Janice M. Marshall

Research data on menstrual health in Honduras are limited, particularly in rural and ethnic minority areas. This pilot study aimed to assess women’s perceptions of menstrual healthcare in rural Honduran communities, focusing on menstrual health education, access to menstrual products and healthcare, and community attitudes towards menstruation. This study was conducted at a 3-day medical clinic set up by Global Brigades in the rural Potrerillos community. Seventy-three female participants (aged 18–55 years) completed a paper-based survey on menstrual health using a Likert scale. Results are reported as descriptive statistics, including median with interquartile range, and 95% confidence intervals. Main findings were that 73.9% of the participants received menstrual health education predominantly at home, with 25% receiving insufficient education before menarche. Additionally, 52.8% of participants reported a lack of and an inadequate range of menstrual products, while 52.9% experienced menstruation anxiety. These findings suggest that community educational initiatives and increased access to menstrual products could significantly improve the menstrual health of rural Honduran women and help reduce negative menstruation experiences.

Cocoa flavan-3-ols affect endothelium-dependent responses in resistance vessels and microcirculation has received little attention. We tested the effects of dark chocolate consumption (396 mg total flavanols/day for 3 days) in two Groups of 10 men (18–25 years; non-smokers) each comprising equal numbers of White European (WE) and South Asian (SA) ethnicity. In Group 1, dark chocolate did not affect reactive hyperaemia in forearm muscle, but augmented muscle dilatation evoked by acute mental stress, and reactive hyperaemia and acetylcholine (ACh)-evoked dilatation in cutaneous microcirculation. Conversely, in Group 2, chocolate did not affect cutaneous reactive hyperaemia or ACh-evoked dilatation, but these responses were blunted in Group 1 relative to Group 2. Further, when Groups 1 and 2 were combined, responses were blunted in SAs relative to WEs, augmented by chocolate in SAs only. In Group 2 individuals whose ACh-evoked dilatation was attenuated by nitric oxide synthase (NOS) inhibition, ACh-evoked dilatation was not altered after chocolate, but the attenuating effect of NOS inhibition was lost. Conversely, in Group 2 individuals whose ACh-evoked dilatation was enhanced by NOS inhibition, ACh-evoked dilatation was also augmented by chocolate. We propose that in resistance and microvessels of young men, cocoa flavan-3-ols preferentially augment endothelium-dependent dilator responses whose responses are depressed by familial and lifestyle factors more prevalent in SAs than Wes. Flavan-3-ols may facilitate the NOS pathway but also influence other endothelium-dependent dilators.

Introduction: Prevalence of cardiovascular disease (CVD) is higher in South Asians than white Europeans. The offspring of hypertensive parents (OH) have greater risk of hypertension than offspring of normotensive parents (ON). We hypothesized that endothelium-dependent dilatation is already blunted in young South Asians, relative to young white European women, particularly in South Asian OH women. Methods: In young white European ON, South Asian ON and OH women (18–25 years old; 10 per group) who were normotensive, we recorded cutaneous perfusion by laser Doppler fluximetry during reactive hyperaemia and iontophoresis of acetylcholine (ACh), before and after inhibiting NO synthesis (NOS) or/and cyclooxygenase (COX). In these and an additional 135 age-matched South Asian and white European women, physical activity and life-style factors were assessed by questionnaire. Results: ACh-evoked dilatation was blunted in young South Asians, relative to white European women. It was attenuated by NOS or COX inhibition in white European ON; by NOS inhibition only in South Asian ON, but not OH women. After combined NOS and COX inhibition, ACh-evoked dilatations were similar to control ACh responses. Similar findings were made for reactive hyperaemia. Questionnaire data indicated young South Asians have lower physical activity levels, fresh fruit and vegetable intake than white European women, South Asian OH being lower than white European ON, or OH women. Conclusion: Endothelium-dependent dilatation is blunted in young South Asians, relative to white European women, especially in South Asian OH in whom NO-dependent and prostaglandin-dependent dilatation is blunted. We suggest improved diet and greater physical activity could be particularly effective in improving endothelium-dependent dilatation and reducing future CVD risk in young South Asian OH women.

The risk of cardiovascular disease (CVD) including hypertension is higher in South Asians (SAs) than White Europeans (WEs). But, whether disturbances in autonomic control of the cardiovascular system are present in early adulthood in SAs has not been tested. Thus, we performed studies on young 20 WEs and 21 SAs aged (21.9±0.36, 20.7±0.41 respectively, equal numbers of men and women in each group) in whom arterial blood pressure (ABP), electrocardiogram (ECG), heart rate (HR) and respiration were recorded at rest, during mental stress (3 min Colour Stroop test) and during 5 min slow breathing (6 breaths/min). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were computed from the pulse contour. Baroreflex sensitivity (BRS) was calculated by the sequence method as change in R‐R interval evoked by spontaneous up and down sequences in systolic pressure (SP) at rest and during mental stress and as the relationship between R‐R interval and the fall in SP evoked by standing from a squat before and at 0, 3, 6 min following the stress test. HRV was computed in time‐domain during mental stress and slow breathing. Comparisons within and between WEs and SAs were done by paired and un‐paired t‐tests respectively. At rest, WEs and SAs had similar mean ABP (mABP, 86.9±1.42 vs 87.1±1.77mmHg), HR (71.1±2.45 vs 76.2±3.56 beats/min), CO (4.8±0.21 vs 5.2±0.21L/min), SV (76.5±3.86 vs 81.5±2.97ml), TPR (1.14±0.06 vs 1.01±0.04 resistance units), and BRS (up‐sequence: 1.2±0.05, down‐sequence: 1.2±0.05 vs 1.0±0.09 and 1.2±0.09ms/mmHg). Further, mental stress evoked similar increases in mABP and HR in WEs and SAs but was accompanied by an increase CO in WEs and by an increase in TPR in SAs. Concomitantly, vagal indices of HRV were depressed during mental stress in SAs only (RMSSD: 66.2±7.8 to56.2±11.4 and 67.6±8.7 to 50.0±6.5*ms, *: P<0.05 within WE or SAs). Further during up‐sequences in SP, BRS was depressed in both SAs and WEs during mental stress, but during down‐sequences, BRS was depressed in WE only (to 0.59±0.10 vs 0.96±0.08*ms/mmHg). Also, following mental stress, BRS during squat to stand, an index of vagosympathetic activity, was depressed in WEs only (0.5±0.04 at rest to 0.3±0.04* vs 0.5±0.06 to 0.5±0.06ms/mmHg). On the other hand, slow breathing, tended to decrease ABP in both WEs and SAs (82.1±1.8 to 79.2±2.1mmHg: P<0.05; 79.4±2.0 to 77.4±2.0mmHg: P=0.09 respectively) and increased vagal indices of HRV in both WEs and SAs (66.3±8.6 to 86.0±13.2*ms; 67.6±8.7 to 86.48.8*ms). These results suggest that during and after mental stress, young normotensive SAs show greater sympathetic vasoconstriction than WEs, and attenuated respiratory modulation of HR, while their ability to evoke baroreflex tachycardia by vagal inhibition and sympathetic activation is preserved relative to young WEs. Such disturbances in would be expected to increase the risk of future CVD and hypertension in SAs, particularly in those with high levels of daily stress. The finding that slow breathing increased vagal activity in young SAs raises the possibility that regular slow breathing may help to normalize autonomic regulation of ABP in SAs and limit future CVD.

The role of prostaglandins (PGs) in exercise hyperemia is controversial. We tested their contributions in moderate intensity forearm exercise, whether their release is oxygen (O2 )-dependent or affected by aging. A total of 12 young (21 ± 1 years) and 11 older (66 ± 2 years) recreationally active men performed rhythmic and isometric handgrip contractions at 60% maximum voluntary contraction for 3 min during air breathing after placebo, after cyclooxygenase (COX) inhibition with aspirin, while breathing 40% O2 and during their combination (aspirin + 40% O2 ). Forearm blood flow (FBF) was recorded with venous occlusion plethysmography (forearm vascular conductance (FVC): FBF/mean arterial pressure). Venous efflux of PGI2 and PGE2 were assessed by immunoassay. Postcontraction increases in FVC were similar for rhythmic and isometric contractions in young and older men, and accompanied by similar increases in efflux of PGI2 and PGE2 . Aspirin attenuated the efflux of PGI2 by 75%-85%, PGE2 by 50%-70%, (p < .05 within group; p > .05 young versus. older), and postcontraction increases in FVC by 22%-27% and 17%-21% in young and older men, respectively (p < .05 within group and young versus. older). In both age groups, 40% O2 and aspirin + 40% O2 caused similar inhibition of the increases in FVC and efflux of PGs as aspirin alone (p < .05 within group). These results indicate that PGs make substantial contributions to the postcontraction hyperemia of rhythmic and isometric contractions at moderate intensities in recreationally active young and older men. Given PGI2 is mainly released by endothelium and PGE2 by muscle fibers, we propose PG generation is dependent on the contraction-induced falls in O2 at these sites.

The contribution of prostaglandins (PGs) to exercise hyperaemia is controversial. In this review, we argue this is partly explained by differences in exercise intensity between studies. The effects of cyclooxygenase (COX) inhibition and PG assays indicate that PGs contribute more at moderate to heavy than at light workloads and are mainly released by low tissue O₂. But, the release and actions of PGs also depend on other O₂‐dependent dilators including ATP, adenosine and NO. K⁺ may inhibit the action of PGs and other mediators by causing hyperpolarization, but contributes to the hyperaemia. Thus, at lighter loads, the influence of PGs may be blunted by K⁺, while COX inhibition leads to compensatory increases in other O₂‐dependent dilators. In addition, we show that other sources of variability are sex and ethnicity. Our findings indicate that exercise hyperaemia following rhythmic contractions at 60% maximum voluntary contraction, is smaller in young black African (BA) men and women than in their white European (WE) counterparts, but larger in men than in women of both ethnicities. We propose the larger absolute force in men causes greater vascular occlusion and accumulation of dilators, while blunted hyperaemia in BAs may reflect lower oxidative capacity and O₂ requirement. Nevertheless, COX inhibition attenuated peak hyperaemia by ∼30% in WE, BA men and WE women, indicating PGs make a substantial contribution in all three groups. There was no effect in BA women. Lack of PG involvement may provide early evidence of endothelial dysfunction, consistent in BA women with their greater risk of cardiovascular disease. image

Purpose We tested whether the values of limb blood flow calculated with strain-gauge venous occlusion plethysmography (VOP) differ when venous occlusion is achieved by automated, or manual inflation, so providing rapid and slower inflation, respectively. Method In 9 subjects (20–30 years), we calculated forearm blood flows (FBF) values at rest and following isometric handgrip at 70% maximum voluntary contraction (MVC) when rapid, or slower inflation was used. Result Rapid and slower cuff inflation took 0.23 ± 0.01 (mean ± SEM) and 0.92 ± 0.02 s, respectively, reflecting the range reported in published studies. At rest, FBF calculated from the 1st cardiac cycle after rapid and slower inflation gave similar values: 10.5 ± 1.4 vs. 9.6 ± 1.3 ml dl^− 1 min^− 1, respectively (P > 0.05). However, immediately post-contraction, FBF was ~ 40% lower with slower inflation: 54.6 ± 5.1 vs. 33.8 ± 4.2 ml dl^− 1 min^− 1 (P < 0.01). The latter value was similar to that calculated over the 3rd cardiac cycle following rapid inflation: 2nd cardiac cycle: 40.5 ± 4.5; 3rd cycle: 32.6 ± 4.5 ml dl^− 1 min^− 1. Regression analyses of FBFs recorded at intervals post-contraction showed those calculated over the 1st, 2nd, or 3rd cardiac cycles with rapid inflation correlated well with those from the 1st cardiac cycle with manual inflation (r = 0.79, 0.82, 0.79; P < 0.01). However, only the slope for the 3rd cycle with rapid inflation vs. slower inflation was close to unity (2.07, 1.34, and 0.94, respectively). Conclusion These findings confirm that the 1st cardiac cycle following venous occlusion should be used when calculating FBF using VOP and, but importantly, indicate that cuff inflation should be almost instantaneous; just ≥ 0.9 s leads to substantial underestimation, especially at high flows.

Background: Across ethnicities, offspring of hypertensive parents (OH) have higher risk of hypertension than offspring of normotensive parents (ON). Sympathetic hyperactivity and reduced nitric oxide availability have been reported in normotensive OH; but the role of vasodilator cyclooxygenase (COX) products is unclear. Methods: In 12 OH and 12 ON men (19–24 years old), each group comprising six white Europeans and six South Asians with resting ABP less than 129/89 mmHg, reactive hyperaemia and responses evoked by iontophoresis pulses of acetylcholine (ACh) were recorded in forearm skin by laser Doppler fluximetry before and after COX inhibition. Results: Peak reactive hyperaemia was larger in ON than OH (71.0 ± 7.8 vs. 43.4 ± 8.3 perfusion units (perf.units); P < 0.05). It was attenuated by COX inhibition in ON (24.8 ± 5.2 perf.units, P < 0.01), not OH (54.2 ± 7.5 perf.units). Similarly, increases in perfusion evoked by ACh were greater in ON than OH (169.1 ± 20.4 vs. 142.1 ± 19.9 perf.units; P < 0.05) and attenuated by COX inhibition in ON (94.5 ± 13.7; P < 0.05), not OH (132.6 ± 16.1 perf.units). Considering ethnicities, ACh-evoked dilation, though not reactive hyperaemia was greater in Europeans than Asians (176.8 ± 21.7 vs. 130.4 ± 15.0; P < 0.01; 61.0 ± 8.7 vs. 51.7 ± 9.2 perf.units). However, within both Europeans and Asians, COX inhibition attenuated reactive hyperaemia and ACh-induced dilatation in ON only. Conclusion: Reactive hyperaemia and ACh-evoked dilatation in cutaneous circulation are blunted in young, normotensive OH relative to ON men irrespective of white European, or South Asian ethnicity and are attributable to impaired contribution of COX vasodilator products in OH. These features may provide early markers of endothelial dysfunction that contribute to hypertensive risk in OH men.

Purpose: Prevalence of cardiovascular disease (CVD) is greater in South Asians (SAs) than White Europeans (WEs). Endothelial dysfunction and blunted forearm vasodilatation to environmental stressors have been implicated in CVD. We investigated whether these features are present in young SA men.Methods: In 15 SA and 16 WE men (19–23 years), we compared changes in forearm blood flow, arterial blood pressure (ABP), forearm vascular conductance (FVC), heart rate, and electrodermal resistance (EDR; sweating) following release of arterial occlusion (reactive hyperaemia endothelium-dependent) and 5 single sounds at 5–10 min intervals (stressors).Results: All were normotensive. Peak reactive hyperaemia was smaller in SAs than WEs (FVC increase: 0.36 ± 0.038 vs 0.44 ± 0.038 units;P < 0.05). Furthermore, in WEs, mean FVC increased at 5, 15, and 20 s of each sound (vasodilatation), but increased at 5 s only in SAs, decreasing by 20 s (vasoconstriction). This reflected a smaller proportion of SAs showing forearm vasodilatation at 15 s (5/15 SAs vs 11/16 WEs:P < 0.01), the remainder showing vasoconstriction. Concomitantly, WEs showed greater bradycardia and EDR changes. Intra-class correlation analyses showed that all responses were highly reproducible over five sounds in both WEs and SAs. Moreover, sound-evoked changes in ABP and FVC were negatively correlated in each ethnicity (P < 0.01). However, WEs showed preponderance of forearm vasodilatation and depressor responses; SAs showed preponderance of vasoconstriction and pressor responses.Conclusions: Endothelium-dependent vasodilatation is blunted in young SA men. This could explain their impaired forearm vasodilatation and greater pressor responses to repeated environmental stressors, so predisposing SAs to hypertension and CVD.