The anaesthetist and the cardiac catheterisation laboratory.

Interventional cardiology is an innovative and expanding field. Anaesthetists are increasingly involved in managing complex congenital and acquired heart lesions in the cardiac catheterisation laboratory. This article provides an overview of common lesions encountered in the cardiac catheterisation laboratory, the anaesthetic management of patients with congenital and acquired heart lesions, the procedures performed and the complications encountered during such procedures.

Upper airway obstruction as a result of massive subcutaneous emphysema following accidental removal of an intercostal drain.

A case is described of extensive subcutaneous emphysema with rapid and life-threatening airway obstruction. The incident followed inadvertent removal of a chest drain in a patient with a persistent air leak from an iatrogenic pneumothorax. The pneumothorax had developed during pacemaker insertion.

The capsaicin analogue SDZ249-665 attenuates the hyper-reflexia and referred hyperalgesia associated with inflammation of the rat urinary bladder.

This study assessed the effects of the systemically administered capsaicin analogue SDZ249-665 in an animal model of visceral pain and hyper-reflexia. The effects of prophylactic administration of SDZ249-665 (in the dose range 0.05-1 mg/kg) on the viscero-visceral hyper-reflexia (VVH) and the referred viscero-somatic hyperalgesia to mechanical stimuli (VSH) associated with turpentine inflammation of the rat urinary bladder were evaluated. SDZ249-665 attenuated both the VVH and the VSH in a dose related fashion. In the VVH model, following solvent control administration, intra-vesical turpentine administration was associated with a significant reduction in micturition threshold to 43.7% (SEM 6.3) of baseline, indicating the presence of a VVH. This effect was not observed when animals were prophylactically treated with SDZ249-665 alone. At a dose of 0.1 mg/kg the micturition threshold was 90.7% (SEM 10.2) of baseline at 1 h after intra-vesical instillation of turpentine. In the VSH model, curves were plotted of the difference in fore and hind limb withdrawal latencies from a mechanical stimulus and the area under these curves (AUCs) were compared between different treatment protocols. Intra-vesical turpentine was associated with a negative deflection of the curve (AUC -5.2x10(3) SEM 1.7) in comparison with naïve animals (AUC -0.02x10(3) SEM 0.6), indicative of a referred hyperalgesia. This was prevented, in a dose-related manner, by prophylactic administration of SDZ249-665. For example, at a dose of 0.5 mg/kg the AUC was +0.4x10(3) (SEM 0.8). These findings support previous work indicating that capsaicin sensitive neurones participate in patho-physiological events occurring following inflammation of the bladder, and provides evidence that systemically active capsaicin based compounds may be developed for use in the clinical setting.

Inflammation of the rat urinary bladder is associated with a referred thermal hyperalgesia which is nerve growth factor dependent.

We have assessed whether a referred somatic hyperalgesia to thermal stimulation of the hind limb of rats occurs after inflammation of the urinary bladder. Furthermore, we evaluated whether any such viscero-somatic hyperalgesia (VSH) is dependent on the neurotrophin nerve growth factor (NGF). Limb withdrawal thresholds from thermal stimulation of both fore and hind limbs were assessed simultaneously at baseline and at fixed times for 24 h after various interventions. After plotting curves for the difference in withdrawal time of fore and hind limbs against time, the area under the curve (AUC) was calculated to provide a single measure over the 24-h period. A negative value indicated relative hyperalgesia of the hind limb. With simple catheterization, although there was a trend towards hind limb hyperalgesia, there was no significant difference in this AUC (mean -100.5) compared with naïve control animals (mean AUC +53.6). However, inflammation with 50% turpentine oil was associated with a significant change in AUC (mean -676.8), indicative of relative hyperalgesia of the hind limb. This hyperalgesia was mimicked by intra-vesical instillation of NGF (in place of turpentine) (mean AUC -1418.3 while mean AUC in naïve animals was +439.4). Furthermore, prior administration of an NGF sequestering molecule, trkA-IgG, attenuated turpentine-induced VSH. These findings increase our knowledge of the nature of visceral and referred pain and further implicate NGF in the hyperalgesic response to inflammation of the urinary bladder.

The endogenous cannabinoid anandamide, but not the CB2 ligand palmitoylethanolamide, prevents the viscero-visceral hyper-reflexia associated with inflammation of the rat urinary bladder.

Anandamide, an endogenous ligand at the CB1 cannabinoid receptor and palmitoylethanolamide (a putative endogenous ligand at the CB2 receptor) have both been shown to possess anti-hyperalgesic properties in models of somatic and visceral inflammation. In the turpentine-inflamed rat urinary bladder a reversal of the inflammation-associated viscero-visceral hyperreflexia (VVH) was observed when the cannabinoids were administered 135 min after the induction of inflammation. Therefore, in this study we determined the efficacy of these two N-acylethanolamides in the prevention of VVH in the same model, using a prophylactic dosing regimen. Palmitoylethanolamide did not prevent the VVH (in the dose range 10-30 mg/kg, i.a), but anandamide attenuated the response in a dose related manner, with a threshold of 25 mg/kg (i.a). These findings provide further support for an acute anti-nociceptive and anti-hyperalgesic role for CB1 receptor agonists, with CB2 agonist effects only becoming important once the effects of inflammation are established.

The anti-hyperalgesic actions of the cannabinoid anandamide and the putative CB2 receptor agonist palmitoylethanolamide in visceral and somatic inflammatory pain.

This study assessed the effects of two N-acylethanolamides in established rat models of visceral and somatic inflammatory pain. (1) The therapeutic effects of the cannabinoid anandamide and the putative CB2 agonist palmitoylethanolamide were tested in a model of persistent visceral pain (turpentine inflammation of the urinary bladder). Both anandamide (at a dose of 25 mg/kg) and palmitoylethanolamide (at doses of 10-30 mg/kg) were able to attenuate the viscero-visceral hyper-reflexia (VVH) induced by inflammation of the urinary bladder. (2) The effects of the same compounds on the behavioural response to subcutaneous formalin injection were assessed. The characteristic biphasic response was observed in control animals. Anandamide (dose range 5-25 mg/kg) and palmitoylethanolamide (dose range 5-10 mg/kg) both reduced the second phase of the response. The results confirm the analgesic potential of endogenous ligands at cannabinoid receptor sites. The anti-nociceptive effect of the putative CB2 receptor agonist, palmitoylethanolamide, is particularly interesting since it is believed to be a peripherally mediated effect. This observation might be exploited to separate central psychotropic effects from peripheral analgesic actions of the cannabinoids, under inflammatory conditions.

The modulatory effects of bradykinin B1 and B2 receptor antagonists upon viscero-visceral hyper-reflexia in a rat model of visceral hyperalgesia.

This study assessed the relative involvement of the two bradykinin (Bk) receptors (B1 and B2) in the viscero-visceral hyper-reflexia (VVH) and plasma extravasation observed in an animal model of cystitis. The effects of the competitive receptor antagonists des-Arg9[Leu8]-Bk (B1) and HOE 140 (B2) were tested both in prophylactic (pre-inflammation administration) and therapeutic (post-inflammation administration) scenarios. Compared with control animals, des-Arg9[Leu8]-Bk had no effect on the hyper-reflexic response of the bladder to inflammation unless it was administered 5 h after inflammation. However, HOE 140 was able to attenuate the inflammation-induced viscero-visceral hyper-reflexia (VVH) at doses of 1 mg/kg, 2 mg/kg and 7.5 mg/kg. This effect was apparent whether the drug was administered before, or after inflammation. In contrast, neither compound was effective in attenuating the intravesical plasma extravasation induced by turpentine. The data therefore suggest that the VVH and tissue inflammation responses are mediated via different mechanisms. In addition, the turpentine-induced VVH appears to be mediated, at least partially, by the B2 receptor in the early phase, with the B1 receptor only becoming important later.