Bridging the Radiology-Pediatrics Interaction Gap by Incorporating a PGY4 Radiology Resident into the General Pediatrics Team.

To bridge the gap between clinicians and radiologists, radiology residents rounded with inpatient pediatric medicine teams to present and interpret daily imaging studies, as well as assist with decisions and indications for radiologic exams. Surveys were sent to team members who rotated with radiology residents, and the consensus strongly favored having radiology residents on future rotations. Team members responded that they benefitted from a better understanding of radiology exams, their indications and limitations.

Pulmonary hemodynamic response to acute combination and monotherapy with sildenafil and brain natriuretic peptide in rats with monocrotaline-induced pulmonary hypertension.

BACKGROUND: The lungs of patients with pulmonary arterial hypertension (PAH) exhibit decreased bioavailability of nitric oxide and downstream signaling through cyclic guanosine monophosphate (cGMP). Therapies that enhance cGMP-mediated vasodilation have shown efficacy in treating PAH. We tested the hypothesis that combination therapy with sildenafil, a cGMP phosphodiesterase type 5 inhibitor, and brain natriuretic peptide (BNP), a receptor-mediated guanosine cyclase stimulator, synergistically attenuates monocrotaline-induced PAH in rats compared with either monotherapy. METHODS: Adult male Sprague-Dawley rats were subcutaneously injected with monocrotaline (n = 41, 50 mg/kg). After approximately 4 weeks, the rats were infused intravenously with vehicle solution, sildenafil (42 and 85 microg/kg/min), or BNP (50 and 100 ng/kg/min), alone and in varied combination. The primary endpoint was the relative change in right ventricular systolic pressure (RVSP) and mean arterial systemic pressure (MAP). Secondary endpoints included heart rate and dP/dt. RESULTS: Vehicle infusions did not alter hemodynamic variables. Sildenafil85 (85 microg/kg/min) alone decreased RVSP (-16.6 +/- 5.6%) and decreased MAP (-4.0 +/- 4.7%). BNP50 (50 ng/kg/min) and BNP100 (100 ng/kg/min) decreased RVSP (-23.3 +/- 5.7% and -27.1 +/- 2.9%, respectively) and MAP (-6.4 +/- 5.8% and -14.3 +/- 4.1%, respectively). Combination therapy with sildenafil42 and BNP50 decreased RVSP (-20.7 +/- 5.6%) and showed a lessened systemic effect (MAP = -11.6 +/- 5.9%). Combination therapy with sildenafil85 and BNP100 decreased RVSP (-27.6 +/- 3.2%, P = NS) and showed increased systemic effect (MAP = -20.7 +/- 3.1%, P < 0.05) in comparison with sildenafil85. CONCLUSIONS: This study suggests that intravenous administration of both sildenafil and BNP monotherapy produces significant improvement in RVSP, making them potentially viable options for the treatment of PAH, whereas combination therapy produces no additional improvement in pulmonary hemodynamics.

Oxidative stress contributes to pulmonary hypertension in the transgenic (mRen2)27 rat.

The transgenic (mRen2)27 (Ren2) rat overexpresses mouse renin in extrarenal tissues, causing increased local synthesis of ANG II, oxidative stress, and hypertension. However, little is known about the role of oxidative stress induced by the tissue renin-angiotensin system (RAS) as a contributing factor in pulmonary hypertension (PH). Using male Ren2 rats, we test the hypothesis that lung tissue RAS overexpression and resultant oxidative stress contribute to PH and pulmonary vascular remodeling. Mean arterial pressure (MAP), right ventricular systolic pressure (RVSP), and wall thickness of small pulmonary arteries (PA), as well as intrapulmonary NADPH oxidase activity and subunit protein expression and reactive oxygen species (ROS), were compared in age-matched Ren2 and Sprague-Dawley (SD) rats pretreated with the SOD/catalase mimetic tempol for 21 days. In placebo-treated Ren2 rats, MAP and RVSP, as well as intrapulmonary NADPH oxidase activity and subunits (Nox2, p22phox, and Rac-1) and ROS, were elevated compared with placebo-treated SD rats (P < 0.05). Tempol decreased RVSP (P < 0.05), but not MAP, in Ren2 rats. Tempol also reduced intrapulmonary NADPH oxidase activity, Nox2, p22phox, and Rac-1 protein expression, and ROS in Ren2 rats (P < 0.05). Compared with SD rats, the cross-sectional surface area of small PA was 38% greater (P < 0.001) and luminal surface area was 54% less (P < 0.001) in Ren2 rats. Wall surface area was reduced and luminal area was increased in tempol-treated SD and Ren2 rats compared with untreated controls (P < 0.05). Collectively, the results of this investigation support a seminal role for enhanced tissue RAS/oxidative stress as factors in development of PH and pulmonary vascular remodeling.