linked to placenta endothelial dysfunction –Two new updates
Am J Physiol Heart Circ Physiol. 2017 Jun 23:ajpheart.00745.2016. doi: 10.1152/ajpheart.00745.2016. [Epub ahead of print] The human coronary vasodilatory response to acute mental stress is mediated by neuronal nitric oxide. Khan SG1, Melikian N1, Shabeeh H2, Cabaco AR1, Martin K1, Khan F1, O’Gallagher K1, Chowienczyk P1, Shah AM3. Author information 1King’s College London.2King’s College London British Heart Foundation Centre.3King’s College London British Heart Foundation Centre of Excellence ajay.shah@kcl.ac.uk. Abstract INTRODUCTION: Mental stress-induced ischemia approximately doubles the risk of cardiac events in patients with coronary artery disease, yet the mechanisms underlying changes in coronary blood flow in response to mental stress are poorly characterized. Neuronal nitric oxide synthase (nNOS) regulates basal coronary blood flow in healthy humans and mediates mental stress-induced vasodilation in the forearm. However, its possible role in mental-stress-induced increases in coronary blood flow is unknown. METHODS: We studied eleven patients (6 men, mean age 58±14 years) undergoing elective diagnostic cardiac catheterization, and assessed the vasodilator response to mental stress elicited by the Stroop color-word test. Intra-coronary substance P (20pmol/min) and isosorbide dinitrate (1mg) were used to assess endothelium-dependent and -independent vasodilation respectively. Coronary blood flow was estimated using intra-coronary Doppler recordings and quantitative coronary angiography to measure coronary artery diameter. RESULTS: Mental stress increased coronary flow by 34±7.0% over the preceding baseline during saline infusion (p<0.01), and this was reduced to 26±7.0% in the presence of the selective nNOS inhibitor S-methyl L-thiocitrulline (SMTC, 0.625µmol/min; p<0.001). Mental stress increased coronary artery diameter by 6.9±3.7% (p=0.02), and by 0.5±2.8% (p=0.51) in the presence of SMTC. The response to substance P did not predict the response to mental stress (r2 = -0.22, p=0.83). CONCLUSION: nNOS mediates the human coronary vasodilator response to mental stress, predominantly through actions at the level of coronary resistance vessels. Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology. KEYWORDS: endothelial function; mental stress-induced ischemia; nitric oxide J Clin Endocrinol Metab. 2017 Jun 23. doi: 10.1210/jc.2017-00434. [Epub ahead of print] Does a first-degree of family history of diabetes impact placental maternal and fetal vascular circulation and inflammatory response? Shargorodsky M1,2, Kovo M3,2, Schraiber L4,2, Bar J3,2. Author information 1Department of Endocrinology, Edith Wolfson Medical Center, Holon, Israel.2Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.3Department of Obstetrics & Gynecology, Edith Wolfson Medical Center, Holon, Israel.4Department of Pathology, Edith Wolfson Medical Center, Holon, Israel. Abstract CONTEXT: Heritability of diabetes is associated with hyperinsulinemia, impaired endothelial function, and inflammatory up-regulation. However, no studies have examined whether a family history of diabetes effects placental vascular circulation. OBJECTIVE: The present study was designed to investigate the impact of a first-degree family history of type 2 diabetes (FHD) on placental vascular circulation and inflammatory lesions. DESIGN: Observational cohort study. SETTING: Pregnant women who gave birth at Edith Wolfson Medical Center. PATIENTS: 339 pregnant women were divided into two groups according to presence of FHD: Group 1 included 225 subjects without FHD, and group 2 included 114 subjects with FHD. INTERVENTION: Placental histopathological examination. MAIN OUTCOME MEASURES: Placental vascular supply abnormalities of maternal and fetal origin. RESULTS: Maternal vascular supply (MVS) abnormalities of the placenta were significantly higher in subjects with FHD, compared to subjects without FHD (p<0.005). Fetal vascular supply (FVS) abnormalities, as well as maternal and fetal inflammatory response did not differ significantly between groups. In the GLM analysis, FHD was an independent and significant predictor of MVS abnormalities and more than doubled the risk of this outcome. Gestational diabetes incidence was significantly higher in subjects with FHD (p<0.0001). Significant by-group differences in gestational diabetes persisted even after adjustment for age and BMI. Although incidence of gestational hypertensive disorders was significantly higher in individuals with FHD, after adjustment FHD did not significantly predict this outcome. CONCLUSIONS: A first-degree FHD is significantly and independently associated with an increased rate of maternal vascular perfusion abnormalities and risk of gestational diabetes. Endothelial Function Scientific Update Sponsored by Endothelix Inc. www.endothelix.com
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