Agents for change: nonphysician medical providers and health care quality.

Quality medical care is a clinical and public health imperative, but defining quality and achieving improved, measureable outcomes are extremely complex challenges. Adherence to best practice invariably improves outcomes. Nonphysician medical providers (NPMPs), such as physician assistants and advanced practice nurses (eg, nurse practitioners, advanced practice registered nurses, certified registered nurse anesthetists, and certified nurse midwives), may be the first caregivers to encounter the patient and can act as agents for change for an organization's quality-improvement mandate. NPMPs are well positioned to both initiate and ensure optimal adherence to best practices and care processes from the moment of initial contact because they have robust clinical training and are integral to trainee/staff education and the timely delivery of care. The health care quality aspects that the practicing NPMP can affect are objective, appreciative, and perceptive. As bedside practitioners and participants in the administrative and team process, NPMPs can fine-tune care delivery, avoiding the problem areas defined by the Institute of Medicine: misuse, overuse, and underuse of care. This commentary explores how NPMPs can affect quality by 1) supporting best practices through the promotion of guidelines and protocols, and 2) playing active, if not leadership, roles in patient engagement and organizational quality-improvement efforts.

The effect of diabetes on endothelin, interleukin-8 and vascular endothelial growth factor-mediated angiogenesis in rats.

In diabetes mellitus, there is a problem of both premature atherosclerosis as well as impaired collateralization. Studies were performed using the rat corneal angiogenesis model as a surrogate for collateralization to determine the effect of diabetes mellitus on endothelin (ET)-1, ET-3, vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8)-mediated angiogenesis. In an initial group of experiments, streptozotocin-induced diabetes resulted in impairment of ET-1-mediated angiogenesis from 69% to 32%, but was only impaired from 74% to 59% for ET-3. When rats were fluid-resuscitated, mortality fell, and the incidence of inhibition of angiogenesis decreased for ET-1, but was still at 47%. Inhibition of ET-3-mediated angiogenesis in fluid-resuscitated rats was essentially unaffected from 74% to 75%. Studies of VEGF and IL-8 in fluid-resuscitated rats demonstrated that VEGF-mediated angiogenesis was only inhibited from 49% to 45%, but there was inhibition of IL-8-mediated angiogenesis from 62% to 31%. We concluded that there may be two mechanisms by which ET-1-mediated corneal angiogenesis is inhibited: a decrease in intravascular volume and dynamic forces affecting angiogenesis, and a direct effect of diabetes on some aspect of cell growth or angiogenic process. Diabetes also appeared to inhibit IL-8-mediated angiogenesis, but had very little or no effect on ET-3- or VEGF-mediated angiogenesis.

Elevated immunoreactive endothelin-1 levels in newborn rabbit lungs after meconium aspiration.

OBJECTIVE: Our prime objective was to study the production of big endothelin-1 (Big ET-1) and its conversion to ET-1 in the lungs of newborn rabbits exposed to meconium. Our second objective was to study the effect of captopril on endothelin expression. DESIGN: Prospective, comparative study. SETTING: Research laboratory of the Michael Reese Hospital and the University of Illinois, Chicago. SUBJECTS: Two-wk-old rabbit pups. INTERVENTIONS: Rabbit pups were instilled with meconium or saline into the lungs. Another group, pretreated with captopril, was also instilled with either meconium or saline. MEASUREMENTS AND MAIN RESULTS: After meconium or saline instillation, lung lavage was performed. Big ET-1 and ET-1 were measured in lung lavage fluid by using a commercially available enzyme-linked immunosorbent assay kits in all groups. Also, lungs were studied by histochemistry analysis for a morphologic evaluation of meconium-induced damage. In the lavage fluid of saline-instilled pups, ET-1 remained low and no increase in Big ET-1 levels was observed. In meconium-instilled animals, bioactive ET-1 levels were significantly higher, with a peak at 8 hrs after instillation. The conversion ratio of Big ET-1 to ET-1 in the meconium group increased from 2.19 at the initial period to 7.19 at 8 hrs after meconium instillation. CONCLUSIONS: Our conclusion is that aspiration of meconium causes lung injury in the newborn and that this injury is associated with a significant increase in ET peptide production in the lungs. We also showed that ET production is inhibited by pretreatment of rabbits with captopril before meconium-induced injury. ET-1 and its conversion from ET-1 in response to meconium may play important roles in increasing pulmonary vascular resistance and lung cell death, even in the absence of hypoxia. In general, we conclude, that ET-1 levels are significantly elevated in meconium-instilled rabbits compared with saline-instilled ones, and both can be significantly inhibited by pretreatment with captopril. Whether ET-1 contributes directly to the pathophysiology of or is simply a marker of meconium aspiration syndrome remains speculative.