In a bid to test the wound healing effect of a crude methanolic extract of Ageratum conyzoides (Linn.), 20 animals were divided into two groups of ten animals each representing control and experimental groups. Each animal had a 2cm x 2cm area of skin on the right dorsolateral flank area marked and excised. The resulting area of skin wound in the experimental group was dressed with crude methanolic extract of Ageratum conyzoides at a five daily interval while the animals in the control group were dressed with normal saline at the same interval. The wound area was measured at the tenth post-operative day for animals in both groups and the percentage wound contraction calculated. Sample of granulation tissues and end scar obtained from these animals and prepared by routine paraffin wax method. Fibroblast and blood vessel counts were determined in both groups. The result showed a significant increase in the percentage wound contraction at day 10 in the experimental group compared with the control (82.3 ± 1.6 % vs 55.0 ± 4.2 %), P < 0.05. The wound of animals in both groups showed excellent granulation tissue formation and minimal signs of wound infection. There was a significant reduction in the mean fibroblast count in the experimental group compared with the control (44.2 ± 5.8/ high power field vs 90.2 ± 17. 4 / high power field),P < 0.05. The exact significance of this cannot however be determined. There was no significance difference in the vessel count. It was concluded that extract of Ageratum conyzoides has a better wound healing enhancing action compared with normal saline treated controls. This effect may be due to the antimicrobial properties of Ageratum conyzoides.
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.
People of Black African ethnicity (BA) have greater prevalence of hypertension compared with those of White European ethnicity (WE) and are at greater risk of developing hypertension‐associated cardiovascular disease (CVD). Older WE non‐dipper hypertensives show endothelial dysfunction. Endothelial dysfunction and higher prevalence of non‐dipping nocturnal blood pressure have been documented in Blacks relative to Whites. Novel environmental stress stimuli evoke sympathetic vasoconstriction in renal and splanchnic vasculature, but vasodilatation in limb muscle, which may habituate on repetition. In young adults altered response to novel stimuli is predictive of developing hypertension later on in life. However, It is not known whether non‐dippers also show endothelial dysfunction and altered responses to environmental stressors. Thus, we hypothesized that non dippers would show smaller muscle vasodilator or muscle vasoconstrictive responses on repetition of an environmental stressor and blunted reactive hyperaemia relative to dippers. Experiments were performed on 17 WEs (21±0.64 years) and 16 BAs (22±0.77 years) who were resident in the UK. Responses were recorded following release of arterial occlusion for 2 min (reactive hyperaemia) and by 5 sound stimuli (S1–5; 100 dB, 2 KHz). Continuous arterial blood pressure (ABP) was recorded by finger photoplethysmography. Forearm blood flow (FBF) was recorded by venous occlusion plethysmography; forearm vascular conductance (FVC) was calculated as FBF/ABP. 24 hour Ambulatory blood pressure monitoring was done. Relative to WES, BAs showed higher 24 hour systolic blood pressure (SBP)(110±1.33 vs 117±3.17 mmHg) and higher sleep‐time SBP (99±1.36 vs 108±3.05 mmHg) p<0.05 as well as higher proportion of pre‐/hypertensives (7/16, 40%) compared with WE (1,5.8%). 40% BAs were non‐ dippers compared to 17.6 % WE. Six of the pre‐/hypertensive BAs were nocturnal dippers. Relative to normotensive BA dippers, BA non‐dippers showed higher sleep SBP (93±4.65 vs 108±3.01 mmHg) and heart rate (59±4.69 vs 72±3.11 bpm) p<0.05. Relative to WE dippers, the WE non dippers showed higher day‐time and night time mean ABP (85.25±1.14 vs 91.57±2.39 mmHg) ; (71.55±0.88 vs 81.25±1.71 mmHg) p<0.05. During reactive hyperaemia, there was no difference between dippers and non‐dippers in the two ethnic groups ( WE: +0.39± 0.03 vs +0.45± 0.08; BA : +0.41± 0.05 vs +0.34± 0.05 p>0.05 ). During S1–5, WE and BA dippers showed a net increase in FVC indicating forearm vasodilatation (WE, +0.005±0.002 CU; BA, +0.007±0.002 CU) whilst WE and BA non‐dippers showed a net decrease in FVC indicating forearm vasoconstriction, (WE − 0.007±0.004 CU; BA −0.007±0.003 CU). These results indicate that in young normotensive non‐dippers, sympathetic vasoconstriction to mental stress precedes development of endothelial dysfunction and could serve as an early indicator of cardiovascular disorder. Thus, we propose that exaggerated sympathetic vasoconstrictor response to environmental stressors contributes to the development of hypertension and CVD in non‐dippersThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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