Hyperemic Blood Flow Response Research Articles

CVN-AD Alzheimer's mice show premature reduction in neurovascular coupling in response to spreading depression and anoxia compared to aged controls.

We compared the efficacy of neurovascular coupling and substrate supply in cerebral cortex during severe metabolic challenges in transgenic Alzheimer's [CVN‐AD] and control [C57Bl/6] mice, to evaluate the hypothesis that metabolic insufficiency is a critical component of degeneration leading to dementia. We analyzed cerebral blood flow and metabolic responses to spreading depression (induced by K+ applied to the cortex) and anoxia across aging in CVN‐AD + C57Bl/6 genotypes. In the CVN‐AD genotype progression to histological and cognitive hallmarks of dementia is a stereotyped function of age. We correlated physiology and imaging of the cortex with the blood flow responses measured with laser doppler probes. The results show that spreading depression resulted in a hyperemic blood flow response that was dramatically reduced (24% in amplitude, 70% in area) in both middle‐aged and aged CVN‐AD mice compared to C57Bl/6 age‐matched controls. However, spreading depression amplitude and conduction velocity (≈6 mm/min) did not differ among groups. Anoxia (100% N2) showed significantly decreased (by 62%) reactive blood flow and autoregulation in aged AD‐CVN mice compared to aged control animals. Significantly reduced neurovascular coupling occurred prematurely with aging in CVN‐AD mice. Abbreviated physiological hyperemia and decreased resilience to anoxia may enhance early‐onset metabolic deficiency through decreased substrate supply to the brain. Metabolic deficiency may contribute significantly to the degeneration associated with dementia as a function of aging and regions of the brain involved.

Implementing local cooling to increase skin tolerance to ischemia during normal seating in people with spinal cord injury

The purpose of this study was to investigate the effectiveness of local cooling in reducing reactive hyperemia after ischemia at the ischial tuberosities for people with spinal cord injury (SCI) during normal seating. The degree of the reactive hyperemic response is indicative of the extent of cellular stress caused by the ischemia. We hypothesized that reactive hyperemic skin blood flow (SBF) responses will be lower when local cooling is implemented by the wheelchair seat cushion. This study used a repeated measures design, and each subject underwent two conditions: normal seating with temperature control ‘on’ (cooling) and ‘off’ (non-cooling) for 30 min. Twenty-three participants with traumatic SCI were recruited. SBF and skin temperature were collected before, during and after seating. SBF signals were processed with short-time Fourier analyses to examine the underlying vascular control mechanisms, including the following (corresponding frequency bands): metabolic (0.0095–0.02 Hz), neurogenic (0.02–0.05 Hz), and myogenic (0.05–0.15 Hz) spectral densities. Our results showed that with cooling, skin temperature decreased (range −0.4 ~ −3.1 °C, p = 0.002), and reactive hyperemia parameters (normalized peak SBF and perfusion area) were reduced (p = 0.02, p = 0.033, respectively). In addition, changes in normalized peak SBF (non-cooling – cooling) was moderately correlated with changes in normalized metabolic and neurogenic spectral densities. Our findings suggested that local cooling has a positive effect on reducing the cellular stress caused by ischemia during normal seating. Metabolic and neurogenic SBF control mechanisms may play a minor role. Further exploration of the effect of temperature control on pressure injury prevention is warranted.

Comparison of maximal hyperemic myocardial blood flow response between regadenoson and adenosine: A quantitative positron emission tomography 13n-ammonia study

Comparison of maximal hyperemic myocardial blood flow response between regadenoson and adenosine: A quantitative positron emission tomography 13n-ammonia study

The Effects of AT1 Receptor Blockade on Skin Microcirculatory Blood Flow and Thromboxane A2 (TXA2) Production in Young Healthy Women

AT1 receptor activation has an important role in maintaining the vascular release of prostaglandins responsible for mediating hypoxic dilation in skeletal muscle microvessels in normotensive rats. High salt diet leads to impairment of vasodilator responses that could be restored by infusion of subpressor dose of ANG II via its interaction with AT1 receptors. In addition to AT1 receptors blockade, losartan blocks thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptor. The aim of this study was to determine the effect of one week AT1 receptor blockade by losartan in 10 healthy normotensive women (20±2 years old) on law salt diet (LSD) on post occlusive hyperemic blood flow response in skin microcirculation by Laser Doppler Flowmetry (LDF) and to determine the plasma renin activity (PRA) and plasma thromboxane A2 (TXA2) concentration. Participants maintained LSD (<40 mmol of Na/day) and took 50 mg of losartan/day for 7 days. After one week of losartan administration the post occlusive hyperemic tissue blood flow was unchanged. However, plasma PRA and TXA2 levels were significantly increased compared to pre‐losartan values. Our results indicate that although one week of AT1 receptor blockade increases the plasma TXA2 concentration and PRA, the skin microcirculatory blood flow remained unchanged, possibly due to losartan blockade of TXA2 receptors and ANG II interaction with AT2 receptors.

Impaired neurovascular coupling to ictal epileptic activity and spreading depolarization in a patient with subarachnoid hemorrhage: Possible link to blood–brain barrier dysfunction

Spreading depolarization describes a sustained neuronal and astroglial depolarization with abrupt ion translocation between intraneuronal and extracellular space leading to a cytotoxic edema and silencing of spontaneous activity. Spreading depolarizations occur abundantly in acutely injured human brain and are assumed to facilitate neuronal death through toxic effects, increased metabolic demand, and inverse neurovascular coupling. Inverse coupling describes severe hypoperfusion in response to spreading depolarization. Ictal epileptic events are less frequent than spreading depolarizations in acutely injured human brain but may also contribute to lesion progression through increased metabolic demand. Whether abnormal neurovascular coupling can occur with ictal epileptic events is unknown. Herein we describe a patient with aneurysmal subarachnoid hemorrhage in whom spreading depolarizations and ictal epileptic events were measured using subdural opto-electrodes for direct current electrocorticography and regional cerebral blood flow recordings with laser-Doppler flowmetry. Simultaneously, changes in tissue partial pressure of oxygen were recorded with an intraparenchymal oxygen sensor. Isolated spreading depolarizations and clusters of recurrent spreading depolarizations with persistent depression of spontaneous activity were recorded over several days followed by a status epilepticus. Both spreading depolarizations and ictal epileptic events where accompanied by hyperemic blood flow responses at one optode but mildly hypoemic blood flow responses at another. Of note, quantitative analysis of Gadolinium-diethylene-triamine-pentaacetic acid (DTPA)-enhanced magnetic resonance imaging detected impaired blood-brain barrier integrity in the region where the optode had recorded the mildly hypoemic flow responses. The data suggest that abnormal flow responses to spreading depolarizations and ictal epileptic events, respectively, may be associated with blood-brain barrier dysfunction.

Influence of venous emptying on the reactive hyperemic blood flow response

BackgroundPrevious research indicates that venous emptying serves as a stimulus for vasodilation in the human forearm. This suggests the importance of recognizing the potential influence of venous volume on reactive hyperemic blood flow (RHBF) following occlusion. The purpose of this study was to examine the influence of venous emptying on forearm vascular function.MethodsForearm RHBF, venous capacitance and venous outflow were examined in 35 individuals (age = 22 ± 2 years), using mercury in-Silastic strain gauge plethysmography, at rest and following five minutes of upper arm occlusion using standard procedures (Control). In addition, the same measures were obtained following five minutes of upper arm occlusion preceded by two minutes of passive arm elevation (Pre-elevation).ResultsAverage resting arterial inflow was 2.42 ± 1.11 ml·100 ml-1·min-1. RHBF and venous capacitance were significantly greater during Pre-elevation compared to Control (RHBF; Pre-elevation: 23.76 ± 5.95 ml·100 ml-1 ·min-1 vs. Control: 19.33 ± 4.50; p = 0.001), (venous capacitance; Pre-elevation: 2.74 ± 0.89 % vs. Control: 2.19 ± 0.97, p = 0.001). Venous outflow did not differ between the two conditions.ConclusionVenous emptying prior to upper arm occlusion results in a significant greater RHBF response and venous capacitance. Recognition of the influence of venous volume on RHBF is particularly important in studies focusing on arterial inflow, and also provides further evidence for the interplay between the venous and arterial system.

Influence of Vascular Function on VO2 Off-Kinetics

0174 Excess post-exercise oxygen consumption (EPOC) has been attributed to metabolic, hemodynamic, neuroendocrine, and pulmonary factors. More recently, van Beekvelt et al. (Am J Physiol Heart Circ Physiol 280: H1741, 2001) reported a marked and prolonged post exercise hyperemia following intense exercise indicating an important role of the vasculature during the recovery phase. Interestingly, few studies have examined the Influence of venous function on EPOC. PURPOSE: To examine the relationship between measures of vascular function and EPOC. METHODS: Nondominant forearm in-flow, venous capacitance and outflow were examined in 15 individuals [age = 22±2.25y]. Forearm blood inflow was estimated at rest and following 5 min of upper arm occlusion (using a 240 mmHg occluding pressure). Forearm venous capacitance and outflow were obtained following 5 min of upper arm venous occlusion pressure at 7 mmHg below diastolic blood pressure. Participants underwent a symptom-limited upright incremental cycle ergometer test with gas exchange analysis and a 10-minute constant work rate protocol at 60% of VO2R. Recovery measurements were obtained with the participants seated on the ergometer for 10 minutes. RESULTS: Average VO2peak was 33.92±8.61 ml/kg/min (Range: 18.70 to 46.10 ml/kg/min). Recovery half-time (T1/2) for the submax test was 16.84±2.44 sec. Resting in-flow, reactive hyperemic flow response and venous outflow were 2.71±1.15, 19.15±4.25 and 37.07±10.86 ml/100ml/min, respectively. Venous capacitance was 2.11±0.82%. Bivariate correlations revealed significant associations between T1/2 and reactive hyperemic response (r = −0.68, p = 0.01) and T1/2 and venous outflow (r = −0.60, p = 0.02). Moreover, venous outflow responses were significantly correlated with reactive hyperemic responses (r = 0.54, p = 0.001) CONCLUSIONS: Reactive hyperemic blood flow response and venous outflow were significantly associated with recovery T1/2 following a 10-minute constant submaximal work rate protocol. These findings suggest an important role of both the arterial and venous circulations on EPOC.

The effects of raloxifene and simvastatin on plasma lipids and endothelium.

Raloxifene is a selective estrogen receptor modulator and an attractive alternative to estrogen replacement as it obviates the need for a progestin and does not increase C-reactive protein levels. We compared the effects of simvastatin and raloxifene treatments on the lipid profile, the levels of adhesion molecules and the endothelium dependent and independent vasoreactivity. We treated 12 postmenopausal women with hypercholesterolemia and coronary artery disease with raloxifene 60 mg/day and simvastatin 20 mg/day in a randomized, double-blind, crossover study. Each treatment period was 8 weeks long with a 4-week washout interval. Plasma lipids and cellular adhesion molecules were evaluated and peripheral blood flow studies with venous occlusion plethysmography were performed. Both simvastatin and raloxifene significantly reduced total [33% (27-40), 12% (0-24)] and LDL [44% (36-52), 16% (0-33)] cholesterol compared to baseline values (p < 0.05) but simvastatin was more effective than raloxifene (p < 0.005). None of the treatments had any significant effect on HDL cholesterol and triglyceride levels. Only raloxifene significantly reduced Lp(a) [18% (1-36)] and ICAM-1 [17% (8-25)] and VCAM-1 [24% (15-33)] plasma levels compared to baseline (p = 0.019, p < 0.0001 and p = 0.003, respectively). Hyperemic blood flow response on raloxifene was significantly higher compared to baseline [52% (0-105)], (p < 0.05), whereas no significant change was noted on simvastatin. Endothelium independent blood flow induced by nitroglycerine was not influenced by either active treatment. Raloxifene administration is associated with lower ICAM-1, VCAM-1 and Lp(a) plasma levels and enhanced endothelium dependent dilation compared to simvastatin although simvastatin is more powerful in total and LDL cholesterol reduction.

Impaired vasodilator responses in obstructive sleep apnea are improved with continuous positive airway pressure therapy.

Obstructive sleep apnea causes cardiovascular morbidity and premature death. Potential links between sleep apnea and cardiovascular complications are chronically elevated activity of the sympathetic nervous system and abnormal vascular function. To explore vascular function, we determined the reactive hyperemic blood flow (RHBF) responses to 10 minutes of forearm arterial occlusion (plethysmography), blood pressure, and muscle sympathetic nerve activity (MSNA, microneurography) in eight patients with sleep apnea and in nine nonapneic control subjects. Peak RHBF and vascular conductance were markedly attenuated in sleep apnea compared with control subjects (p < 0.05). Seven sleep apnea patients were retested after at least two weeks of continuous positive airway pressure (CPAP) therapy. MSNA decreased after CPAP therapy (p < 0.05, n = 6), whereas blood pressure did not change. After CPAP therapy, peak RHBF and vascular conductance were increased compared with before treatment (p < 0.05; n = 7). Thus, vascular function is abnormal in sleep apnea and is improved by CPAP therapy. Furthermore, effective CPAP therapy decreases sympathetic activity in sleep apnea. Thus, sympathoexcitation and abnormal vascular function in patients with sleep apnea appear to be linked to the repetitive nocturnal apneic events.

Dose-dependent vasodilating effects of insulin on adenosine-stimulated myocardial blood flow.

In the peripheral vasculature, insulin induces time- and dose-dependent vasodilation. We have recently demonstrated that insulin potentiates adenosine-stimulated myocardial blood flow. However, it is unknown whether insulin's effects on the coronary vasculature are dose dependent. In this study, we quantitated myocardial blood flow and adenosine-stimulated coronary flow (140 microg.kg(-1).min(-1) for 5 min) in 10 healthy men (age, 32 +/- 6 years; BMI, 24.1 +/- 1.8 kg/m(2)) using positron emission tomography and (15)O-labeled water. Hyperemic myocardial blood flow was measured in the basal state, during euglycemic physiological hyperinsulinemia (serum insulin approximately 65 mU/l) and during supraphysiological hyperinsulinemia (serum insulin approximately 460 mU/l). Basal myocardial blood flow was 0.84 +/- 0.17 ml.g(-1).min(-1). Physiological hyperinsulinemia increased the adenosine-stimulated flow by 20% (from 3.92 +/- 1.17 to 4.72 +/- 0.96 ml.g(- 1).min(-1); P < 0.05). Supraphysiological hyperinsulinemia further enhanced the adenosine-stimulated flow by 19% (to 5.61 +/- 1.03 ml.g(-1).min(-1); P < 0.05). These effects were not explained by changes in systemic hemodynamics, since coronary resistance decreased during each insulin infusion (P < 0.05). In addition, hyperemic myocardial blood flow responses during insulin stimulation were positively correlated with whole-body glucose uptake. The results demonstrate that insulin is able to enhance hyperemic myocardial blood flow in a dose-dependent manner in healthy subjects. These effects might contribute to the known beneficial dose-dependent effects of insulin on myocardial ischemia.

Relevance and methods for determining coronary flow reserve

The assessment of coronary flow reserve, defined as the ratio of hyperemic to resting coronary blood flow, allows a more functional analysis of the coronary vasculature in addition to coronary angiography. Three different kinds of cardiac catherization procedures for measurement of coronary flow reserve will be reviewed with respect to reliability, feasibility and clinical significance in the diagnosis and treatment of diseases of coronary conductance and resistive vessels: first, from the techniques utilizing selective catherization of coronary sinus, the thermodilution and the oxymetry have to be considered qualitatively rather than quantitatively because of a large variance and an underestimation of hyperemic blood flow responses. The gas chromatographic argon method provides a more quantitative rationale for the selective measurement of resting and hyperemic coronary flow, and thus to more exact differentiation between a reduced hyperemic vs an increased resting flow as a major cause of a reduced flow reserve. Furthermore, because of a reliable reproducibility this approach allows to proceed follow up studies to assess impact of therapeutic interventions on coronary flow reserve in individual patients. Second, angiographic methods utilize either densitometry or time-to-arrival measurements of defined boluses of contrast medium. The utility of the TIMI-frame count and of densitometric algorithms will be discussed. These methods offer the advantage of being rather easy to handle and to be performed within routine coronary angiography. However, they can be applied to a only rather small group of patients because of methodological limitations in patients with multivessel disease, with disturbed left ventricular function and with irregular heart rate. Third, this group comprises methods in which devices have to be advanced into coronary circulation such as pressure or doppler guide wires, which allows selective assessment of regional coronary flow and reserve. Currently evaluated approaches to assess significance of coronary stenosis will be discussed. In conclusion, currently different methods for the assessment of coronary flow reserve are available in cardiac catherization laboratories and each of these methods provides specific advantages and disadvantages, which have to be considered to select the appropriate approach for the diagnosis of functional disturbances of the coronary conductance and resistance vessels. The obtained functional data on coronary circulation should always be interpreted only in context with myocardial function and clinical symptoms of the individual patient.

Head-down-tilt bed rest alters forearm vasodilator and vasoconstrictor responses.

To test the hypothesis that head-down-tilt bed rest (HDBR) for 14 days alters vascular reactivity to vasodilatory and vasoconstrictor stimuli, the reactive hyperemic forearm blood flow (RHBF, measured by venous occlusion plethysmography) and mean arterial pressure (MAP, measured by Finapres) responses after 10 min of circulatory arrest were measured in a control trial (n = 20) and when sympathetic discharge was increased by a cold pressor test (RHBF + cold pressor test; n = 10). Vascular conductance (VC) was calculated (VC = RHBF/MAP). In the control trial, peak RHBF at 5 s after circulatory arrest (34.1 +/- 2.5 vs. 48.9 +/- 4.3 ml . 100 ml-1 . min-1) and VC (0.34 +/- 0.02 vs. 0.53 +/- 0.05 ml . 100 ml-1 . min-1 . mmHg-1) were reduced in the post- compared with the pre-HDBR tests (P < 0. 05). Total excess RHBF over 3 min was diminished in the post- compared with the pre-HDBR trial (84.8 vs. 117 ml/100 ml, P < 0.002). The ability of the cold pressor test to lower forearm blood flow was less in the post- than in the pre-HDBR test (P < 0.05), despite similar increases in MAP. These data suggest that regulation of vascular dilation and the interaction between dilatory and constrictor influences were altered with bed rest.

Vasodilator effects of estrogen are not diminished by androgen in postmenopausal women

Objective: To compare the effects of estrogen with estrogen-androgen treatment on vaginal blood flow velocity and fingertip postocclusive hyperemic blood flow response. Design: Prospective, randomized, parallel, double-blind study. Setting: Healthy human volunteers in an academic research environment. Patient(s): Postmenopausal women receiving estrogen replacement therapy for at least 12 months and treated with placebo before this investigation. Intervention(s): Esterified estrogens or esterified estrogen + methyltestosterone were administered orally; laser Doppler velocimetry was used to determine vaginal and fingertip blood flow responses at baseline and after 4 and 8 weeks of daily drug administration. Main Outcome Measure(s): Fingertip postocclusive area under curve (AUC); vaginal blood flow velocities. Result(s): The AUC for postocclusive fingertip blood flow and vaginal blood flow increased to a greater extent in the estrogen-androgen group, but changes were not statistically significant between groups. Conclusion(s): Estrogen-androgen treatment does not diminish the vasodilator effects of estrogen treatment in postmenopausal women.

Diabetes impairs sciatic nerve hyperemia induced by surgical trauma: implications for diabetic neuropathy.

The most widely used methods to assess nerve blood flow in diabetics rats are hydrogen clearance polarography and laser Doppler flowmetry, techniques requiring surgical exposure of the nerve. In these experiments, we examined the hypothesis that the trauma of surgical exposure introduces an important and hitherto largely unrecognized variable that could account for discordant reports on nerve blood flow changes induced by diabetes. We used the noninvasive (for sciatic nerve) reference sample microsphere method to quantify sciatic nerve blood flow in unexposed va. surgically exposed nerves in rats with streptozotocin-induced diabetes (at different temperatures and after curarization) and in unexposed vs. surgically exposed nerves in galactose-fed rats. Baseline resting blood flow in unexposed nerves in both animal models of diabetes was either normal or increased (but was decreased in diabetic rats given d-tubocurarine). Furthermore, the normal brisk hyperemic nerve blood flow response to the minimal trauma associated with surgical exposure of the nerve was markedly impaired in diabetic and in galactose-fed rats. Normalization of the blood flow response to trauma in galactose-fed rats by an aldose reductase inhibitor suggests that the impairment is linked to increased polyol pathway metabolism. These findings 1) confirm our previous findings that sciatic nerve blood flow in diabetic rats is increased or unchanged in unexposed nerves, while also confirming reports that in surgically exposed nerves blood flow is higher in control than in diabetic rats, and 2) indicate that blood flows in surgically exposed nerves are largely a measure of vascular responses to injury rather than (patho)physiological blood flow in undisturbed nerves.

Contributions of vascular tone and structure to elastic properties of a medium-sized artery.

Isobaric compliance and distensibility of the radial artery were recently reported to be normal or slightly increased in untreated hypertensive patients. However, these findings provide no information on the intrinsic mechanical properties of the wall material. To address this question, we determined intima-media wall thickness, wall-to-lumen ratio, and incremental elastic modulus in the radial artery of 25 untreated hypertensive patients with blood pressure of 150 +/- 14/103 +/- 6 mm Hg (mean +/- SD) and 25 matched control subjects with blood pressure of 118 +/- 9/79 +/- 6 mm Hg. High-resolution echotracking for assessment of internal diameter and intima-media wall thickness was combined with measurements of blood flow velocity by Doppler and blood pressure by photoplethysmography. In addition, isobaric compliance and distensibility and incremental elastic modulus were measured at peak diameter during reactive hyperemia after a 5-minute brachial occlusion. No significant difference was found between the two groups for isobaric compliance or distensibility at baseline or during hyperemia. However, incremental elastic modulus at 100 mg Hg tended to be lower in hypertensive patients than control subjects (1.9 +/- 1.1 versus 2.5 +/- 1.2 mm Hg x 10(4), P = .1) in resting conditions. Hypertensive patients and control subjects had similar internal diameters (2.47 +/- 0.32 versus 2.41 +/- 0.35 microm), but intima-media wall thickness and wall-to-lumen ratio were significantly increased in hypertensive patients compared with control subjects (0.268 +/- 0.032 versus 0.236 +/- 0.025 mm -P < or = .01- and 0.220 +/- 0.038 versus 0.195 +/- 0.028 -P < or = .05-, respectively). Peak hyperemic blood flow response (hypertensive patients versus control subjects: 349% versus 360% increase from baseline) and reactive hyperemic dilation (7.2% versus 7.9%) were similar in amplitude and duration in the two groups. These results suggest that wall thickening is an adaptive process that reduces wall tension in hypertensive patients while preserving a normal mechanical behavior of the radial artery. This is most likely accomplished by modification of the incremental elastic modulus of wall components rather than by a change in vascular tone.

Impaired cholinergic peripheral vasodilation and its relationship to hyperemic calf blood flow response and exercise intolerance in patients with chronic heart failure

This study examined the peripheral endothelium-dependent vasodilatory response to acetylcholine and the endothelium-independent vasodilatory response to nitroprusside in 19 patients with chronic heart failure and eight controls. These peripheral blood flow responses were compared with hyperemic calf blood flow changes after maximum leg exercise and 5-min femoral occlusion. The peripheral blood flow response to forearm intra-arterial infusion of acetylcholine and sodium nitroprusside, and reactive hyperemic calf blood flow changes were measured by plethysmography. All peripheral blood flow responses were significantly reduced in patients with chronic heart failure ( P < 0.05). Reduction of acetylcholine-mediated changes in peripheral blood flow was correlated with exercise-induced calf blood flow response ( r = 0.51, P < 0.05), but not with occlusion-induced calf blood flow response ( r = 0.02, NS). Sodium nitroprusside-mediated changes were not correlated with any reactive hyperemic blood flow responses (exercise: r = 0.27, NS; occlusion: r = 0.11, NS). When the patients were divided into two subgroups based on the median exercise-induced calf blood flow change, the subgroup with the lower calf blood flow response showed a reduction in exercise capacity (anaerobic threshold: 11.8 ± 0.6 vs. 14.6 ± 1.0 ml/kg/min; P < 0.05). These findings suggest that endothelial dysfunction is related to a decrease in exercise-induced skeletal muscle blood flow and exercise capacity in patients with chronic heart failure.

Reactive hyperemia in term neonates and adults—A laser Doppler fluxmetry study of skin microcirculation

The reactivities of neonatal and adult microcirculation have been studied and compared. The cutaneous reactive hyperemia after 1 and 4 min of arterial occlusion (AO) was measured with a laser-Doppler fluxmeter in 21 healthy neonates and 10 adults. Local skin temperature, mean arterial blood pressure (MAP), and skin prick hematocrit were also determined at the same time. The magnitude of neonatal reactive hyperemia was approximately one-third that of the adult response regardless of the duration of AO. In both groups, with age-specific regressions, the hyperemic blood flow response after 4 min of AO developed more slowly in subjects with low MAP and was of low magnitude in subjects with high hematocrit values. In response to a prolongation of AO, from 1 to 4 min, the magnitude and duration of hyperemia increased significantly and similarly in both neonates and adults. We conclude that compared to adults neonates have a less pronounced ability to increase skin microcirculation in response to local ischemia. The normally low blood pressure and high hematocrit in newborn infants contribute further to this conclusion.

Assessment of human muscle blood perfusion with single-fiber laser Doppler flowmetry

Laser Doppler flowmetry (LDF) is a technique for continuous monitoring of microvascular perfusion. Commercially available flowmeters in general are equipped with probes constructed for performing measurements on superficial tissue surfaces, but small (∅ = 0.45 mm) metallic needle probes for in-tissue measurements are also available. In this study a flexible single-fiber LDF probe with a total diameter of 0.5 mm has been inserted into human tibial muscle and used for assessment of local muscle blood flow. Local muscle perfusion shows a considerable spatial variation. If the probe position is not changed between consecutive measurements, reproducible curve parameters are obtained. Vasomotion was not observed in any measurement. The hyperemic blood flow response was recorded after tourniquet deflation. Time to reach peak magnitude as well as duration of the hyperemic blood flow response was increased significantly ( P < 0.01) with prolonged occlusion time. The response was found in both skin and muscle blood flow recordings. Increasing occlusion time from 3 to 5 min did not significantly enhance the results. Comparison of skin and muscle responses with respect to time to reach peak magnitude showed a significant difference ( P < 0.02) for the 1-min occlusion. A significant increase ( P < 0.01 and 0.05 for muscle and skin, respectively) in peak flux was seen in muscle and skin when tourniquet occlusion was increased from 1 to 3 min. Further increases in occlusion time did not produce significant increases in peak flux. The technique is easy to use, and may be of value in studies of disturbances of perfusion in muscle and possibly in parenchymatous organs (transplantation surgery) and central nervous system circulation.

Physiologic and structural indices of vascular function in paraplegics

In an effort to determine whether chronic physical forearm activity would increase both structural and physiologic indices of peripheral forearm vasodilation, we studied a group (N = 7) of individuals chronically performing high levels of arm work, young wheelchair-confined paraplegics, and compared them with ten young, able bodied control subjects. The index of vasodilator capacity was the flow response following the release of 10 min of arterial occlusion, the peak reactive hyperemic blood flow response (RHBF). The index of a structural effect of training on the vasculature was the brachial artery diameter (cm) derived by simultaneous measurement of velocity and forearm blood flow (area = flow.forearm volume.velocity-1). Vascular function differed significantly between the groups, with a greater RHBF (paraplegics, 53.8 +/- 3.7; controls, 38.2 +/- 1.5 ml.min-1.100 ml-1; P less than 0.05) and a larger brachial artery diameter at rest (paraplegics, 0.4 +/- 0.01 vs controls, 0.3 +/- 0.02 cm; P less than 0.05) in the paraplegics. We conclude that chronic upper extremity activity leads to an enhanced capability to vasodilate resistance vessels acutely and to a structural dilation of large conductance vessels.

Left subclavian flap aortoplasty for coarctation of the aorta: Effects on forearm vascular function and growth

This study evaluated vascular function and growth of the forearm in nine children (mean age 9.2 years) who had undergone left subclavian flap aortoplasty for the infantile type of coarctation of the aorta many years (mean 9.0) earlier. Variables used to investigate bilateral forearm vascular function included forearm blood flow and resistance measured by strain gauge plethysmography under rest conditions, in response to 30 s of static handgrip exercise at 40% maximal voluntary contraction and in response to 10 min of forearm arterial occlusion (that is, the reactive hyperemic blood flow response). Forearm growth was ascertained by measuring right and left forearm volumes, lengths, circumferences and skinfold thicknesses.Mean arterial pressure at rest in the right and left arms differed by 9% (right 78.2 ± 2.1, left 71.0 ± 2.7 mm Hg; p < 0.05). Forearm blood flow, however, was not significantly different between the surgically altered left arm and the normal right arm under any of the study conditions. Likewise, forearm vascular resistance was not statistically different under any conditions, although the left arm tended to have a lower resistance at rest (right 23.5 ± 3.2, left 18.7 ± 2.0 mm Hg·min·100 ml/ml; p = 0.057). Left forearm anthropometric measurements showed a 9% reduction in volume and a 3 % reduction in circumference and length. In addition, skinfold thickness tended to be larger on the left arm, suggesting that this limb had a smaller muscle mass.In conclusion, early repair with a subclavian flap does not impair vascular function in the altered limb and is associated with only minor reductions in forearm growth variables. Hence, left subclavian flap aortoplasty appears to be a safe and effective procedure for repair of coarctation of the aorta.