RESUMO
BACKGROUND: The World Health Organization (WHO) recommends that antenatal care (ANC) commence before 12 weeks' gestation to reduce the risk of obstetric and perinatal complications. Immigrants, refugees, and asylum seekers are at higher risk for late or non-initiation of ANC, and exclusion from universal healthcare (UHC) may be a contributing factor. AIMS: The aims were to synthesise evidence regarding uptake of ANC and to examine if this is associated with inadequate access to UHC and to evaluate the link between ANC and the risk of pregnancy outcomes in the immigrant, refugee and asylum seeker population. METHODS: The review was performed according to meta-analysis of observational studies in epidemiology (MOOSE) guidelines. Five databases were systematically searched. Abstracts were screened against inclusion criteria, and eligible papers underwent data extraction by two independent reviewers per paper. The ROBINS-I tool was used to assess risk of bias. RESULTS: Twelve studies were included in the final review. All studies reported that ANC was delayed for women who were classified as immigrants, refugees, and asylum seekers as per the WHO recommendations, and this was statistically significant compared to controls in 11 of 12 studies (P < 0.05). Findings regarding ANC uptake and pregnancy complications were too heterogeneous to conclusively report an association. CONCLUSION: Immigrants, refugees and asylum seekers who are excluded from UHC present significantly later to ANC than receiving-country-born women with full access to UHC. The link between delayed ANC due to inadequate UHC access and pregnancy complications remains unclear due to the heterogeneous nature of the studies.
RESUMO
A 60-year-old gentleman who presented with features of end-organ hypoperfusion despite initial hypertension was promptly diagnosed with cardiogenic shock following evidence of hyperlactatemia on biochemistry and left ventricular global hypokinesis with severe mitral regurgitation on transthoracic echocardiogram. He responded well to dobutamine and later underwent definitive surgical mitral valve replacement.
RESUMO
BACKGROUND AND PURPOSE: The physiological role of vascular ß3 -adrenoceptors is not fully understood. Recent evidence suggests cardiac ß3 -adrenoceptors are functionally effective after down-regulation of ß1 /ß2 -adrenoceptors. The functional interaction between the ß3 -adrenoceptor and other ß-adrenoceptor subtypes in rat striated muscle arteries was investigated. EXPERIMENTAL APPROACH: Studies were performed in cremaster muscle arteries isolated from male Sprague-Dawley rats. ß-adrenoceptor expression was assessed through RT-PCR and immunofluorescence. Functional effects of ß3 -adrenoceptor agonists and antagonists and other ß-adrenoceptor ligands were measured using pressure myography. KEY RESULTS: All three ß-adrenoceptor subtypes were present in the endothelium of the cremaster muscle artery. The ß3 -adrenoceptor agonists mirabegron and CL 316,243 had no effect on the diameter of pressurized (70 mmHg) cremaster muscle arterioles with myogenic tone, while the ß3 -adrenoceptor agonist SR 58611A and the nonselective ß-adrenoceptor agonist isoprenaline caused concentration-dependent dilation. In the presence of ß1/2 -adrenoceptor antagonists nadolol (10 µM), atenolol (1 µM) and ICI 118,551 (0.1 µM) both mirabegron and CL 316,243 were effective in causing vasodilation and the potency of SR 58611A was enhanced, while responses to isoprenaline were inhibited. The ß3 -adrenoceptor antagonist L 748,337 (1 µM) inhibited vasodilation caused by ß3 -adrenoceptor agonists (in the presence of ß1/2 -adrenoceptor blockade), but L 748,337 had no effect on isoprenaline-induced vasodilation. CONCLUSION AND IMPLICATIONS: All three ß-adrenoceptor subtypes were present in the endothelium of the rat cremaster muscle artery, but ß3 -adrenoceptor mediated vasodilation was only evident after blockade of ß1/2 -adrenoceptors. This suggests constitutive ß1/2 -adrenoceptor activity inhibits ß3 -adrenoceptor function in the endothelium of skeletal muscle resistance arteries.