Moderate-intensity exercise training reduces vasorelaxation of mesenteric arteries: role of BKCa channels and nitric oxide.

Exercise training (ET) is well established to induce vascular adaptations on the metabolically active muscles. These adaptations include increased function of vascular potassium channels and enhanced endothelium-dependent relaxations. However, the available data on the effect of ET on vasculatures that normally constrict during exercise, such as mesenteric arteries (MA), are scarce and not conclusive. Therefore, this study hypothesized that 10 weeks of moderate-intensity ET would result in adaptations towards more vasoconstriction or/and less vasodilatation of MA. Young Fischer 344 rats were randomly assigned to a sedentary group (SED; n=24) or exercise training group (EXE; n=28). The EXE rats underwent a progressive treadmill ET program for 10 weeks. Isometric tensions of small (SED; 252.9+/-29.5 microm, EXE; 248.6+/-34.4 microm) and large (SED; 397.7+/-85.3 microm, EXE; 414.0+/-86.95 microm) MA were recorded in response to cumulative phenylephrine concentrations (PE; 0-30 microM) in the presence and absence of the BKCa channel blocker, Iberiotoxin (100 nM). In another set of experiments, tensions in response to cumulative concentration-response curves of acetylcholine (ACh) or sodium nitroprusside (SNP) were obtained, and pEC50s were compared. Immunoblotting was performed to measure protein expression levels of the BKCa channel subunits and eNOS. ET did not alter the basal tension of small and large MA but significantly increased their responses to PE, and reduced the effect of BKCa channels in opposing the contractile responses to PE without changes in the protein expression level of BKCa subunits. ET also elicited a size-dependent functional adaptations that involved reduced endothelium-independent and endothelium-dependent relaxations. In large MA the sensitivity to SNP was decreased more than in small MA suggesting impaired nitric oxide (NO)-dependent mechanisms within the vascular smooth muscle cells of ET group. Whereas the shift in pEC50 of ACh-induced relaxation of small MA would suggest more effect on the production of NO within the endothelium, which is not changed in large MA of ET group. However, the eNOS protein expression level was not significantly changed between the ET and SED groups. In conclusion, our results indicate an increase in contraction and reduced relaxation of MA after 10 weeks of ET, an adaptation that may help shunt blood flow to metabolically active tissues during acute exercise.

Developing patient safety system using WHO tool in hospitals in Oman.

OBJECTIVE: Oman is progressively implementing the Patient Safety Friendly Hospital Initiative (PSFHI), a tool formulated by the World Health Organization (WHO) to achieve optimal patient safety in hospitals. This paper describes its implementation in selected government and private hospitals in Oman and analyses the performance of four hospitals whose implementations of PSFHI were assessed by WHO. DESIGN: The PSFHI initiative was launched in 11 hospitals in Oman during 2016. The enrolled hospitals implemented a 1-year plan composed of several steps such as formation of steering committees, working groups, full orientation about the standards, training of staff, documents development and community involvement. One year later, four hospitals which were the earliest to join the initiative were subjected to WHO assessment. SETTING: Secondary level government and private hospitals. INTERVENTION(S): The WHO-PSFHI standards. MAIN OUTCOME MEASURE: Hospitals' adherence to the standards. RESULTS: Three of the four hospitals (one government and two private) scored level two. One government hospital scored level three, earning it the distinction of being the first hospital in the Eastern Mediterranean Region to reach level three in the very first assessment. CONCLUSIONS: Implementation of PSFHI in selected hospitals of Oman had successful outcomes in improving patient's safety.

Insulin infusion via an intraosseous needle in diabetic ketoacidosis.

We report the successful management of a five-year-old child with severe diabetic ketoacidosis with dehydration, who received his initial resuscitative fluids and a continuous infusion of insulin via an intraosseous needle. The patient had presented to a remote community hospital and intravenous access could not be gained. The correction of hyperglycaemia and metabolic acidaemia was achieved at a rate comparable to intravenous therapy. No complications were observed. Although intraosseous access is well described in paediatric resuscitation guidelines, it is not mentioned in International Diabetes Society guidelines for the management of diabetic ketoacidosis. Alternatives to intravenous administration of insulin delivery recommended in such guidelines, such as the subcutaneous or intramuscular routes, may be less appropriate than the intraosseous route. This route can also allow resuscitation fluids and other drugs to be reliably administered in children with diabetic ketoacidosis and severe dehydration where intravenous access can not be attained. We suggest that the potential role of intraosseous access, when intravenous access can not be obtained, should be considered when management guidelines for paediatric diabetic ketoacidosis with dehydration are reviewed.