Role of ventral medullary catecholaminergic neurons for respiratory modulation of sympathetic outflow in rats

Sympathetic activity displays rhythmic oscillations generated by brainsteminspiratory and expiratory neurons. Amplification of these rhythmic respiratory-related oscillations is observed in rats under enhanced central respiratory drive or during development of neurogenic hypertension. Herein, we evaluated the involvement of ventral medullary sympatho-excitatory catecholaminergic C1 neurons, using inhibitory Drosophila allatostatin receptors, for the enhanced expiratory-related oscillations in sympathetic activity in rats submitted to chronic intermittent hypoxia (CIH) and following activation of both peripheral (hypoxia) and central chemoreceptors (hypercapnia). Pharmacogenetic inhibition of C1 neurons bilaterally resulted in reductions of their firing frequency and amplitude of inspiratory-related sympathetic activity in rats in normocapnia, hypercapnia or after CIH. In contrast, hypercapnia or hypoxia-induced enhanced expiratory-related sympathetic oscillations were unaffected by C1 neuronal inhibition. Inhibition of C1 neurons also resulted in a significant fall in arterial pressure and heart rate that was similar in magnitude between normotensive and CIH hypertensive rats, but basal arterial pressure in CIH rats remained higher compared to controls. C1 neurons play a key role in regulating inspiratory modulation of sympathetic activity and arterial pressure in both normotensive and CIH hypertensive rats, but they are not involved in the enhanced late-expiratory-related sympathetic activity triggered by activation of peripheral or central chemoreceptors

Ambient air pollution and birth defects in Brisbane, Australia

BACKGROUND: Birth defects are a major public health concern as they are the leading cause of neonatal and infant mortality. Observational studies have linked environmental pollution to adverse birth outcomes, including congenital anomalies. This study examined potential associations between ambient air pollution and congenital heart defects and cleft lip or palate among births in Brisbane, Australia (1998–2004).---- METHODS: Ambient air pollution levels were averaged over weeks 3–8 of pregnancy among 150,308 births. Using a case–control design, we used conditional logistic regression and matched cases to 5 controls. Analyses were conducted using all births, and then births where the mother resided within 6 and 12 kilometers of an ambient air quality monitor.---- FINDINGS: When analyzing all births there was no indication that ambient air pollution in Brisbane was associated with a higher risk of cardiac defects. Among births where the mother resided within 6 kilometers of an ambient air quality monitor, a 5 ppb increase in O3 was associated with an increased risk of pulmonary artery and valve defects (OR 2.96, 95% CI: 1.34, 7.52) while a 0.6 ppb increase in SO2 was associated with an increased risk of aortic artery and valve defects (OR 10.76, 95% CI: 1.50, 179.8). For oral cleft defects among all births, the only adverse association was between SO2 and cleft lip with or without cleft palate (OR 1.27, 95% CI: 1.01, 1.62). However, various significant inverse associations were also found between air pollutants and birth defects.---- CONCLUSIONS: This study found mixed results and it is difficult to conclude whether ambient air pollution in Brisbane has an adverse association with the birth defects examined. Studies using more detailed estimates of air pollution exposure are needed