No abstract

Recent clinical and animal studies have shown that collateral artery growth is impaired in the presence of vascular risk factors, including hypertension. Available evidence suggests that angiotensin-converting enzyme inhibitors (ACEI) promote collateral growth in both hypertensive humans and animals; however, the specific mechanisms are not established. This study evaluated the hypothesis that collateral growth impairment in hypertension is mediated by excess superoxide produced by NAD(P)H oxidase in response to stimulation of the ANG II type 1 receptor. After ileal artery ligation, mesenteric collateral growth did not occur in untreated, young, spontaneously hypertensive rats. Significant luminal expansion occurred in collaterals of spontaneously hypertensive rats treated with the superoxide dismutase mimetic tempol, the NAD(P)H oxidase inhibitor apocynin, and the ACEI captopril, but not ANG II type 1 (losartan) or type 2 (PD-123319) receptor blockers. The ACEI enalapril produced equivalent reduction of arterial pressure as captopril but did not promote luminal expansion. This suggests the effects of captopril on collateral growth might result from its antioxidant properties. RT-PCR demonstrated that ANG II type 1 receptor and angiotensinogen expression was reduced in collaterals of untreated rats. This local suppression of the renin angiotensin system provides a potential explanation for the lack of effect of enalapril and losartan on collateral growth. The results demonstrate the capability of antioxidant therapies, including captopril, to reverse impaired collateral artery growth and the novel finding that components of the local renin angiotensin system are naturally suppressed in collaterals.

The majority of GAS pharyngitis testing in this practice before intervention was inconsistent with IDSA guideline recommendations. A quality improvement initiative, which was approved for Part 4 Maintenance of Certification credit, led to improvement in guideline-based testing for GAS pharyngitis.

KEY WORDS POTENTIAL CONFLICT OF INTEREST:The authors have indicated they have no potential confl icts of interest to disclose.A Quality Improvement Initiative to Achieve High Nursing Presence During Patient-and Family-Centered Rounds abstract OBJECTIVES: The objectives of this study were to: (1) identify local barriers to nursing presence on patient-and family-centered rounds (PFCR); and (2) increase nursing attendance during PFCR. METHODS:An electronic survey needs assessment was administered to nursing staff on a single acute medical care unit to identify local barriers to nursing presence on PFCR. Daily tracking of nursing presence on rounds was then performed over a 7-month period. During this time period, 2 Plan-DoStudy Act cycles were conducted. The fi rst intervention was a workshop for nurses about PFCR. The second intervention was the development of a strategy to contact nurses by using a hands-free communication device so that nurses were notifi ed when rounds were starting on their patients. To evaluate the impact of our interventions, a p-chart was generated for the outcome of average daily nursing attendance (%) on PFCR per week over the 7-month period. RESULTS:Two barriers identifi ed on the survey were: (1) nurses were uncertain if physicians valued their input during PFCR; and (2) nurses were unsure when the physician team would be conducting rounds on their patients. On the p-chart, the average percentage of nursing attendance before interventions was 47%. After the nursing workshop, no change in the mean nursing attendance on PFCR was noted. After initiation of the hands-free contact strategy, nursing attendance on PFCR rose to 80%. CONCLUSIONS:A nursing contact strategy using a hands-free device led to a sustained increase in nursing attendance during PFCR.Patient-and family-centered rounds (PFCR) have been identifi ed as an effective model for high-quality patient care. Research has shown that families are more satisfi ed when they are included on rounds and that patient care is optimal when both the patient and family are included in medical decision-making.

Calmodulin (CaM) binds to the cardiac ryanodine receptor Ca2+ release channel (RyR2) with high affinity and may act as a regulatory channel subunit. Here we determine the role of CaM Met residues in the productive association of CaM with RyR2, as assessed via determinations of [3H]ryanodine and [35S]CaM binding to cardiac muscle sarcoplasmic reticulum (SR) vesicles. Oxidation of all nine CaM Met residues abolished the productive association of CaM with RyR2. Substitution of the COOH-terminal Mets of CaM with Leu decreased the extent of CaM inhibition of cardiac SR (CSR) vesicle [3H]ryanodine binding. In contrast, replacing the NH2-terminal Met of CaM with Leu increased the concentration of CaM required to inhibit CSR [3H]ryanodine binding but did not alter the extent of inhibition. Site-specific substitution of individual CaM Met residues with Gln demonstrated that Met124 was required for both high-affinity CaM binding to RyR2 and for maximal CaM inhibition. These results thus identify a Met residue critical for the productive association of CaM with RyR2 channels.