A novel, integrated curriculum for dental hygiene-therapists and dentists.

Introduction: In certain communities patients may struggle to find access to adequate dental treatment. One proposed strategy to help meet population need is to train more dental hygiene-therapists. However, established attitudes and hierarchies, along with a lack of clear understanding of different roles within some general practice environments has led to underutilised shared-care approaches. Integrating dentists and dental hygiene-therapists in undergraduate education may be an effective approach to promote inter-professional education, dispel inappropriate biases and hierarchies, and nurture team working from an early career stage. As such, we have developed a novel BSc Dental Therapy and Hygiene (BDHT) curriculum, which is integrated with the Bachelor of Dental Surgery (BDS) programme. Aims: The aim of this paper is to describe how two separate BDHT and BDS undergraduate programmes have been uniquely integrated, and to share areas of best practice. Design: The BDHT curriculum was developed based on our established BDS programme introduced in 2013 and is novel in two respects: BDHT students complete their academic and clinical training jointly with BDS students, and are assessed and trained to the same standards; and our patient-centred, primary care clinical training model is designed to prepare BDHT graduates to work under direct access. Results: Key success indicators of the integrated BDHT-BDS programmes are: award of GDC sufficiency; 100% BDHT graduate employment; and 100% BDHT final year pass rate. Conclusion: Inter-professional education is an established pedagogic approach to inhibit the formation of hierarchy and barriers that impede collaborative care. Our BDHT programme is the first of its kind to embed inter-professional education through the entirety of both the BDHT and BDS course structures and be entirely integrated. Further studies are required to provide quantitative and qualitative data to validate the success of our new integrated training programme. This paper presents our curriculum journey, from conception, to design, implementation and review. It describes our vision and its relevance for the future of inter-professional dental education.

Role of L-type calcium channels in altered microvascular responses to propofol in hypertension.

BACKGROUND: Propofol acts as an L-type calcium channel (LTCC) antagonist to decrease peripheral resistance and initiate hypotension. This study investigated LTCC sensitivity/expression in hypertension and the role of LTCCs in exaggerated hypotension to propofol in this situation. METHODS: Age-matched 12- to 15-week-old normotensive rats [male Wistar Kyoto (WKY)] and spontaneously hypertensive rats (SHR) were used. Propofol (10 mg kg(-1), 10-50 mg kg(-1) h(-1) i.v.) was administered and the mesenteric microcirculation (<70 µm) observed with fluorescent in vivo microscopy using fluorescein isothiocyanate-conjugated bovine serum albumin (100 mg kg(-1) i.v.). Western blotting was used to measure tissue expression of the α(1C) LTCC subtype. Pressure myography was used to assess isolated mesenteric arterioles (<350 µm) in response to BAYK8644 (0.1 nM-1 µM), a specific LTCC channel agonist. RESULTS: Propofol dilated isolated arterioles {336.6 µM [mean (sd) change 16.2 (5.8)%]}. However, constriction to BAYK8644 was reduced at this concentration of propofol [EC(50)=8.3 (0.1) log mol(-1)] compared with controls [7.4 (0.1) log mol(-1), P<0.05], suggesting that propofol inhibited LTCCs. The sensitivity of LTCCs increased during hypertension, as in vivo there was a greater increase in mean arterial pressure (MAP) to BAYK8644 [10 µg kg(-1), WKY: 59.5 (9.3)%; SHR: 97.7 (6.3)%, P<0.05] with exaggerated constriction of arterioles [10 µg kg(-1), WKY: 9.1 (2.5)%; SHR: 19.1 (2.6)%, P<0.05]. Propofol also decreased MAP in SHR over time (P<0.05), but remained unchanged in WKY. Using western blotting, expression of α(1C) was greater in SHR compared with WKY (P<0.05). CONCLUSIONS: Propofol acts via LTCC channels, with increased channel expression and sensitivity in genetically hypertensive rats. We suggest that increased sensitivity and expression of LTCCs may be a mechanism for exaggerated hypertension during propofol anaesthesia.

Beneficial microvascular and anti-inflammatory effects of pravastatin during sepsis involve nitric oxide synthase III.

BACKGROUND: Sepsis induces microvascular inflammation and production of the vasodilator nitric oxide (NO) via endothelial and inducible nitric oxide synthase (eNOS or NOS III and iNOS or NOS II). Statins are cholesterol-lowering drugs; however, they also attenuate inflammation. This study aimed to determine whether pravastatin protected against sepsis-induced hypotension, loss of vascular tone, and microvascular inflammation via NOS pathways. METHODS: Male Wistar rats (n=18) were anaesthetized and the mesentery prepared for fluorescent intravital microscopy. Animals received either lipopolysaccharide (LPS; n=6); LPS+pravastatin (18 and 3 h before LPS; n=6), or saline as a control, for 4 h. RESULTS: Mean arterial pressure decreased in LPS-treated animals (P<0.05), but not in those also receiving pravastatin. Acetylcholine-induced relaxation of venules was abolished by LPS but improved by pravastatin. Pravastatin also reduced the increase in nitrite concentration and macromolecular leak from venules induced by LPS (P<0.05). The increased leucocyte adhesion seen in LPS-treated rats was also reduced in those also treated with pravastatin. Immunohistochemical analysis showed that pravastatin increased endothelial cell expression of NOS III during sepsis, but had no effect on LPS-induced up-regulation of NOS II. CONCLUSIONS: Pravastatin improved NOS III-mediated vessel relaxation and exerted anti-inflammatory effects within the microcirculation after LPS administration in rats. Pravastatin therefore appears to have beneficial effects during sepsis, as a result of increased microvascular expression and function of NOS III.

Statins for all: the new premed?

The use of statins is widespread and many patients presenting for surgery are regularly taking them. There is evidence that statins have beneficial effects beyond those of lipid lowering, including reducing the perioperative risk of cardiac complications and sepsis. This review addresses the cellular mechanisms by which statins may produce these effects. Statins appear to have actions on vascular nitric oxide through the balance of inducible and endothelial nitric oxide synthase. The clinical evidence for these benefits is also briefly reviewed with the objective of clarifying the current status of statin use in the perioperative period. There is reasonably strong evidence that patients already taking statins should continue on them perioperatively. However, the evidence for the prophylactic use of statins perioperatively is weak and lacks prospective controlled studies.

Beneficial effects of statins on the microcirculation during sepsis: the role of nitric oxide.

This review describes the laboratory evidence and microvascular mechanisms responsible for the beneficial effects of statins in sepsis. During sepsis, changes occur within the microcirculation including alterations in arteriolar tone influencing blood pressure, adaptations to endothelial cell integrity causing leakage of proteins and macromolecules, and adhesion and migration of leucocytes through the vascular endothelium. Statins are widely used as cholesterol-lowering agents, but appear to have anti-inflammatory actions during sepsis. We have discussed the effects of statins on specific pathological processed within the microcirculation and focused on the role of nitric oxide (NO). The main mechanism by which statins appear to be an effective treatment for sepsis is increased expression of endothelial nitric oxide synthase (eNOS), in conjunction with down-regulation of inducible nitric oxide synthase. Combined, this results in an increase in physiological concentrations of NO, thus restoring endothelial function. Laboratory studies have therefore suggested that enhancement of eNOS activity during sepsis may lead to restoration of microvascular tone, maintenance of microvascular integrity, and inhibition of cell adhesion molecules. However, other mechanisms independent of lipid-lowering effects, including antioxidant activity and alterations in the development of vascular atherosclerosis, may also contribute to the beneficial effects of statins. We have also addressed the influence on the effects of statins of lipid solubility and pre- and pro-phylactic administration.

Differential effects of propofol, ketamine, and thiopental anaesthesia on the skeletal muscle microcirculation of normotensive and hypertensive rats in vivo.

BACKGROUND: This study utilized the dorsal microcirculatory chamber (DMC) model to determine differential effects of i.v. propofol, ketamine, and thiopental anaesthesia on the skeletal muscle microcirculation (10-180 micro m) of normotensive (Male Wistar Kyoto, WKY) and hypertensive (spontaneously hypertensive Harlan, SHR) rats, importantly, comparing responses to a conscious baseline. METHODS: Three weeks following implantation of the DMC in WKY (n=8) and SHR (n=6) (130 g) 0.25 ml 100 g(-1) FITC-BSA (i.v.) was administered and the microcirculation viewed using fluorescent in vivo microscopy for a 30 min baseline (t=0-30 min). This was followed by either propofol, thiopental, ketamine, or saline (i.v. bolus induction over 5 min (t=30-35 min)), then maintenance step-up infusion for 60 min (t=45-105 min), so that animals received all four agents 1 week apart (56 experiments). RESULTS: Dilation of A3 arterioles (15-30 micro m) and V3 venules (20-40 microm) with propofol was greater in SHR (t=95 min, A3 36.7 (12)%, V3 15.5 (2.3)%) than WKY (t=95 min, A3 19.4 (7.4)%, V3 8.0 (2.3)%) (P<0.05). Constriction of A3 with ketamine was greater in SHR (t=95 min, A3 -29.1 (6.4)%) than WKY (A3 -17.5 (8.8)%) (P<0.05). This was accompanied by hypotension with propofol in SHR (-32% decrease in systolic arterial pressure), but not WKY (-6%) and hypertension with ketamine in WKY (-15%) and SHR (-24%) (P<0.05). During thiopental anaesthesia there was dilation of A1 (80-180 microm), A3, and V3 in WKY (P<0.05). Conversely, in SHR dilation of venules (29.2 (8.7)%) was accompanied by constriction of A1 and A3 (t=95 min, A1 -25.1 (5.9)%, A3-45.2 (3.1)%) (P<0.05). CONCLUSION: Within the skeletal muscle microcirculation of hypertensive rats there is enhanced dilation with propofol and constriction with ketamine, associated with exaggerated changes in arterial pressure. Thus, dysfunctional control mechanisms at the level of the microcirculation alter responses to anaesthesia during hypertension.

Differential effects of intravenous anaesthetic agents on the response of rat mesenteric microcirculation in vivo after haemorrhage.

BACKGROUND: The differential effects of i.v. anaesthesia on the response of the mesenteric microcirculation after haemorrhage in vivo are previously unexplored. METHODS: Male Wistar rats (n=56) were anaesthetized intravenously either with propofol and fentanyl (propofol/fentanyl), ketamine or thiopental. A tracheostomy and carotid cannulation were performed and the mesentery surgically prepared for observation of the microcirculation using fluorescent in vivo microscopy. Animals were allocated to one of three groups: control, haemorrhage or haemorrhage re-infusion. RESULTS: After haemorrhage, the response of the microcirculation differed during propofol/fentanyl, ketamine and thiopental anaesthesia. During propofol/fentanyl anaesthesia there was constriction of arterioles (-16.7 (3.9)%), venules (-5.9 (1.7)) and capillaries (-16.3 (2.8)) (n=12). During ketamine and thiopental anaesthesia both constriction and dilation was observed. After haemorrhage and re-infusion, macromolecular leak occurred from venules during propofol/fentanyl and thiopental anaesthesia (P<0.05), but not during ketamine anaesthesia. CONCLUSION: In summary, i.v. anaesthetic agents differentially alter the response of the mesenteric microcirculation to haemorrhage.

Intravenous anaesthesia and the rat microcirculation: the dorsal microcirculatory chamber.

The use of the dorsal microcirculatory chamber in male Wistar rats (n=7) to study the effects of induction and maintenance of anaesthesia on the microcirculation is described. Different patterns of responses were observed. At induction, arteriolar dilation was found following propofol and thiopental but ketamine produced constriction. During maintenance, constriction of arterioles was seen with ketamine and thiopental but dilation persisted with propofol. The dorsal microcirculatory chamber appears to be a useful tool for the study of microcirculatory changes related to anaesthesia.