This double-blind, placebo-controlled, crossover study investigated the effect of blackcurrant anthocyanin (BCA) intake on peripheral circulation during rest and during typing work by using near-infrared spectroscopy (NIRS), and it also assessed improvement in shoulder stiffness caused by poor local circulation. In a resting circulation study, nine healthy male subjects took capsules of BCA at a dosage of 17 mg kg(-1) or placebo (isoenergetic sugar). NIRS was used to measure left forearm blood flow (FBF) following venous occlusion and muscle oxygen consumption following arterial occlusion prior to and hourly for 4 h after ingestion of BCA. Plasma anthocyanin concentration was measured prior to ingestion and 1, 2, and 4 h later. FBF increased significantly 2 h after BCA ingestion [BCA 1.22 (0.13)-fold increase relative to pre-values vs placebo 0.83 (0.06) of pre-values; P < 0.05] and then tended to increase for a further 3 h after ingestion [BCA 1.26 (0.15)-fold increase relative to pre-values vs placebo 0.82 (0.07) of pre-values; P = 0.078]. There was, however, no significant difference in muscle oxygen consumption between BCA and placebo intake at any time point. In a typing work study, 11 healthy subjects took capsules of BCA (7.7 mg kg(-1)) or placebo (isoenergetic sugar) daily for 2 weeks. The subjects then performed intermittent typing workload for 30 min in order to induce acute shoulder stiffness. During the workload, total hemoglobin and oxygenated hemoglobin (oxy-Hb) were determined using NIRS and myoelectric signals measured in the right trapezius muscle using electromyography (EMG). The viscoelasticity of the trapezius muscle was also evaluated using a muscle stiffness meter before and after the typing workload. BCA intake prevented the decrease in oxy-Hb significantly (P < 0.05), and also tended to alleviate the increase in root mean square (RMS) of the EMG during the typing workload, and also muscle stiffness after the workload. There was no improvement in typing performance with BCA intake. The results of this study suggest that intake of BCA may improve shoulder stiffness caused by typing work by increasing peripheral blood flow and reducing muscle fatigue.

Anthocyanin (AC) is widely used as supplement of eye health in Europe and in East Asia. In this review, I describe AC effects to clarify the mechanism is important in order to understand the effects of AC on vision health. The bioavailability of AC is quite low but, reported as intact form and many kinds of metabolite. And AC passes through the blood-aqueous fluid barrier and blood-retinal barrier. In vitro study, AC had a relaxing effect on ciliary muscle which is important to treat both myopia and glaucoma. And AC stimulate the regeneration of rhodopsin in frog rod outer segment. Furthermore, AC could inhibit the axial length and ocular length elongation in a negative lens-induced chick myopia model. In addition, we summarized clinical studies of AC intake improved dark adaptation and transient myopic shift and the improvement on retinal blood circulation in normal tension glaucoma patients.

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Abstract. We examined the involvement of nitric oxide (NO) and / or endothelium-derived hyperpolarizing factor (EDHF) in decreasing peripheral vascular resistance in the rat hind limb perfusion model and analyzed the identity of EDHF in this model. The potency of carbachol (CCh) to produce relaxation was quantitatively similar to sodium nitroprusside (SNP). CChinduced relaxation was abolished after endothelial denudation, but resistant to nitroarginine and indomethacin. The relaxation was inhibited by tetraethylammonium, ouabain, charybdotoxin plus apamin, and under depolarization. SNP-induced relaxation was accompanied by increased cGMP production, which was inhibited by ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-l-one). Although CCh produced a similar extent of relaxation to SNP, the cGMP level was 24 times lower than that with SNP. Low KCl produced a definite relaxation, which was inhibited by ouabain, but independent of NO, prostacyclin, and endothelium. 1-EBIO (1-ethyl-2-benzimidazolinone) as an activator of IK Ca channel also produced a concentration-dependent relaxation, which was inhibited by charybdotoxin, ouabain, and depolarization, but independent of NO and prostacyclin. Clotrimazole and 17-octadecynoic acid as inhibitors of P 450 monooxygenase inhibited the CCh-induced relaxation. Meanwhile, catalase at a concentration sufficient to inhibit H 2 O 2 -induced relaxation did not exert definite inhibition of the CCh-induced relaxation. These results suggest that CCh produces an endothelium-dependent, EDHF-dependent, and NO-cGMPindependent relaxation and that K + and metabolite(s) of P 450 monooxygenase possibly play an important role for this relaxation.