Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

The ins and outs of caveolar signaling. m2 muscarinic cholinergic receptors and eNOS activation versus neuregulin and ErbB4 signaling in cardiac myocytes.

Endothelial cells constitutively express the NOS isoform eNOS, which generates NO in response to specific extracellular signals to regulate vascular smooth muscle tone, vascular permeability, and platelet adhesion, among other actions. In addition to coronary vascular and endocardial endothelium, both atrial and ventricular myocytes express eNOS, the activation of which is also dependent on specific intracellular and extracellular signals. eNOS is targeted in cardiac myocytes to caveolae in plasma membranes and, in the case of cardiac myocytes, possibly T-tubular membranes as well. eNOS targeting to caveolae in cardiac myocytes requires co-translational myristoylation and subsequent palmitoylation for efficient targeting of the enzyme to the specialized lipid microdomains characteristic of caveolae. Although eNOS also contains a caveolin binding motif, this is insufficient for correct targeting of eNOS to caveolae. Recent evidence obtained from ventricular myocytes of mice with targeted disruption of the eNOS gene indicates that the lack of functional eNOS interrupts muscarinic cholinergic control of ICa-L in these cells. eNOS-/- mice are hypertensive and develop cardiac hypertrophy as they age, and these animals also exhibit an accelerated degree of vascular remodeling in response to injury. Reconstitution experiments confirm both the essential role of eNOS in coupling m2 AchR signaling to the control of ICa-L and myocyte automaticity and the importance of eNOS subcellular localization within caveolae in mediating this signal transduction pathway. It appears that translocation into caveolae is essential for signaling. However, this is not the case with all receptors associated with caveolae