A review of minimal access surgery provision and training within the United Kingdom.

When combined with healthcare pressures, the exponential growth of robotic-assisted surgery (RAS) has impacted UK-based training outcomes, including the learning curve to competency. Aim: To ascertain the current provision of RAS and investigate differences in access to minimal access surgical (MAS) facilities and training across the UK. A two-armed electronic survey was conducted. The first arm questioned clinical leads regarding robotic practice and future training provisions. The second investigated trainee and trainers' perceptions of MAS training and facilities. 64% (52/81) of responding trusts utilise a robotic system. The majority (68% [55/81]) have plans to expand or acquire a system within 3 years. 171 responses from 112 UK and Republic of Ireland hospitals were collected for Arm 2. Laparoscopic categories queried whether trainees had access to a formal curriculum, training days and sim-boxes. Most consultants (51.9%) and trainees (51.6%) reported that there was no formal local training curriculum for robotic surgery. Combined responses demonstrated 42.1% (n = 195/463) said "yes", 39.5% (n = 183) "no" and 18.4% (n = 85) "don't know". For combined robotic categories (simulation, training days and operative lists) 28.3% (n = 134/473) responded "yes", 51.6% (n = 244) said "no" and 20.1% (n = 95) said "don't know". This study provides insight into the current provision of robotic-assisted surgery at UK trusts and highlights the need to facilitate regular clinical training and equitable access to MAS simulation within a formal curriculum. This may aid regulation of training in parallel with the expansion of robotic practice and avoid a significant skill acquisition gap and risks to patient safety.

TRPA1 activation leads to neurogenic vasodilatation: involvement of reactive oxygen nitrogen species in addition to CGRP and NO.

BACKGROUND AND PURPOSE: Transient receptor potential ankyrin-1 (TRPA1) activation is known to mediate neurogenic vasodilatation. We investigated the mechanisms involved in TRPA1-mediated peripheral vasodilatation in vivo using the TRPA1 agonist cinnamaldehyde. EXPERIMENTAL APPROACH: Changes in vascular ear blood flow were measured in anaesthetized mice using laser Doppler flowmetry. KEY RESULTS: Topical application of cinnamaldehyde to the mouse ear caused a significant increase in blood flow in the skin of anaesthetized wild-type (WT) mice but not in TRPA1 knockout (KO) mice. Cinnamaldehyde-induced vasodilatation was inhibited by the pharmacological blockade of the potent microvascular vasodilator neuropeptide CGRP and neuronal NOS-derived NO pathways. Cinnamaldehyde-mediated vasodilatation was significantly reduced by treatment with reactive oxygen nitrogen species (RONS) scavenger such as catalase and the SOD mimetic TEMPOL, supporting a role of RONS in the downstream vasodilator TRPA1-mediated response. Co-treatment with a non-selective NOS inhibitor L-NAME and antioxidant apocynin further inhibited the TRPA1-mediated vasodilatation. Cinnamaldehyde treatment induced the generation of peroxynitrite that was blocked by the peroxynitrite scavenger FeTPPS and shown to be dependent on TRPA1, as reflected by an increase in protein tyrosine nitration in the skin of WT, but not in TRPA1 KO mice. CONCLUSION AND IMPLICATIONS: This study provides in vivo evidence that TRPA1-induced vasodilatation mediated by cinnamaldehyde requires neuronal NOS-derived NO, in addition to the traditional neuropeptide component. A novel role of peroxynitrite is revealed, which is generated downstream of TRPA1 activation by cinnamaldehyde. This mechanistic pathway underlying TRPA1-mediated vasodilatation may be important in understanding the role of TRPA1 in pathophysiological situations.