerves. Imaging of cultured bladder interstitial cells reveals spontaneous firing that could contribute to detrusor overactivity, while optical imaging of the spinal cord and brain could identify changes in central pathways that underlie lower urinary tract dysfunction. Conclusions: LCL161 The animal models and methods described

allow for the study of neurogenic overactivity at the peripheral, spinal and cortical levels. This may lead to greater understanding of sensory and motor mechanisms involved in incontinence, the contributions of interstitial cells and spontaneous detrusor contractions, and the involvement of the cortex. Neurourol. Urodynam 30:658-667, 2011. (C) 2011 Wiley-Liss, Inc.”
“Background: Resuscitation of hemorrhagic shock with isotonic crystalloids has been shown to activate polymorphonuclear neutrophils (PMNs). Although hypertonic saline (HTS) can reduce PMN activation and interactions with endothelial cells (EC) in systemic microvascular beds, no data exist demonstrating that the same occurs in the unique blood-brain barrier microcirculation. We hypothesized that resuscitation MK-8931 research buy of hemorrhagic shock with HTS would blunt brain in vivo PMN-EC interactions.

Methods: Wistar rats (250-350 g) underwent craniotomy and placement of a window for live intravital viewing of pial vessels. Twenty animals were bled to a mean arterial pressure of 30 mm Hg to 35 mm Hg for 1 hour and resuscitated with shed blood and either 5% HTS (6 mL/kg) or Ringer’s lactate (RL) (2 X shed blood volume).

Circulating rhodamine-6G-labeled PMN in pial venules were captured by videomicroscopy at baseline (preshock), end of the shock period, after resuscitation, and every 15 minutes to 30 minutes for 2 hours. Hemodynamics and arterial gases were monitored. Off-line footage analysis allowed comparisons of PMN-EC interactions between groups.

Results: Animals in both groups developed significant metabolic acidosis (p < 0.01) after hemorrhage, but postresuscitation blood pressures were similar at all time points. Crystalloid resuscitation volumes were 10 X greater in RL than HTS animals (p < 0.001). For all time points, we did not observe the expected reduction in PMN rolling and adhesion in HTS animals, instead noted trends of consistently lower interactions in RL counterparts.