Neonatologists less frequently discuss long term complications: A simulation-based study of prenatal consults beyond the threshold of viability.

BACKGROUND: Guidelines exist for counseling expectant families of infants at periviable gestational ages (22-25 weeks), but it is much more common for neonatologists to counsel families at gestational ages beyond the threshold of viability when several aspects of these guidelines do not apply. We aimed to develop an understanding of what information is shared with mothers at risk of preterm delivery beyond periviability and to evaluate communication skills of our participants. METHODS: We developed a checklist of elements to include in counseling based on a comprehensive literature review. The checklist was divided into an information sharing section and a connect score. The information sharing list was sub-divided into general information and specific complications. Neonatologists engaged in a simulated prenatal counseling session with a standardized patient. Videotaped encounters were then analyzed for checklist elements. RESULTS: Neonatologists all scored well in communication using our tool and two other validated communication tools - the SEGUE and the analytic global OSCE. There was no difference in scoring based on years of experience or level of training. Information sharing from neonatologists more often discussed general information over specific. Neonatologists also focused more on early outcomes over long-term outcomes. Only 12% of neonatologists quoted the correct survival rate for the case. CONCLUSIONS: Neonatologists generally communicate well but share less information specific to prematurity and the long-term sequelae of prematurity. Our tool may be used to test if other interventions improve information sharing or communication.

Angiotensin II stimulates hyperplasia but not hypertrophy in immature ovine cardiomyocytes.

Rat and sheep cardiac myocytes become binucleate as they complete the 'terminal differentiation' process soon after birth and are not able to divide thereafter. Angiotensin II (Ang II) is known to stimulate hypertrophic changes in rodent cardiomyocytes under both in vivo and in vitro conditions via the AT1 receptor and intracellular extracellular regulated kinase (ERK) signalling cascade. We sought to develop culture methods for immature sheep cardiomyocytes in order to test the hypothesis that Ang II is a hypertrophic agent in the immature myocardium of the sheep. We isolated fetal sheep cardiomyocytes and cultured them for 96 h, added Ang II and phenylephrine (PE) for 48 h, and measured footprint area and proliferation (5-bromo-2'-deoxyuridine (BrdU) uptake) separately in mono- vs. binucleate myocytes. We found that neither Ang II nor PE changed the footprint area of mononucleated cells. PE stimulated an increase in footprint area of binucleate cells but Ang II did not. Ang II increased myocyte BrdU uptake compared to serum free conditions, but PE did not affect BrdU uptake. The MAP kinase kinase (MEK) inhibitor UO126 prevented BrdU uptake in Ang II-stimulated cells and prevented cell hypertrophy in PE-stimulated cells. This paper establishes culture methods for immature sheep cardiomyocytes and reports that: (1) Ang II is not a hypertrophic agent; (2) Ang II stimulates hyperplastic growth among mononucleate myocytes; (3) PE is a hypertrophic agent in binucleate myocytes; and (4) the ERK cascade is required for the proliferation effect of Ang II and the hypertrophic effect of PE.