Household infrastructure in aboriginal communities and the implications for health improvement.

OBJECTIVE: To evaluate housing survey data, describe the state of household infrastructure in Aboriginal communities in the Northern Territory (NT), and to discuss implications for health improvement for people in these communities. DESIGN: Quantitative analysis of survey data and qualitative analysis of the survey process. SETTING: All NT houses funded for repairs and maintenance through the Indigenous Housing Authority of the Northern Territory (IHANT). MAIN OUTCOME MEASURE: Status of infrastructure necessary for four key "healthy living practices" (washing people, washing clothes and bedding, waste removal, and food storage and preparation). RESULTS: 3906 houses (79% of all houses funded by IHANT) were surveyed. Infrastructure components most frequently identified as not functional or not present were those required for the storage and preparation of food (62% not functional). The facilities required for personal hygiene and safe removal of human waste were not functional in 45%-46% of houses. CONCLUSIONS: These findings highlight the significance of absent or non-functioning household infrastructure as a potential contributory factor in the poor nutritional status and high rates of respiratory, skin and gastrointestinal infections in Indigenous communities. The environmental health and housing survey in the NT is an important tool for monitoring progress on addressing a key underlying determinant of the health of Indigenous people, and potentially for facilitating research aimed at gaining an improved understanding of the relationship of the household environment to health in Indigenous communities.

Inhibition of sympathetic cholinergic vasodilatation by a selective NPY Y2 receptor agonist in the gracilis muscle of anaesthetised dogs.

Neuropeptide Y (NPY) is known to be co-stored and co-released from sympathetic nerve terminals. In the cardiovascular system NPY acts on two main receptor subtypes. At the postjunctional or Y1 receptor NPY causes constriction directly in addition to potentiating other vasoconstrictor agents. NPY acting at the prejunctional, or Y2 receptor, inhibits the release of neurotransmitter from autonomic nerve terminals. In these experiments we used the selective Y2 receptor agonist N-acetyl[Leu28,Leu31]NPY24-36 to examine the role of NPY in the modulation of sympathetic vascular control in skeletal muscle in anaesthetised dogs. No systemic pressor or local constrictor activity was observed in response to N-acetyl[Leu28, Leu31]NPY24-36 administration, therefore allowing us to examine the neuroinhibitory actions of NPY in the absence of direct vascular effects on blood flow. Stimulation of the sympathetic nerves to the gracilis muscle engages both sympathetic cholinergic and sympathetic adrenergic fibres and produces an initial vasodilatation followed by a slower vasoconstriction. Nerve evoked vasodilatation was inhibited by over 50% in the presence of the selective NPY Y2 agonist N-acetyl[Leu28,Leu31]NPY24-36. This dilatation was abolished by atropine, confirming its cholinergic nature. N-Acetyl[Leu28,Leu31]NPY24-36 was found to have no effect on nerve evoked vasoconstriction. The results demonstrate a NPY Y2-receptor mediated inhibition of nerve evoked sympathetic cholinergic vasodilatation but not of sympathetic vasoconstriction.

Effects of pituitary adenylate cyclase-activating polypeptide on cardiovascular and respiratory responses in anaesthetised dogs.

This study examines some of the cardiovascular and respiratory effects of pituitary adenylate cyclase-activating polypeptide (PACAP) in anaesthetised dogs. Intravenous injection of PACAP 27 caused an increase in arterial blood pressure and an increase in heart rate. The blood pressure response was significantly reduced by adrenoceptor blockade suggesting a mechanism of action mediated in part via catecholamines. The heart rate increase was unaltered by adrenoceptor blockade suggesting a direct effect of PACAP 27. PACAP 27 also caused potentiation of cardiac slowing caused by stimulation of the vagus nerve. In addition, PACAP 27 powerfully stimulated breathing. This was probably evoked by stimulation of arterial chemoreceptors, because bilateral section of the carotid sinus nerves abolished this effect. PACAP 27 had no effect on the ability of the cardiac sympathetic nerve to increase heart rate, nor on the interaction between the sympathetic and parasympathetic systems in the heart.