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Improvement of cutaneous microcirculation by cold atmospheric plasma (CAP): Results of a controlled, prospective cohort study.
Kisch, T, Helmke, A, Schleusser, S, Song, J, Liodaki, E, Stang, FH, Mailaender, P, Kraemer, R
Microvascular research. 2016;:55-62
Abstract
BACKGROUND Cold atmospheric plasma (CAP) has proven its benefits in the reduction of various bacteria and fungi in both in vitro and in vivo studies. Moreover, CAP generated by dielectric barrier discharge (DBD) promoted wound healing in vivo. Charged particles, chemically reactive species (such as O3, OH, H2O2, O, NxOy), ultraviolet radiation (UV-A and UV-B), strong oscillating electric fields as well as weak electric currents are produced by DBD operated in air. However, wound healing is a complex process, depending on nutrient and oxygen supply via cutaneous blood circulation. Therefore, this study examined the effects of CAP on cutaneous microcirculation in a prospective cohort setting. HYPOTHESIS Cold atmospheric plasma application enhances cutaneous microcirculation. METHODS Microcirculatory data of 20 healthy subjects (11 males, 9 females; mean age 35.2 ± 13.8 years; BMI 24.3 ± 3.1 kg/m(2)) were recorded continuously at a defined skin area at the radial forearm. Under standardized conditions, microcirculatory measurements were performed using a combined laser Doppler and photospectrometry system. After baseline measurement, CAP was applied by a DBD plasma device for 90 s to the same defined skin area of 22.5 cm(2). Immediately after the application cutaneous microcirculation was assessed for 30 min at the same site. RESULTS After CAP application, tissue oxygen saturation immediately increased by 24% (63.8 ± 13.8% from 51.4 ± 13.2% at baseline, p<0.001) and stayed significantly elevated for 8 min. Cutaneous blood flow increased by 73% (41.0 ± 31.2 AU from 23.7 ± 20.8 AU at baseline, p<0.001) and remained upregulated for 11 min. Furthermore, cutaneous blood flow showed two peaks at 14 (29.8 ± 25.0 AU, p=0.049) and 19 min (29.8 ± 22.6 AU, p=0.048) after treatment. Postcapillary venous filling pressure continuously increased, but showed no significant change vs. baseline in the non-specific BMI group. Subgroup analysis revealed that tissue oxygen saturation, postcapillary venous filling pressure and blood flow increased more in case of a lower BMI. CONCLUSION CAP increases cutaneous tissue oxygen saturation and capillary blood flow at the radial forearm of healthy volunteers. These results support recently published data on wound healing after CAP treatment. However, further studies are needed to determine if this treatment can improve the reduced microcirculation in diabetic foot ulcers. Moreover, repetitive application protocols have to be compared with a single session treatment approach.
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Oral atorvastatin therapy restores cutaneous microvascular function by decreasing arginase activity in hypercholesterolaemic humans.
Holowatz, LA, Santhanam, L, Webb, A, Berkowitz, DE, Kenney, WL
The Journal of physiology. 2011;(Pt 8):2093-103
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Abstract
Elevated low-density lipoproteins (LDLs) are associated with vascular dysfunction evident in the cutaneous microvasculature. We hypothesized that uncoupled endothelial nitric oxide synthase (NOS3) through upregulated arginase contributes to cutaneous microvascular dysfunction in hyperocholesterolaemic (HC) humans and that a statin intervention would decrease arginase activity. Five microdialysis fibres were placed in the skin of nine normocholesterolaemic (NC: LDL level 95±4 mg dl⁻¹) and nine hypercholesterolaemic (HC: LDL: 177±6 mg dl⁻¹) men and women before and after 3 months of systemic atrovastatin. Sites served as control, NOS inhibited, arginase inhibited, L-arginine supplemented and arginase inhibited plus L-arginine supplemented. Skin blood flow was measured while local skin heating (42°C) induced NO-dependent vasodilatation. L-NAME was infused after the established plateau in all sites to quantify NO-dependent vasodilatation. Data were normalized to maximum cutaneous vascular conductance (CVC(max)). Skin samples were obtained to measure total arginase activity and arginase I and arginase II protein. Vasodilatation was reduced in hyperocholesterolaemic subjects (HC: 76±2 vs. NC: 94±3%CVC(max), P < 0.001) as was NO-dependent vasodilatation (HC: 43±5 vs. NC: 62±4%CVC(max), P < 0.001). The plateau and NO-dependent vasodilatation were augmented in HC with arginase inhibition (92±2, 67±2%CVC(max), P < 0.001), L-arginine (93±2, 71±5%CVC(max), P < 0.001) and combined treatments (94±4, 65±5%CVC(max), P < 0.001) but not in NC. After statin intervention (LDL: 98±5 mg dl⁻¹) there was no longer a difference between control sites (88±4, 61±5%CVC(max)) and localized microdialysis treatment sites (all P > 0.05). Arginase activity and protein were increased in HC skin (P < 0.05 vs. NC) and activity decreased with atrovastatin treatment (P < 0.05). Reduced NOS3 substrate availability through upregulated arginase contributes to cutaneous microvascular dysfunction in hyperocholesterolaemic humans, which is corrected with atorvastatin therapy.
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Evaluation of renal microcirculation by contrast-enhanced ultrasound with Sonazoid as a contrast agent.
Tsuruoka, K, Yasuda, T, Koitabashi, K, Yazawa, M, Shimazaki, M, Sakurada, T, Shirai, S, Shibagaki, Y, Kimura, K, Tsujimoto, F
International heart journal. 2010;(3):176-82
Abstract
Chronic kidney disease (CKD) is a major and serious risk factor for cardiovascular disease (CVD). Continuous hypoxia due to hypoperfusion in peritubular capillaries is one of the factors aggravating CKD, but evaluation of perfusion in this region is difficult using clinically available imaging methods. Since the second-generation ultrasound contrast agent Sonazoid has a stable shell, it enables visualization of the renal vasculature for a long period of time. We therefore evaluated changes in contrast-enhanced ultrasound (CEUS) imaging with Sonazoid in CKD patients.Sonazoid was used in 85 CKD patients and 5 control subjects, and images were recorded for 10 minutes. Time-intensity curves were generated from the images of 62 time points in both cortex and medulla.In control samples, contrast enhancement spread from the hilar portion to the periphery along the direction of arterial flow, and renal cortex and medulla were then enhanced in sequence. Enhancement was maximal soon after, then gradually decreased, but was still visible at 600 seconds. In CKD patients, renal contrast enhancement was attenuated in both cortex and medulla. On time-intensity curves, the attenuation of enhancement was composed of delayed rising, reduction of peak, and acceleration of decay in both cortex and medulla with progression of renal dysfunction. No side effects of the contrast agent were observed in any subjects.The attenuation of renal contrast enhancement observed in CKD patients appears to reflect disturbance of perfusion in peritubular capillaries. CEUS with Sonazoid is a useful and safe means of visualizing the renal microvasculature.
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WISE 2005: chronic bed rest impairs microcirculatory endothelium in women.
Demiot, C, Dignat-George, F, Fortrat, JO, Sabatier, F, Gharib, C, Larina, I, Gauquelin-Koch, G, Hughson, R, Custaud, MA
American journal of physiology. Heart and circulatory physiology. 2007;(5):H3159-64
Abstract
Sedentary behavior has deleterious effects on the cardiovascular system, including reduced endothelial functions. A 2-mo bed rest study in healthy women [women international space simulation for exploration (WISE) 2005 program] presented a unique opportunity to analyze the specific effects of prolonged inactivity without other vascular risk factors on the endothelium. We investigated endothelial properties before and after 56 days of bed rest in 8 subjects who performed no exercise (control group: No-EX) and in 8 subjects who regularly performed treadmill exercise in a lower body negative pressure chamber as well as resistance exercise (countermeasure group, EX). A functional evaluation of the microcirculation in the skin was assessed with laser Doppler. We studied endothelium-dependent and -independent vasodilation using iontophoresis of acetylcholine and sodium nitroprusside, respectively. We also measured circulating endothelial cells (CECs), an index of endothelial damage. In the No-EX group, endothelium-dependent vasodilation was significantly reduced (35.4 +/- 4.8% vs. 24.1 +/- 3.8%, P < 0.05) by bed rest with a significant increase in the number of CECs (3.6 +/- 1.4 vs. 10.6 +/- 2.7 ml(-1), P < 0.05). In the EX group, endothelium-dependent vasodilation and number of CECs were preserved. Our study shows that in humans prolonged bed rest causes impairment of endothelium-dependent function at the microcirculatory level, along with an increase in circulating endothelial cells. Microcirculatory endothelial dysfunction might participate in cardiovascular deconditioning, as well as in several bed rest-induced pathologies. We therefore conclude that the endothelium should be a target for countermeasures during periods of prolonged deconditioning.
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Effect of low-density lipoprotein apheresis on plasma endothelin-1 levels in diabetic hemodialysis patients with arteriosclerosis obliterans.
Nakamura, T, Ushiyama, C, Osada, S, Inoue, T, Shimada, N, Koide, H
Journal of diabetes and its complications. 2003;(6):349-54
Abstract
Endothelin (ET)-1 has been implicated in the pathogenesis of diabetes, arteriosclerosis, and chronic renal failure. We studied whether low-density lipoprotein (LDL) apheresis alters plasma ET-1 levels in diabetic hemodialysis patients with arteriosclerosis obliterans (ASO). Plasma ET-1 levels were measured in 30 healthy control subjects (Group A), 30 diabetes patients without ASO (Group B), 20 diabetes patients with ASO (Group C), 20 diabetes patients without ASO who were undergoing hemodialysis (Group D), and 6 diabetes patients with ASO who were undergoing hemodialysis (Group E). Hemodialysis patients were dialyzed three times weekly with a bicarbonate dialysate. Six diabetic hemodialysis patients with ASO underwent LDL apheresis once weekly for 10 weeks, and the change in plasma ET-1 levels due to LDL apheresis was measured. LDL apheresis resulted in a statistically significant decrease in levels of total cholesterol and LDL cholesterol. In addition, LDL apheresis improved clinical symptoms in all patients. Plasma ET-1 levels in Group E (15.0+/-1.9 pg/ml) were significantly higher than those in Groups A (1.0+/-0.6 pg/ml, P<.001), B (1.3+/-0.5 pg/ml, P<.001), C (5.6+/-1.0 pg/ml, P<.001), and D (10.4+/-1.6 pg/ml, P<.01). Plasma ET-1 levels decreased progressively and significantly after a single LDL apheresis began (9.4+/-1.0 pg/ml after 60 min, P<.001, and 6.0+/-1.0 pg/ml after 120 min, P<.001). These data suggest that ET-1 may be associated with arteriosclerosis and that LDL apheresis enhances peripheral microcirculation in part by reducing the production of ET-1 in diabetic hemodialysis patients with ASO.
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Skin microvascular vasodilatory capacity in offspring of two parents with Type 2 diabetes.
Lee, BC, Shore, AC, Humphreys, JM, Lowe, GD, Rumley, A, Clark, PM, Hattersley, AT, Tooke, JE
Diabetic medicine : a journal of the British Diabetic Association. 2001;(7):541-5
Abstract
AIMS: Microvascular dysfunction occurs in Type 2 diabetes and in subjects with fasting hyperglycaemia. It is unclear whether this dysfunction relates to dysglycaemia. This study investigated in normogylcaemic individuals whether a genetic predisposition to diabetes, or indices of insulin resistance including endothelial markers, were associated with impaired microvascular function. METHODS Maximum microvascular hyperaemia to local heating of the skin was measured using laser Doppler flowmetry in 21 normoglycaemic subjects with no family history of diabetes (Group 1) and 21 normoglycaemic age, sex and body mass index-matched offspring of two parents with Type 2 diabetes (Group 2). RESULTS Although Group 2 had normal fasting plasma glucose and glucose tolerance tests, the 120-min glucose values were significantly higher at 6.4 (5.3-6.6) mmol/l (median (25th - 75th centile)) than the control group at 4.9 (4.6-5.9) mmol/l (P = 0.005) and the insulinogenic index was lower at 97.1 (60.9-130.8) vs. 124.0 (97.2-177.7) (P = 0.027). Skin maximum microvascular hyperaemia (Group 1: 1.56 (1.39-1.80) vs. Group 2: 1.53 (1.30-1.98) V, P = 0.99) and minimum microvascular resistance which normalizes the hyperaemia data for blood pressure (Group 1: 52.0 (43.2-67.4) vs. Group 2: 56.0 (43.7-69.6) mmHg/V, P = 0.70) did not differ in the two groups. Significant positive associations occurred between minimum microvascular resistance and indices of the insulin resistance syndrome; plasminogen activator inhibitor type 1 (R(s) = 0.46, P = 0.003), t-PA (R(s) = 0.36, P = 0.03), total cholesterol (R(s) = 0.35, P = 0.02), and triglyceride concentration (R(s) = 0.35, P = 0.02), and an inverse association with insulin sensitivity (R(s) = -0.33, P = 0.03). CONCLUSIONS In normoglycaemic adults cutaneous microvascular vasodilatory capacity is associated with features of insulin resistance syndrome, particularly with plasminogen activator inhibitor type 1. A strong family history of Type 2 diabetes alone does not result in impairment in the maximum hyperaemic response. Diabet. Med. 18, 541-545 (2001)