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Biomedical subjects

A C Shore

Publications and source records attributed to A C Shore.

At least 19 recordsLinked to original sources
PubMed2007

Reduced endothelial progenitor cells in European and South Asian men with atherosclerosis.

BACKGROUND: Circulating endothelial progenitor cells (EPCs) play a role in the repair and regeneration of the endothelium and may represent a novel cardiovascular risk factor. South Asian subjects have an increased risk of cardiovascular disease which is not fully explained by known risk factors. This study examined associations of EPCs with atherosclerosis and possible ethnic differences in EPCs. MATERIALS AND METHODS: A population sample of 58 European and South Asian adult men was enriched with the recruitment of an additional 59 European and South Asian men with known coronary disease. The coronary artery calcification score was measured by multi-slice computerized tomography (CT), carotid and femoral intima-media thickness (IMT), and femoral plaques were measured by ultrasound. The subjects were further subdivided into three categories of coronary artery disease on the basis of coronary artery calcification score and clinical history. Total EPCs and non-senescent EPCs (ns-EPCs) were quantified after 5 days cell culture and the number of late outgrowth colonies was measured over a 6-week test period. Circulating CD34+ haematopoietic precursor cells were measured by flow cytometry. RESULTS: Individuals with femoral plaques had reduced total and ns-EPCs. The number of ns-EPCs were reduced in individuals with the most coronary atheroma and were inversely related to the coronary calcification score and femoral IMT. These relationships persisted after multivariate adjustment for other risk factors. The numbers of late outgrowth colonies or circulating CD34+ cells were unrelated to the presence of atherosclerosis. There were no differences in the number of EPCs between European and South Asian subjects. CONCLUSION: The number of EPCs are reduced in subjects with atherosclerosis independent of other risk factors. Reduction in EPC numbers may be an independent risk factor for atherosclerosis but does not explain ethnic differences in cardiovascular risk.

Aged↗
PubMed2006

Six months of aerobic exercise does not improve microvascular function in type 2 diabetes mellitus.

AIMS/HYPOTHESIS: Adults with type 2 diabetes mellitus have impaired microvascular function. It has been hypothesised that microvascular function may be restored through regular exercise. The aim of this study was to investigate whether 6 months of regular aerobic exercise would improve microvascular function in adults with type 2 diabetes. MATERIALS AND METHODS: Fifty-nine patients with type 2 diabetes (32 males, age 62.9+/-7.6 years, HbA(1c) 6.8+/-0.9%) were randomised to either a 6-month aerobic exercise programme (30 min, three times a week, 70-80% of maximal heart rate) or a 'standard care' control group. Before and after the intervention period, microvascular function was assessed as the maximum skin hyperaemia to local heating and endothelial and non-endothelial responsiveness following the iontophoretic application of acetylcholine and sodium nitroprusside. Maximal oxygen uptake, as an index of aerobic fitness, was assessed using a maximal exercise test. RESULTS: No significant improvement was seen in the exercise group compared with the control group for any of the variables measured: maximal oxygen uptake (control pre: 1.73+/-0.53 [means+/-SD] vs post: 1.67+/-0.40; exercise pre: 1.75+/-0.56 vs post: 1.87+/-0.62 l/min, p=0.10); insulin sensitivity (insulin tolerance test) (control pre: -0.17+/-0.06 vs post: -0.17+/-0.06; exercise pre: -0.16+/-0.1 vs post: -0.17+/-0.07 mmol l(-1) min(-1), p=0.97); maximal hyperaemia (control pre: 1.49+/-0.43 vs post: 1.52+/-0.57; exercise pre: 1.42+/-0.36 vs post: 1.47+/-0.33 V, p=0.85); peak response to acetylcholine (control pre: 1.37+/-0.47 vs post: 1.28+/-0.37; exercise pre: 1.27+/-0.44 vs post: 1.44+/-0.23 V, p=0.19) or to sodium nitroprusside (control pre: 1.09+/-0.50 vs post: 1.10+/-0.39; exercise pre: 1.12+/-0.28 vs post: 1.13+/-0.40 V, p=0.98). CONCLUSIONS/INTERPRETATION: In this group of type 2 diabetic patients with good glycaemic control a 6-month aerobic exercise programme did not improve microvascular function or aerobic fitness.

Adult↗
PubMed2006

The insulin sensitiser pioglitazone does not influence skin microcirculatory function in patients with type 2 diabetes treated with insulin.

AIMS/HYPOTHESIS: Insulin resistance is associated with abnormal microvascular function. Treatment with insulin sensitisers may provoke oedema, suggesting microvascular effects. The mechanisms underlying the peripheral oedema observed during glucose-lowering treatment with thiazolidinediones are unclear. Therefore we examined the effect of pioglitazone on microvascular variables involved in oedema formation. METHODS: Subjects (40-80 years) with type 2 diabetes and on insulin were randomised to 9 weeks of pioglitazone therapy (30 mg/day; n=14) or placebo (n=15). The following assessments were performed at baseline and 9 weeks: microvascular filtration capacity; isovolumetric venous pressure; capillary pressure; capillary recruitment following venous or arterial occlusion; postural vasoconstriction; and maximum blood flow. A number of haematological variables were also measured including vascular endothelium growth factor (VEGF), IL-6 and C-reactive protein (CRP). RESULTS: Pioglitazone did not significantly influence any microcirculatory variable as compared with placebo (analysis of covariance [ANCOVA] for microvascular filtration capacity for the two groups, p=0.26). Mean VEGF increased with pioglitazone (61.1 pg/ml), but not significantly more than placebo (9.76 pg/ml, p=0.94). HbA(1c) levels and the inflammatory markers IL-6 and CRP decreased with pioglitazone compared with placebo (ANCOVA: p=0.009, p=0.001 and p=0.004, respectively). CONCLUSIONS/INTERPRETATION: Pioglitazone improved glycaemic control and inflammatory markers over 9 weeks but had no effect on microcirculatory variables associated with oedema or insulin resistance in type 2 diabetic patients treated with insulin.

Adult↗
PubMed2006

A novel automated waterline cleaning system that facilitates effective and consistent control of microbial biofilm contamination of dental chair unit waterlines: a one-year study.

Microbial contamination of dental chair unit (DCU) output water caused by biofilm growth in dental unit waterlines (DUWs) is a universal problem and a potentially significant source of cross-infection. The microbial quality of output water from a Planmeca Compact i DCU equipped with the novel Water Management System (WMS), an integrated and automated DUW cleaning system, was investigated over a 12-month period with the hydrogen peroxide- and silver ion-containing disinfectants Planosil and Planosil Forte. Four weeks after connection to the potable-water quality mains supply the density of aerobic heterotrophic bacteria, rose from the low levels consistently found in the supply water throughout this study (mean average 77 cfu/mL) to 15,400 cfu/mL. Disinfection of DUWs once weekly with Planosil for 10 weeks resulted in a dramatic reduction in bacterial density immediately following disinfection (mean average 26 cfu/mL). Bacterial density rose steadily between disinfections and by 7 days post-disinfection, water quality failed (mean average 384 cfu/mL) the American Dental Association DCU water quality standard of <or=200 cfu/mL. The DCU was then disinfected once weekly for 40 weeks with Planosil Forte. The average bacterial density immediately post-disinfection was 20 cfu/mL and 7 days post-disinfection was 113 cfu/mL. Electron microscopy showed that improved output water quality following disinfection with both disinfectants was associated with marked elimination of DUW biofilm, but deterioration of water quality following disinfection was associated with its regrowth. The most common bacterial species cultured from the mains water and the DCU output water were Microcococcus luteus and Sphingomonas spp., respectively, the latter of which are known opportunistic pathogens. The findings of this study show that the Planmeca Compact i DCU equipped with the easy to use and automated WMS, that requires minimal effort on the part of the operator, consistently provides output water that passes the ADA quality standard of <or=200 cfu/mL for up to 7 days following once-weekly disinfection with Planosil Forte.

Automation↗
PubMed2005

Differences in the association between type 2 diabetes and impaired microvascular function among Europeans and African Caribbeans.

AIMS/HYPOTHESIS: Diabetes is associated with microvascular damage in all populations, but diabetic patients of Black African descent (African Caribbeans) have a greater risk of vascular target organ damage than would be anticipated for any given blood pressure level. We investigated whether this may be due to differences in the microvasculature. MATERIALS AND METHODS: To assess the maximum hyperaemic response to heating and the post-ischaemic response, Laser Doppler fluximetry was performed on 51 and 100 Europeans, and on 66 and 88 African Caribbeans with and without diabetes, respectively. Subjects were aged between 40 and 65 years and recruited from the general population. Echocardiographic interventricular septal thickness (IVST) was measured as a proxy for vascular target organ damage. RESULTS: In diabetic subjects of both ethnic groups, the maximum hyperaemic response and peak response to ischaemia were attenuated as compared to the corresponding non-diabetic subjects (p=0.08 for diabetic and 0.03 for non-diabetic Europeans; p=0.03 and 0.1 for African Caribbeans). Adjustment for cardiovascular risk factors, in particular insulin and blood pressure, abolished these differences in Europeans (p=0.8 for diabetic and 0.2 for non-diabetic Europeans), but not in African Caribbeans (p=0.03 and 0.05). CONCLUSIONS/INTERPRETATION: Persisting microvascular dysfunction in African Caribbeans may contribute to the increased risk of target organ damage observed in diabetes in this population. The weak contribution of conventional cardiovascular risk factors to these disturbances indicates that conventional therapeutic interventions may be less beneficial in these patients. There was a risk-factor-independent, inverse association between IVST and maximal hyperaemia. These ethnic differences in microvascular responses to temperature and arterial occlusion could account for increased target organ damage in African Caribbeans.

Aged↗
PubMed2005

A role for heterotrimeric GTP-binding proteins and ERK1/2 in insulin-mediated, nitric-oxide-dependent, cyclic GMP production in human umbilical vein endothelial cells.

AIMS/HYPOTHESIS: Insulin is known to stimulate endothelial nitric oxide synthesis, although much remains unknown about the intracellular mechanisms involved. This study aims to examine, in human endothelial cells, the specific contribution of heterotrimeric Gi proteins and extracellular signal-regulated protein kinases 1/2 (ERK1/2) in insulin signalling upstream of nitric-oxide-dependent cyclic GMP production. METHODS: Human umbilical vein endothelial cells were treated with 1 nmol/l insulin in the presence or absence of inhibitors of tyrosine kinases (erbstatin), Gi proteins (pertussis toxin) or ERK1/2 (PD098059 or U0126), and nitric oxide production was examined by quantification of intracellular cyclic GMP. Activation/phosphorylation of ERK1/2 by insulin was examined by immunoblotting with specific antibodies, and direct association of the insulin receptor with Gi proteins was examined by immunoprecipitation. RESULTS: Treatment of cells with a physiological concentration of insulin (1 nmol/l) for 5 min increased nitric-oxide-dependent cyclic GMP accumulation by 3.3-fold, and this was significantly inhibited by erbstatin. Insulin-stimulated cyclic GMP production was significantly reduced by pertussis toxin and by the inhibitors of ERK1/2, PD098059 and U0126. Immunoblotting indicated that insulin stimulated the phosphorylation of ERK1/2 after 5 min and 1 h, and that this was completely abolished by pertussis toxin, but insensitive to the nitric oxide synthase inhibitor L-NAME. No direct interaction of the insulin receptor beta with Gialpha2 could be demonstrated by immunoprecipitation. CONCLUSIONS/INTERPRETATION: This study demonstrates, for the first time, that nitric oxide production induced by physiologically relevant concentrations of insulin, is mediated by the post-receptor activation of a pertussis-sensitive GTP-binding protein and subsequent downstream activation of the ERK1/2 cascade.

Cells, Cultured↗
PubMed2005

Does aerobic fitness influence microvascular function in healthy adults at risk of developing Type 2 diabetes?

AIM: To investigate whether aerobic fitness is associated with skin microvascular function in healthy adults with an increased risk of developing Type 2 diabetes. METHODS: Twenty-seven healthy normal glucose-tolerant humans with either a previous diagnosis of gestational diabetes or having two parents with Type 2 diabetes and 27 healthy adults who had no history of diabetes were recruited. Maximal oxygen uptake was assessed using an incremental exercise test to exhaustion. Skin microvascular function was assessed using laser Doppler techniques as the maximum skin hyperaemic response to a thermal stimulus (maximum hyperaemia) and the forearm skin blood flow response to the iontophoretic application of acetylcholine (ACh) and sodium nitroprusside. RESULTS: Maximal oxygen uptake was not significantly different in the 'at-risk' group compared with healthy controls. Maximum hyperaemia was reduced in those 'at risk' (1.29 +/- 0.30 vs. 1.46 +/- 0.33 V, P = 0.047); however, the peak response to acetylcholine or sodium nitroprusside did not differ in the two groups. A significant positive correlation was demonstrated between maximal oxygen uptake and maximum hyperaemia (r = 0.52, P = 0.006 l/min and r = 0.60, P = 0.001 ml/kg/min) and peak ACh response (r = 0.40, P = 0.04 l/min and r = 0.47, P = 0.013 ml/kg/min) in the 'at-risk' group when expressed in absolute (l/min) or body mass-related (ml/kg/min) terms. No significant correlations were found in the control group. CONCLUSIONS: In this 'at-risk' group with skin microvascular dysfunction maximal oxygen uptake was not reduced compared with healthy controls. However, in the 'at-risk' group alone, individuals with higher levels of aerobic fitness also had better microvascular and endothelial responsiveness.

Adult↗
PubMed2005

Impact of hormone replacement therapy on microvascular function in healthy and Type 2 diabetic postmenopausal women.

AIMS: Hormone replacement therapy (HRT) has been previously reported to modulate vascular function and cardiovascular risk. Its impact on the macrocirculation has previously been explored, however, little data is available on its impact on the microcirculation. This study aimed to determine the impact of HRT on microvascular function in healthy and Type 2 diabetic postmenopausal women (n=20 and 17, respectively). METHODS: Microvascular function was assessed by skin maximum hyperaemia, skin hyperaemic response to iontophoretically applied acetylcholine (endothelial-dependent vasodilator) and sodium nitroprusside (endothelial-independent vasodilator), capillary pressure and the microvascular filtration capacity. Microvascular assessments were carried out at baseline and repeated following 6 months' oral hormone replacement therapy (1 mg oestradiol/0.5 mg norethisterone or 1 mg unopposed oestradiol for hysterectomized women). RESULTS: Following 6 months' therapy there were no significant changes in microvascular assessments in the healthy women. In the diabetic women there was a reduction in the skin hyperaemic response to acetylcholine [median pretreatment peak response: 1.95 (25th, 75th centiles: 1.54, 2.30) V vs. post-treatment peak response: 1.53 (1.30, 1.91) V (P=0.011, Wilcoxon's signed rank test)] and sodium nitroprusside [median peak response 1.59 (1.37, 1.99) vs. 1.35 (0.92, 1.63) V (P=0.011)] with HRT, but no other changes. CONCLUSION: These data suggests that HRT does not affect microvascular function in healthy women, but adversely affects it in diabetic women. These findings may help to explain why HRT fails to provide the predicted cardiovascular protection, and raises the possibility that HRT influences microangiopathy progression in diabetic women.

Acetylcholine↗
PubMed2005

Microvascular endothelial function in subjects with Type 2 diabetes and the effect of lipid-lowering therapy.

AIMS: Abnormalities of microvascular and endothelial function are present in subjects with Type 2 diabetes. Although statin therapy improves cardiovascular risk in diabetes, dyslipidaemia in diabetes may be more responsive to combined statin and fibrate therapy. We examined the effect of cerivastatin and fenofibrate on microvascular function in subjects with Type 2 diabetes with no clinical evidence of cardiovascular disease and near normal lipid levels. METHODS: Age-, sex-, lipid- and blood pressure-matched subjects with Type 2 diabetes were randomized in double-blind fashion to one of four treatment groups: group 1 placebo/placebo (n=12), group 2 fenofibrate/placebo (n=10), group 3 cerivastatin/placebo (n=20) and group 4 cerivastatin/fenofibrate (n=11). The subjects were recruited from the Lipid in Diabetes Study. Microvascular function was assessed by skin blood flow response to iontophoresis of acetylcholine and sodium nitroprusside and by skin maximum hyperaemia to local heating. Measurements were carried out at baseline and 3 months later. RESULTS: Although all lipid parameters improved in groups 2-4 after 3 months' therapy, no difference was detected in skin blood flow to iontophoresis or maximum hyperaemia in any of the groups. Highly sensitive c-reactive protein (Hs-CRP) did not change with therapy. CONCLUSIONS: In conclusion, we were unable to demonstrate any improvement in microvascular endothelial function in non-hyperlipidaemic Type 2 diabetic subjects treated with single or combination lipid-lowering therapy.

Adult↗
PubMed2003

Insulin and lysophosphatidylcholine synergistically stimulate NO-dependent cGMP production in human endothelial cells.

AIMS: Nitric oxide (NO) is an important regulator of cardiovascular homeostasis. Lysophosphatidylcholine (lyso-PC), a major constituent of oxidized low density lipoproteins (oxLDL), has been reported to impair nitric oxide-dependent vasodilatation. This study investigated the possible mechanism of the lyso-PC effect on insulin-stimulated NO-dependent of cyclic guanosine 3',5'-monophosphate (cGMP) generation in human endothelial cells. METHODS: The intracellular concentration of cGMP in cultured human umbilical vein endothelial cells (HUVECs) was used to estimate NO production. The levels of endothelial nitric oxide synthase (eNOS) protein expression were assessed by Western blotting analyses. RESULTS: Both insulin, at physiological concentration, and lyso-PC stimulated rapid and prolonged intracellular of cGMP production, and together induced a marked synergistic response (for short-term stimulation: 1185 +/- 285.9% over control level (100%) compared with insulin and lyso-PC alone (384.8 +/- 67.4% and 357 +/- 205%, respectively; P < 0.001), for long-term stimulation: 3495 +/- 1377%, compared with insulin and lyso-PC alone (663 +/- 131% and 487 +/- 250%, P = 0.002)). Stimulated levels of cGMP accumulation were completely abrogated by NOS inhibitor, indicating NO involvement in the effects of insulin and lyso-PC. Stimulated NO synthesis was not associated with altered eNOS protein expression. Cell subfractionation studies demonstrate that insulin and lyso-PC each alone induced translocation of eNOS from the membrane to the cytosolic compartment and together caused a synergistic translocation. CONCLUSIONS: The presented data suggest that insulin and lyso-PC synergistically upregulate endothelial NO production via eNOS translocation from the membrane fraction to the cytosol. This study raises the possibility that an interplay between various factors accompanying diabetes can lead to endothelial NO overproduction or desensitization of NO-dependent responses. Appropriate rather than necessarily high levels of nitric oxide is the determinant of vascular health.

Biological Transport↗
PubMed2002

Association of calpain-10 gene with microvascular function.

AIMS/HYPOTHESIS: Genotype could influence vascular function. In some populations, Calpain 10 gene polymorphisms increase susceptibility to diabetes or insulin resistance. Alterations in microvascular function could contribute to insulin resistance. This study investigated whether polymorphisms in the Calpain-10 gene influence microvascular function. METHODS: Skin maximum microvascular hyperaemia to local heating on the dorsum of the foot (30 min at 43 degrees C) was measured by Laser Doppler Fluximetry in 37 healthy volunteers. All were normoglycaemic according to World Health Organisation criteria, normotensive and not on any medication. Four polymorphisms in the calpain-10 gene were typed: SNP-44, SNP-43, SNP-19, SNP-63. The SNP common to all the described high risk haplotypes is the G-allele at SNP-43. This intron 3 polymorphism appears to influence gene expression. Microvascular function was examined in relation to polymorphisms at this site alone as well as the effects of the known extended high risk haplotypes using the SNP's above. RESULTS: Maximum microvascular hyperaemia was increased in the 21 subjects with G/G genotypes at SNP-43 compared to the combined group of subjects ( G/ A genotype at SNP-43 ( n=12) + A/ A genotype at SNP-43 ( n=4)), and the minimum microvascular resistance was reduced 49.4 (39.6-94.2) vs 67.5 (39.1-107.3) mmHg/V, p=0.007). Haplotype analysis of the hyperaemic response revealed no significant differences between haplotypes. The two groups did not differ in terms of anthropometric measures, blood pressure, insulin resistance or glucose. CONCLUSIONS/INTERPRETATION: The polymorphism that confers susceptibility to Type II (non-insulin-dependent) diabetes mellitus in some populations is associated in United Kingdom Caucasians with enhanced microvascular function in the presence of normoglycaemia.

Adult↗
PubMed2002

Microvascular correlates of blood pressure, plasma glucose, and insulin resistance in health.

OBJECTIVES: The associations between hypertension, insulin resistance and glucose intolerance are poorly understood. Altered microvascular structure and function could contribute by increasing peripheral vascular resistance and decreasing tissue delivery of glucose. We addressed this hypothesis in a sample of healthy men. METHODS: We studied 105 healthy young men aged 23-33 years. Insulin resistance was calculated using the Homeostasis Model Assessment (HOMA). Video capillaroscopy was used on the dorsum of the finger to measure skin capillary density, and in nailfold capillaries to measure capillary blood velocity. Skin vasodilatation was measured with laser Doppler fluximetry on the forearm following heating and iontophoresis of acetylcholine. RESULTS: Higher systolic blood pressure was associated with insulin resistance (r=0.31, P<0.005), lower dermal capillary density (r= -0.25, P<0.05), and impaired maximum dermal blood flow after heating (r= -0.26, P<0.01), but not with capillary blood velocity (r=0.07) or dilator responses to acetylcholine (r=0.09). Insulin resistance did not correlate with indices of microvascular structure or function (all r<+/-0.15). However, higher fasting plasma glucose was associated with lower capillary density (r= -0.27, P<0.01), and increased capillary blood velocity (r=0.30, P<0.05). CONCLUSIONS: The association between hypertension and insulin resistance is unlikely to be explained by altered microvascular structure and function. However, changes in the microvasculature are found in subjects with early and subtle elevations in blood pressure or fasting plasma glucose in advance of their crossing conventional thresholds for the diagnosis of hypertension or diabetes mellitus.

Acetylcholine↗
PubMed2001

Skin microvascular vasodilatory capacity in offspring of two parents with Type 2 diabetes.

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)

Adult↗
PubMed2001

Impaired microvascular vasodilatory function in 3-month-old infants of low birth weight.

OBJECTIVE: Low birth weight has been linked to an increased risk of type 2 diabetes and cardiovascular disease in adult life. The fetal insulin hypothesis proposed that a genetic predisposition to insulin resistance may also influence vascular development. Therefore, impaired vascular function may be an intrinsic abnormality in low-birth weight infants that antedates clinical features of the insulin resistance syndrome. RESEARCH DESIGN AND METHODS: Two groups of 3-month-old term infants were included in the study: 17 infants of lowest quartile birth weight (LQBW) and 21 infants of highest quartile birth weight (HQBW). Three aspects of skin microvascular function were examined; response to local heating, response to acetylcholine iontophoresis, and capillary density. RESULTS: Median (interquartile ranges) birth weights of the LQBW and HQBW infants were 3,140 g (2,738-3,254) and 3,920 g (3,750-4,020), respectively. Skin maximal hyperemic response to local heating was 2.14 V (1.68-2.30) in the LQBW group vs. 2.44 V (1.96-2.90) in the HQBW group (P = 0.020), and the endothelium-dependent vasodilatory response was 1.03 V (0.62-1.32) in the LQBW group vs. 0.78 V (0.45-1.32) in the HQBW group (P = 0.297). Capillary density in the LQBW and HQBW groups were 46.3 mm(-2) (40.1-53.7) and 44.1 mm(-2) (41.7-56.0), respectively (P = 0.736). CONCLUSIONS: Skin maximal hyperemic response was lower in LQBW infants, although no reduction in capillary density or defect in endothelium-dependent vasodilatation was observed. Such a lower maximal hyperemic response in early life in LQBW subjects who are at risk for type 2 diabetes and cardiovascular disease supports the hypothesis that impaired microvascular function is an early antecedent to diabetes in later life.

Acetylcholine↗
PubMed2000

Capillaroscopy and the measurement of capillary pressure.

Capillaries play a critical role in cardiovascular function as the point of exchange of nutrients and waste products between the tissues and circulation. Studies of capillary function in man are limited by access to the vascular bed. However, skin capillaries can readily be studied by the technique of capillaroscopy which enables the investigator to assess morphology, density and blood flow velocity. It is also possible to estimate capillary pressure by direct cannulation using glass micropipettes. This review will describe the techniques used to make these assessments and will outline some of the changes that are seen in health and disease.

Age Factors↗
PubMed2000

Characteristics of laser Doppler perfusion imaging in vitro and in vivo.

Traditional laser Doppler flowmetry (LDF) employs continuous recording of perfusion at one point with time. In order to eliminate the large spatial and temporal fluctuations that occur in the microcirculation, laser Doppler perfusion imaging (LDI) integrates flow readings over a large area. This paper describes a number of experiments to identify some of the characteristics of the LDI, its relationship to flow and no-flow conditions and to compare it with LDF. We undertook experiments to establish the effect of scanner head height, avascular skin thickness and haematocrit on LDI output. We also investigated the contribution of the biological zero signal (the signal obtained from skin when flow is arrested) to the LDI output. LDI output increased with scanner height in vitro and in vivo. Increasing avascular skin thickness reduced the LDI output although linear output characteristics with flow were maintained over the flow range studied. Increasing the haematocrit resulted in a loss of linearity of output with flow at lower velocities. The biological zero signal contributes a similar proportion of the output signal in LDF and LDI. We have presented a series of experiments that will contribute to the understanding of the characteristics of laser Doppler perfusion imaging, its comparison to laser Doppler flowmetry and its relationship to flow and no flow situations. However, our experiments were restricted to one machine, and may not necessarily be applicable to other instruments.

Blood Flow Velocity↗