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Background Epidural analgesia is considered fundamental in enhanced recovery protocols (ERPs). However, its value in laparoscopic colorectal surgery is unclear. The aim of this study was to examine the effects of different analgesic regimens on outcomes following laparoscopic colorectal surgery in fluid-optimized patients treated within an ERP. Methods Ninety-nine patients were randomized to receive epidural, spinal or patient-controlled (PCA) analgesia. The primary endpoints were time until medically fit for discharge and length of hospital stay. Secondary endpoints included return of bowel function, pain scores, and changes in pulmonary function and quality of life. Results Ninety-one patients completed the study. The median length of hospital stay was 3·7 days following epidural analgesia, significantly longer than that of 2·7 and 2·8 days for spinal analgesia and PCA respectively (P = 0·002 and P < 0·001). There was also a slower return of bowel function with epidural analgesia than with spinal analgesia and PCA. Epidural analgesia did not offer better preservation of pulmonary function or quality of life, although pain scores were higher in the PCA group in the early postoperative period. Conclusion Many of the outcomes in the epidural analgesia group were significantly worse than those in the spinal analgesia and PCA groups, suggesting that either of these two modalities could replace epidural analgesia. Registration number: NCT 18926278 (http://www.clinicaltrials.gov).

Objective: We investigated the role of the inward rectifier potassium (K-IR) channel and the cyclic AMP-dependent pathway in mediating vasorelaxation induced by the prostacyclin analogue cicaprost.Methods: Small vessel myography was used to assess responses to cicaprost in segments of rat tail artery contracted with phenylephline. Microelectrode recordings were made from helical strips to assess effects on membrane potential.Results: Cicaprost caused relaxation and hyperpolarisation that were significantly inhibited by Ba2+ (30-100 mu M), a known blocker of K-IR channels. Raising extracellular K+ from 5 to 15 mM elicited membrane hyperpolarisation and an endothelium-independent relaxation that was blocked by Ba2+ (30-100 mu M), suggesting the existence of functional KIR channels on the smooth muscle. In contrast, neither glibenclamide (10 mu M), a blocker of ATP-sensitive K+ channels, nor fluoxetine hydrochloride (100 mu M), a blocker of G-protein-gated inward rectifier K+ channels, nor pertussis toxin (PTX; 1 mu g/ml), which irreversibly inhibits G(i)/G(o), reduced relaxation to cicaprost. Indeed, PTX significantly potentiated responses. Relaxation to cicaprost was not mediated by NO but was partially endothelium-dependent, consistent with a similar inhibition by a combination of charybdotoxin (0.1 mu M) and apamin (0.5 mu M), blockers of endothelium-derived hyperpolarising factor (EDHF). However, relaxation was unaffected by adenylyl cyclase (SQ22536, dideoxyadenosine) or protein kinase A (Rp-2-O-monobutyryl-cAMP) inhibitors, consistent also with Ba2+ only weakly inhibiting relaxation to the adenylyl cyclase activator forskolin.Conclusion: We conclude that cicaprost relaxes rat tail artery by activating K-IR channels with some involvement from EDHF. The mechanism appears to be largely independent of cyclic AMP and G(i)/G(0), although the latter appears to counteract relaxation through an unknown pathway and/or receptor. (c) 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

Objective: The aim of this study was to investigate changes following regression of left ventricular hypertrophy (LVH). Methods: Electrophysiolological changes were recorded in isolated guinea-pig myocardial preparations. LVH was induced by constriction of the thoracic aorta and regression was followed after removal of the constriction. Sham-operated animals served as controls. Results: During 42 days constriction, heart/body weight ratio increased (3.19±0.49 vs. 3.85±0.83 g kg−1) and was accompanied by an increase of cell size. Forty-two days after clip removal, values had returned to control values. LVH increased action potential (AP) duration (mean 112% of control) and decreased conduction velocity (60.4±3.3 vs. 45.9±4.6 cm−1). These changes did not return to control after regression of LVH. The changes to condition velocity were attributed solely to increases of intracellular resistivity. The positive staircase response also decreased with LVH, but did recover upon regression. In isolated whole hearts, no changes to subepicardial action potential duration, QRS complex duration or AP refractory period were observed in LVH or its regression. During low-flow ischaemia AP duration shortened reversibly, the rate of shortening was more rapid in hypertrophied hearts but similar to control in regressed hearts. The incidence of ventricular tachyarrhythmias of fibrillation during low-flow ischaemia was similar in control, hypertrophied and regressed hearts. Conclusion: Morphological regression of LVH is not accompanied by reversal of electrophysiological changes measured in isolated preparations, whereas some aspects of contractile function to recover.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and paroxysmal AF (PAF) comprises approximately half of all AF cases. PAF poses a particular diagnostic challenge given its intermittency. A physician's choice of investigational device is largely based on symptom frequency although it has been widely established that a significant proportion of PAF episodes are asymptomatic. We aim to determine whether symptom frequency is a reliable method to select a choice of investigational device in a population presenting with palpitations.