These findings provide evidence that the α(1A)-AR subtype mediates adrenergic vasoconstriction in murine ophthalmic arteries.

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Gastrointestinal sequelae in neonates surviving surgery for NEC are frequent. Long-term follow-up assessing defined gastrointestinal outcomes is warranted.

Background: Studies on the influence of congenital heart disease (CHD) on neonates with necrotizing enterocolitis (NEC) have produced varied results. We therefore examined the influence of CHD on NEC outcomes.Methods: We carried out a retrospective single-center study including infants with confirmed NEC, treated between 2004 and 2017. We excluded patients with isolated patent ductus arteriosus or pulmonary hypertension (n = 45) and compared outcomes of patients with hemodynamically relevant CHD (n = 38) and those without CHD (n = 91).Results: Patients with CHD were more mature than those without CHD [gestational age, median, 95% confidence interval (CI95), 37.1, 34.5–37.2w, vs. 32.6, 31.9–33.3w; P < 0.01]. The presence of CHD did not influence the frequencies of severe disease (overall 21% Bell stage III), nor surgical interventions (overall 30%), the occurrence of intestinal complications (overall 13%), nor the duration of hospitalization (overall 38 days in survivors). The overall mortality as well as NEC-related mortality was increased with the presence of CHD, being 50% (19 out of 38) and 13% (5 out of 38), respectively, when compared to patients without CHD, being 8% (7 out of 91) and 3% (3 out of 91). The presence of CHD and of advanced NEC stage III were independent predictors of NEC-associated fatalities with multivariable odds ratios (CI95) of 7.0, 1.3–39.5 for CHD, and of 3.4, 1.6–7.5 for stage III disease.Conclusions: While some outcome parameters in neonates with NEC remained unaffected by the presence of CHD, the mortality risk for patients with CHD was seven times higher than without CHD.

Pharmacological activation of the M1 muscarinic receptor subtype was suggested to promote the survival of retinal neurons. We examined the hypothesis that the M1 receptor is crucial for retinal neuron survival in vivo by using mice devoid of the M1 receptor gene. Muscarinic receptor gene expression was determined in the retina using real-time PCR. The amount of neurons in the retinal ganglion cell layer and of axons in the optic nerve was determined in retinal wholemounts stained with cresyl blue and in optic nerve cross-sections stained with toluidine blue, respectively. mRNA of all five muscarinic receptor subtypes (M1-M5) was detected in the retina from wild-type mice. Remarkably, M2 and M3 receptor mRNA were most abundant. In retinas from M1 receptor-deficient mice, M4 receptor mRNA expression was increased compared to that of wild-type mice, while no marked changes in the mRNA expression levels of the other muscarinic receptor subtypes were observed. The amount of cells in the retinal ganglion cell layer and the amount of axons in the optic nerve did not differ between M1 receptor-deficient and wild-type mice. The present findings suggest that the M1 receptor is not essential for the survival of retinal neurons in vivo.

It is difficult to predict the risk of mortality in necrotizing enterocolitis (NEC). This study aimed at identifying risk factors for severe NEC (Bell stage III) and mortality in preterm children with NEC. In this multicenter retrospective study, we analyzed multiple data from 157 premature children with confirmed NEC in the period from January 2007 to October 2018. We performed univariate, multivariate, stepwise logistic regression, and receiver operator characteristics (ROC) analyses. We were able to demonstrate that low Apgar scores (notably at 1′ and 5′), low hemoglobin concentration (Hgb), and high lactate level at disease onset and during disease correlated with NEC severity and mortality (P < 0.05, respectively). Severe NEC was related to congenital heart disease (CHD — OR 2.6, CI95% 1.2–5.8, P 0.015) and patent ductus arteriosus (PDA — OR 3.3, CI95% 1.6–6.9, P 0.0012), whereas death was related to the presence of PDA (OR 5.5, CI95% 2.3–14, P < 0.001).Conclusion: Low Apgar scores, low Hgb, high lactate levels, and the presence of CHD or PDA correlated with severe NEC or mortality in children with NEC. What is Known:• It remains difficult to predict which infant that suffers from necrotizing enterocolitis at risk of death.• Several clinical and laboratory parameters tools to predict fatal outcome in NEC. What is New:• The following laboratory parameters were associated with the risk of death from NEC: Hemoglobin concentration, base excess and lactate level.• The following clinical variables were associated with the risk of death from NEC: Apgar scores, as well as the presence of congenital heart disease and patent ductus arteriosus.

The α₁-AR-induced mydriasis in mice is mediated mainly by the α₁A-AR, with a smaller contribution of the α₁B-AR, matching the relative abundance of these subtypes at the mRNA level. The lack of a single α₁-AR subtype does not appear to cause atrophy in the mouse iris.

Background: The development of necrotizing enterocolitis (NEC) in neonates with patent ductus arteriosus (PDA) is not well-understood. Our aim was to find risk factors for NEC in children with a significant PDA and to assess differences in mortality and duration of hospital stay between patients with PDA and those with PDA and NEC. Methods: We performed a retrospective single center case control study including infants with PDA scheduled for treatment. We compared multiple patient data between patients with PDA and those with PDA and NEC from 2004 to 2018 using 1:2 and 1:1 matching. Results: We used 1:2 matching with 26 NEC patients (cases) and 52 PDA patients without NEC (controls) and 1:1 matching with 5 NEC patients and 5 PDA patients without NEC. NEC patients had lower Apgar score (1 ′), more congenital malformations, more suspected sepsis, less hypotension, higher minimum platelet count and higher CRP-values during the week before NEC (P < 0.05, respectively). The mortality was higher in NEC cases [29% (9/31)] compared to the control patients [2% (1/57), P < 0.001]. Lower Apgar score (1 ′) was correlated with an increased risk of NEC stage III. Hypotension was inversely correlated with the odds of NEC (OR 0.3). Conclusions: NEC increased mortality in infants with PDA. Hypotension did not increase the risk of NEC in infants with PDA. Routine clinical parameters were not able to predict NEC in infants who suffer from PDA.