Changes In Cutaneous Blood Flow Research Articles

The effects of lumbar spine high velocity low amplitude thrust (HVLAT) manipulation on upper limb cutaneous blood supply

Introduction: Spinal manipulation is commonly employed by osteopaths to correct somatic and visceral dysfunction. Much research has concentrated on the somatovisceral effects of spinal manipulation, with many studies demonstrating sympathoexcitation/inhibition following spinal manipulation. The mechanisms behind the neurophysiological effects of spinal manipulation still remains poorly understood. No published study to date has investigated the effect of spinal manipulation on the sympathetic innervation of regions of the body with no known neural connections. Previous studies that used cutaneous blood flow (CBF) as measures of sympathetic activity have not considered the contribution that breathing or postural perturbation have on study outcomes. The aim of this study was to investigate the effect a unilateral lumbosacral HVLAT on CBF to the upper limb, and to estimate the contribution that breathing or postural perturbation may have on the study outcome. Design: The study was a strictly controlled, carry-over design on a cohort of twenty-eight asymptomatic, male osteopathic students of similar age and body mass index. Methods: CBF to the distal, palmar surface of the both forearms was measured using Laser Doppler Flowmetry (LDF). After 10minute acclimatising period, each subject acted as their own control whilst an initial 5-minute baselinemeasurement of CBFwas established. This was followed directly by the first control, postural perturbation for the HVLAT in right rotation, and a further 5-minute ‘post-control 1’ recording phase. This was then followed directly by the second control, postural perturbation for the HVLAT in right rotation and breathing relaxation, and a further 5-minute ‘post-control 2’ recording phase. The experimental intervention (HVLAT to L5-S1) was then applied, and followed by a further 5-minute ‘post-experimental intervention’ recording of CBF. Results: All raw data for the different interventions were converted into percentiles relative to the baseline reading so the data could be analysed by a one way ANOVA and post-hoc Tukey’s tests. The results indicated that there was a significant change in CBF from baseline level to the experimental intervention (p 0.05). However, the results illustrate the contribution that postural perturbation and especially breathing have on the outcome of this study which was calculated to be 4.2% and 7.5%, and 48% and 65%, respectively for the contralateral and ipsilateral upper limb respectively. Conclusion: This study provides preliminary evidence that a unilaterally applied HVLAT to the right L5/S1 lumbar zygo-apophyseal joint results in side-specific peripheral changes in the upper limbs. However, there is also preliminary evidence in this study that the breathing relaxation technique used in HVLAT’s contributes to the magnitude of the outcome as assessed by changes in CBF. It is concluded that the breathing effect should be included in interpreting past studies and in the design of future studies.

Responses evoked in single sympathetic nerve fibres of the rat tail artery by systemic hypoxia are dependent on core temperature

No direct evidence exists of the changes evoked by systemic hypoxia in sympathetic nerves to the rat cutaneous circulation, and of the concomitant changes in cutaneous blood flow. Here we investigated responses evoked by two levels of systemic hypoxia (12% and 8% inspired O(2)) in single sympathetic units supplying tail caudal ventral artery (CVA) in spontaneously breathing anaesthetized rats, whilst simultaneously recording tail blood flow and vascular resistance (TVR) from the CVA, under conditions of modest hypothermia and hyperthermia. During modest hypothermia and normoxia, TVR was high and CVA unit activity was present, with marked respiratory modulation and a rhythmictiy (T-rhythm) that was often independent of respiration. Hypoxia evoked a graded fall in TVR indicating vasodilatation, but there were no consistent changes in CVA unit firing rate or T-rhythm frequency, although respiratory modulation increased. By contrast, during hyperthermia, TVR was low and CVA unit activity was absent. Systemic hypoxia evoked graded increases in TVR, indicating vasoconstriction, and in 8% O(2) there was recommencement of firing in some CVA units, at low discharge rate, with respiratory modulation but no T-rhythm. These results indicate that the changes evoked by systemic hypoxia in TVR and sympathetic nerve activity to CVA are dependent on core temperature. During modest hypothermia, hypoxia-induced cutaneous vasodilatation in the tail is independent of sympathetic activity, whereas during hyperthermia, when sympathetic activity is 'switched off', severe hypoxia initiates respiratory-related low level activity, causing cutaneous vasoconstriction.

Botulinum Toxin type A reduces capsaicin-evoked pain and neurogenic vasodilatation in human skin

The effect of Botulinum Toxin type A (BoNT/A) on pain and neurogenic vasodilatation induced by application to the human skin of thermal stimuli and capsaicin was evaluated in a double blind study. A capsaicin cream (0.5 ml of a 0.075%) was applied to the skin of both forearms of eighteen subjects randomly pretreated with either BoNT/A (Botox ®) or 0.9% saline (NS). Capsaicin was applied to a skin area either inside (protocol A) or adjacent to the BoNT/A treated area (protocol B). Pre-treatment with BoNT/A did not affect thermal-specific and thermal-pain thresholds (by quantitative sensory testing). However, capsaicin-induced pain sensation (by a visual analogue scale), flare area (by acetate sheet) and changes in cutaneous blood flow (CBF, by laser Doppler flowmetry) were reduced when capsaicin was administered inside (protocol A) the BoNT/A treated area. In Protocol B, capsaicin-induced pain was unchanged, and capsaicin-induced flare/increase in CBF were reduced only in the area treated with BoNT/A, but not in the BoNT/A untreated area. Results indicate that (i) BoNT/A reduces capsaicin-induced pain and neurogenic vasodilatation without affecting the transmission of thermal and thermal-pain modalities; (ii) reduction in capsaicin-induced pain occurs only if capsaicin is administered into the BoNT/A pretreated area; (iii) reduction in neurogenic vasodilatation by BoNT/A does not contribute to its analgesic action. BoNT/A could be tested for the treatment of conditions characterised by neurogenic inflammation and inflammatory pain.

Role of the Na+-K+-2Cl− Cotransporter in the Development of Capsaicin-Induced Neurogenic Inflammation

Recent behavioral and electrophysiological studies have attributed an important role to dorsal root reflexes (DRRs) in the initiation and development of neurogenic inflammation produced by intradermal capsaicin (CAP). The DRRs can occur in peptidergic fibers, resulting in peripheral release of neuromediators that produce vasodilation, plasma extravasation and subsequently hyperalgesia and allodynia. In this study, we have evaluated the effect of spinal administration of bumetanide (a blocker of the Na+-K+-2Cl- cotransporter, NKCC) on DRR activity, changes in cutaneous blood flow (vasodilation), hindpaw edema, mechanical allodynia, and hyperalgesia induced by intradermal injection of 1% CAP in Sprague-Dawley rats. Vasodilation was monitored using laser Doppler flowmetry, neurogenic edema was evaluated by measurements of hindpaw volume, and secondary mechanical allodynia and hyperalesia were tested using von Frey filaments (10 and 200 mN) applied to the plantar surface of the paw. Changes in the blood flow were blocked significantly by intrathecal bumetanide at 10 and 100 microM in both pre- and posttreatment studies. Spinal bumetanide at 10 and 100 microM blocked neurogenic edema when it was administered before CAP injection, but only bumetanide at 100 microM administered after CAP injection reduced the paw edema significantly. Furthermore, the administration of bumetanide onto the spinal cord reduced the increment in DRR activity produced by CAP. Finally, both secondary mechanical allodynia and hyperalesia were reduced by bumetanide at 1, 10, and 100 microM. Taken together these results suggest that NKCC is involved in the increases in DRR activity, neurogenic inflammation and hyperalgesia and allodynia induced by intradermal CAP.

A new method to model change in cutaneous blood flow due to mechanical skin irritation: Part II: Parameter identification procedure

Mechanical skin irritation, for example a light scratch with a needle, induces histamine and neuropeptide release on the line of stroke and in the surrounding tissue. Both histamine and neuropeptides are vasodilators. They cause vasodilation by changing the contraction state of the vascular smooth muscles and hence vessel compliance. Smooth muscle contraction state is very difficult to measure in vivo. For that reason we propose in this article an identification procedure to establish an irritation law. The law gives change in vessel compliance as a function of space, time and the intensity of the stroke. We have showed that vessel compliance increases immediately after the stroke not only on the line of stroke, but also in the surrounding tissue. Then, after a short delay, vessel compliance starts decreasing in the surrounding tissue, whereas vessel compliance on the line of stroke keeps increasing. Hence, blood is transported from the surrounding tissue to the line of stroke. In this way, higher blood volume on the line of stroke can be obtained than by only changing vessel compliance locally.

A new method to model change in cutaneous blood flow due to mechanical skin irritation: Part I: Comparison between experimental and numerical data

Mechanical skin irritation creates vasodilation. Vasodilation of vascular networks induces increase in blood volume and blood velocity. Both can be measured by Laser Doppler Velocimetry. We propose in this article a method permitting comparison between experimental and numerical results. Experimental data was obtained by Laser Doppler Velocimetry. Numerical results were obtained by a continuous model of the vascular network. The model consists of three layers. First and last layer are described by anisotropic and heterogeneous porous media. They represent the irrigation and the drainage of the vascular system. The intermediate layer is described by a lumped parameter model that does not permit horizontal fluxes. All vessels are compliant. The permeabilities depend on the volumes of the specific layer. Skin irritation is modeled by a change in compliance of small arterial blood vessels. The comparison between experimental and numerical data is based on the model proposed by Bonner and Nossal [1981. Model for laser Doppler measurements of blood flow. Appl. Opt. 20, 2097–2107]. The model describes the Doppler frequency spectrum S ( ω ) as a function of the optical phenomena creating the frequency shift. The comparison is based on the model of the first moment M 1 ∼ ∫ ω S ( ω ) d ω . The variables of the first moment can be determined by results of the numerical model. We have shown, that it exists a linear relation between the change in compliance and the following increase in first moment. Using this linear relation experimental and numerical data can be compared.

Involvement of peripheral neuropeptide y receptors in sympathetic modulation of acute cutaneous flare induced by intradermal capsaicin

In a recent study, we have demonstrated that the dorsal root reflex (DRR)-mediated acute cutaneous neurogenic inflammation following intradermal injection of capsaicin (CAP) is sympathetically dependent and subject to modulation by peripheral α 1-adrenoceptors. Postganglionic sympathetic neurons contain not only adrenergic neurotransmitters, but also non-adrenergic substances, including neuropeptide Y (NPY). In this study, we examined if peripheral NPY receptors participate in the flare following CAP injection. Different NPY receptor subtypes were studied by using relatively specific agonists and antagonists for the Y 1 and Y 2 subtypes. Changes in cutaneous blood flow on the plantar surface of the foot were measured using a laser Doppler flowmeter. Following CAP injection, cutaneous flare spread more than 20 mm away from the site of CAP injection. Removal of the postganglionic sympathetic nerves by surgical sympathectomy reduced dramatically the CAP-evoked flare. If the foot of sympathectomized rats was pretreated with either NPY or Y 2 receptor agonists by intra-arterial injection, the spread of flare induced by CAP injection could be restored and prolonged. However, if the spinal cord was pretreated with a GABA A receptor antagonist, bicuculline, to prevent DRRs, NPY or an Y 2 receptor agonist no longer restored the CAP-evoked flare. A Y 1 receptor agonist did not affect the CAP-evoked flare in sympathectomized rats. In sympathetically intact rats, blockade of either peripheral NPY or Y 2 receptors with [ d-Trp 32]-NPY or BIIE0246 markedly reduced the flare induced by CAP injection, whereas blockade of peripheral Y 1 receptors by BIBP3226 did not obviously affect the flare. It is suggested that NPY is co-released with NE from the postganglionic sympathetic terminals to activate NPY Y 2 and α 1 receptors following CAP injection. Both substances are involved, at least in part, in modulation of the responses of CAP sensitive afferents thereby affecting their ability to evoke the release of inflammatory agents from primary afferents.

Sympathetic modulation of acute cutaneous flare induced by intradermal injection of capsaicin in anesthetized rats.

Much of the acute cutaneous neurogenic inflammation after intradermal injection of capsaicin (CAP) in rats is mediated by dorsal root reflexes (DRRs), which cause the release of inflammatory agents from primary afferent terminals. Sympathetic efferents modulate neurogenic inflammation by interaction with primary afferent terminals. In this study, we examined if DRR-mediated flare after CAP injection is subject to sympathetic modulation. Changes in cutaneous blood flow on the plantar surface of the foot were measured using a laser Doppler flow meter. After CAP injection, cutaneous flare spread more than 20 mm away from the site of CAP injection. However, this CAP-induced flare was significantly reduced after surgical sympathectomy. Decentralization of postganglionic neurons did not affect the flare induced by CAP injection. If the foot of sympathectomized rats was pretreated with an alpha(1)-adrenoceptor agonist (phenylephrine) by intra-arterial injection, the spread of flare induced by CAP injection could be restored. However, if the spinal cord was pretreated with a GABA(A) receptor antagonist, bicuculline, to prevent DRRs, phenylephrine no longer restored the CAP-evoked flare. An alpha(2)-adrenoceptor agonist (UK14,304) did not affect the CAP-evoked flare in sympathectomized rats. In sympathetically intact rats, blockade of peripheral alpha(1)-adrenoceptors with terazosin profoundly reduced the flare induced by CAP injection, whereas blockade of peripheral alpha(2)-adrenoceptors by yohimbine did not obviously affect the flare. Therefore the pathogenesis of acute neurogenic inflammation in the intradermal CAP injection model depends in part on intact sympathetic efferents and alpha(1)-adrenoceptors. Peripheral alpha(1)-adrenoceptors thus modulate the ability of capsaicin sensitive afferents to evoke the release of inflammatory agents from primary afferents by DRRs.

Lower brainstem pathways regulating sympathetically mediated changes in cutaneous blood flow.

1. When the individual is alerted by painful or salient stimuli, there is a vigorous sympathetically mediated constriction of the cutaneous vascular bed. We investigated central pathways mediating this response using chronically implanted Doppler ultrasonic probes to measure cutaneous blood flow in the rabbit ear pinna and in the rat tail. 2. Blockade of neuronal function in the amygdala prevents cutaneous vasoconstriction elicited by salient stimuli, but does not prevent the response to painful stimuli. Blockade of neuronal function in raphe magnus/pallidus and the parapyramidal region in anesthetized rabbits prevents cutaneous vasoconstriction elicited by painful stimuli. A similar region of the medullary raphe regulates tail artery vasoconstriction in rats. Inhibition of neuronal function in this region reverses cutaneous vasoconstriction induced by cooling the animal. 3. Bulbospinal presympathetic neurons in the rostral medullary raphe region appear to regulate cutaneous blood flow responses occurring as part of the response to painful or dangerous environmental events and as part of the regulation of body temperature.

The niacin skin flush abnormality in schizophrenia: a quantitative dose–response study

Niacin dilates cutaneous blood vessels, resulting in a pronounced skin flush in most people. The flush response to niacin is attenuated in schizophrenia, but the quantification and physiological mechanism of this abnormality have not been described in detail. It is not clear whether the mechanism involves changes in the pharmacological sensitivity to niacin, or whether there is a reduced ability of the vasculature to dilate adequately in subjects with schizophrenia. We address this question in the present study by characterizing the dose–response relationship between topically applied α-methylnicotinate (AMN) and cutaneous blood flow changes, which were quantified by laser Doppler flowmetry. The dose–response curve was shifted to the right in subjects with schizophrenia. The EC 50 value of AMN was significantly increased in the schizophrenia group (mean: 1.66 mM; 95% confidence interval: 1.04–2.65 mM) as compared to the control group (mean: 0.38 mM; 95% confidence interval: 0.263–0.547 mM). The blood flow responses to higher AMN doses were lower in the schizophrenics; however, there was no statistically significant difference in the extrapolated maximal blood flow response value ( F max) between the two groups. The results suggest that the skin flush abnormality in schizophrenia primarily reflects reduced pharmacological sensitivity to niacin rather than an inadequate cutaneous vasodilatory response to the stimulus. Since vasodilatation in response to niacin requires the release of prostaglandins, the data from this study suggest that schizophrenia is associated with abnormalities in enzymes, receptors, or signal transduction mechanisms that affect the synthesis, release, or response to vasodilatory prostaglandins.

Potential role of medullary raphe-spinal neurons in cutaneous vasoconstriction: an in vivo electrophysiological study.

In rabbits, raphe magnus/pallidus neurons form a link in the CNS pathway regulating changes in cutaneous blood flow elicited by nociceptive stimulation and activation of the central nucleus of the amygdala. To characterize relevant raphe-spinal neurons, we performed extracellular recordings from the rostral medullary raphe nuclei in anesthetized, paralyzed, mechanically ventilated rabbits. All studied neurons were antidromically activated from the dorsolateral funiculus of the spinal cord (C(8)-T(2)). Of 129 studied neurons, 40% were silent. The remaining neurons discharged spontaneously at 0.3-29 Hz. Nociceptive stimulation (lip squeeze with pliers) excited 63 (49%), inhibited 9 (7%), and did not affect 57 (44%) neurons. The same stimulation also elicited falls in ear pinna blood flow. In neurons activated by the stimulation, the increase in discharge preceded the fall in flow. Electrical stimulation of the spinal trigeminal tract excited 61/63 nociception-activated neurons [onset latencies range: 6-75 ms, mean: 28 +/- 3 (SE) ms], inhibited 9/9 nociception-inhibited neurons (onset latencies range: 9-85 ms, mean: 32 +/- 10 ms), and failed to affect 55/57 neurons insensitive to nociceptive stimulation. Neurons insensitive to nociceptive/trigeminal stimulation were also insensitive to nonnociceptive tactile stimulation and to electrical stimulation of the amygdala. They were either silent (32/45) or discharged regularly at low frequencies. They possessed long-duration action potentials (1.26 +/- 0.08 ms) and slow-conducting axons (6.0 +/- 0.5 m/s). These neurons may be serotonergic raphe-spinal cells. They do not appear to be involved in nociceptive-related cutaneous vascular control. Of the 63 neurons sensitive to nociceptive and trigeminal tract stimulation, 35 also responded to tactile stimulation (wide receptive field). These neurons possessed short action potentials (0.80 +/- 0.03 ms) and fast-conducting axons (30.3 +/- 3.1 m/s). In this subpopulation, electrical stimulation of the amygdala activated nearly all neurons tested (10/12), with a mean onset latency of 34 +/- 3 ms. The remaining 28 neurons sensitive to nociceptive and trigeminal stimulation did not respond to tactile stimuli and were mainly unaffected by amygdala stimulation. It may be that fast-conducting raphe-spinal neurons, with wide multimodal receptive fields and with input from the central nucleus of the amygdala, constitute the bulbo-spinal link in the CNS pathway regulating cutaneous blood flow in response to nociceptive and alerting stimuli.

Impairment of skin vasoconstrictive response to sympathetic activation in obese patients: Influence of rheological disorders

Alterations of cardiac vagosympathetic activity have been suggested in obesity. We have previously shown that the skin vasoconstrictive response to sympathetic activation is reduced in non-insulin-dependent diabetic patients. The present study investigates the skin vasoconstrictive response to sympathetic activation in nondiabetic obese patients and the influence of clinical and rheological factors. Fifty-seven obese and 18 healthy women were investigated. The resting cutaneous blood flow (CBF) and CBF response to three tests that activate the sympathetic nervous system (deep breathing, Valsalva maneuver, and sitting to standing) were measured by a laser Doppler device. The red blood cell (RBC) filtration index (FI) and RBC aggregation were measured using a Hanss hemorrheometer and a Myrenne aggregometer (Myrenne, Roetgen, Germany), respectively. Resting CBF was not significantly different in obese and control subjects. The vasoconstrictive response to the deep-breathing and sitting-to-standing tests expressed as the decrease in CBF was significantly lower in obese patients versus controls (43.9% +/- 3.1% v 73.7% +/- 17.9%, P = .01, and 67.1% +/- 3.8% v 89.8% +/- 12.0%, P = .02, respectively). The spontaneous basal CBF variations and the downward slope of the CBF reduction during the Valsalva and sitting-to-standing tests correlated negatively with age in obese patients (P = .042, .022, and .008, respectively). During the sitting-to-standing test, the percent change in CBF correlated positively with RBC aggregation at a shear rate of 0 and 3 s(-1) (P = .011 and .017, respectively). In conclusion, (1) CBF assessment by laser Doppler flowmetry is an effective noninvasive method to investigate sympathetic nervous function in obese patients; (2) obesity is associated with a significant reduction in the vasoconstrictive response to two tests for sympathetic activation, the deep-breathing and sitting-to-standing tests; (3) the severity of this reduction increases with age; and (4) RBC aggregation may contribute to the increase in the vasoconstrictive response and may thus increase the risk of widespread cardiovascular disease.

Progressive calibrated pressure device to measure cutaneous blood flow changes to external pressure strain

The present methodological paper describes a simple and useful device for local, external pressure application. The mechanical devices, the difficulties, the time required, the possibilities and limitations of the technique to apply a progressive calibrated pressure and to measure cutaneous blood flow with a laser Doppler probe at the same site are discussed. This technique was used to study the effects of local pressure on the cutaneous blood flow with laser Doppler technique. Use of this protocol has provided evidence for a transient cutaneous vasodilation in the human hand during progressive externally applied pressure strain. Results from our laboratory thus far suggest that this vasodilator response is mediated by small sensory nerve fibres in the skin. Theme: Autonomic regulation Topic: Cardiovascular regulation

Dorsal root reflexes and cutaneous neurogenic inflammation after intradermal injection of capsaicin in rats.

The role of dorsal root reflexes (DRRs) in acute cutaneous neurogenic inflammation induced by intradermal injection of capsaicin (CAP) was examined in anesthetized rats. Changes in cutaneous blood flow (flare) on the plantar surface of the foot were measured using a laser Doppler flowmeter, and neurogenic edema was examined by measurements of paw thickness. To implicate DRRs in neurogenic inflammation after CAP injection, the ipsilateral sciatic and femoral nerves were sectioned, dorsal rhizotomies were performed at L(3-)-S(1), and antagonists of GABA or excitatory amino acid receptors were administered intrathecally. Intradermal injection of CAP evoked a flare response that was largest at 15-20 mm from the injection site and that spread >30 mm. Acute transection of the sciatic and femoral nerves or dorsal rhizotomies nearly completely abolished the blood flow changes 15-20 mm from the CAP injection site, although there was only a minimal effect on blood flow near the injection site. These procedures also significantly reduced neurogenic edema. Intrathecal bicuculline, 6-cyano-7-nitroquinoxaline-2,3-dione, (CNQX) or D(-)-2-amino-7-phosphonoheptanoic acid (AP7), but not phaclofen, also reduced dramatically the increases in blood flow 15-20 mm from the CAP injection site, but had only a minimal effect on blood flow near the injection site. Neurogenic edema was reduced by the same agents that reduced blood flow. Multiunit DRRs recorded from the central stumps of cut dorsal rootlets in the lumbar spinal cord were enhanced after CAP injection. This enhanced DRR activity could be reduced significantly by posttreatment of the spinal cord with bicuculline, CNQX or AP7, but not phaclofen. It is concluded that peripheral cutaneous inflammation induced by intradermal injection of CAP involves central nervous mechanisms. DRRs play a major role in the development of neurogenic cutaneous inflammation, although a direct action of CAP on peripheral nerve terminals or the generation of axon reflexes also may contribute to changes in the skin near the injection site.

Sensory threshold changes without initial pain or alterations in cutaneous blood flow, in the area of secondary hyperalgesia caused by topical application of capsaicin in humans

Changes in von Frey hair perception, pricking pain, and vibration thresholds were examined in six healthy human adults, in the zone of secondary hyperalgesia, 45 min following the topical application of capsaicin at concentrations of 0.05 and 0.1 mg/ml. In two of these subjects, cutaneous blood flow was monitored at 10-min intervals, before, during and after capsaicin application, using laser Doppler perfusion imaging. Thresholds for all three parameters were significantly reduced after capsaicin treatment, in a dose-dependant manner. However, there was no visible skin flare, and no change in cutaneous blood flow at these doses of capsaicin. The effects on von Frey perception threshold and vibration threshold have not been demonstrated previously, and may be indicative of central changes, initiated by afferent fibres (presumably C fibres) that are not vasoactive.

An ipsilateral superdrainaged transverse rectus abdominis myocutaneous flap for breast reconstruction.

A conventional single pedicled TRAM (transverse rectus abdominis myocutaneous) flap is a musculocutaneous flap widely used for breast reconstruction. However, complications such as partial flap necrosis, fat necrosis, and fatty induration may occur as a result of unstable blood flow circulation to the flap. One major factor is venous congestion in the flap. In an effort to obtain more stable TRAM flap blood circulation, we anastomosed the ipsilateral deep inferior epigastric vein of a pedicled TRAM flap to the thoracodorsal vein. This procedure provides superdrainage by means of enhanced venous perfusion. This flap with superdrainage augmentation is referred to as a superdrainaged TRAM flap (12 patients). Changes in cutaneous blood flow were also assessed by measurement of cutaneous blood flow in zone IV using a laser blood flow meter (8 patients). The patients who underwent breast reconstructive surgery using this technique showed no evidence of postoperative complications such as flap necrosis, fat necrosis, or fatty induration. Satisfactory results were obtained during breast reconstruction in patients who had previously undergone a radical mastectomy with resultant large areas of tissue defects. In addition, the two patient groups, 12 patients with superdrainaged TRAM flap and 20 patients with single pedicled TRAM flap, were compared to assess differences in complications. The incidence of partial flap necrosis, fat necrosis, and fatty induration was lower among patients with superdrainaged flap than those with single pedicled flap.

Spinal integration of antidromic mediated cutaneous vasodilation during dorsal spinal cord stimulation in the rat

The purpose of this study was to determine the involvement of supraspinal centers and spinal synaptic integration in cutaneous vasodilation mediated by dorsal spinal cord stimulation (DCS). Laser Doppler flowmetry was used to assess cutaneous blood flow changes in the rat hindpaw during DCS with a unipolar ball electrode placed at the L2-L3 spinal level. Results demonstrated that transecting the spinal cord at the T10 spinal segment did not alter the DCS response while T13 spinal transection abolished the DCS-induced vasodilation. Inhibition of synaptic activity with topical application of muscimol (0.2 mM) on the dorsal surface of the spinal cord markedly attenuated the DCS response. In conclusion DCS-induced vasodilation involved synaptic integration but did not require input from rostral spinal sites or supraspinal areas.

Applied forces and associated physiologic responses induced by axial spinal unloading with the LTX 3000™ lumbar rehabilitation system

Objective: To measure forces applied to the body and associated changes in physiologic responses during axial spinal unloading (gravity-dependent traction) using the LTX 3000™ Lumbar Rehabilitation System. Design: Lumbar unloading was induced in 17 healthy subjects. The following parameters were measured: (1) percentage of total body weight unloaded; (2) forces applied onto and below the rib cage and local changes in cutaneous blood flow; (3) alteration of the applied forces to the seat strap associated with lumbar lengthening; and (4) changes in respiratory rates, respiratory minute volumes, heart rate, and blood pressure. Results: The average pressure applied to the rib cage for thoracic immobilization without unloading was 73 ± 26mmHg. Lumbar unloading caused these pressures to increase by approximately 30%, causing complete but temporary occlusion of cutaneous blood flow in this region. Significant, but normal, reactive hyperemia occurred upon release of the rib support pads ( p <- .05). Axial spinal unloading using an LTX 3000™ induced changes in heart rate, blood pressure, and respiratory rates of magnitudes similar to those reported with the use of other traction devices. Conclusion: The forces applied to the rib cage by the LTX 3000™ for proper lumbar unloading caused changes in physiologic responses, but these changes were reversible and can be considered clinically unimportant and thus should not be contraindications to the use of this device by the general population.

Peripheral vasoconstrictor responses to sympathetic activation in diabetic patients: Relationship with rheological disorders

The sympathetic nervous system regulates peripheral blood flow. This study investigated sympathetic vascular control in diabetic patients by measuring cutaneous blood flow (CBF) with a laser Doppler device at rest and during three sympathetic activation tests: deep-breathing, changing positions from sitting to standing, and using the Valsalva maneuver. The influence of various factors, particularly rheological changes, was also assessed. Forty-two type II diabetes mellitus (non—insulin-dependent [NIDDM]) patients and 14 control subjects were studied. The mean value and standard deviation (SD) of basal CBF at rest were not significantly different in the two groups. In 12 NIDDM patients, the SD was less than the lowest limit found in the controls. During the three tests, the reduction in CBF and its downward slope were lower in NIDDM patients than in controls, with the greatest difference occurring during the deep-breathing test. During this test, the downward slope of CBF was less than the lowest control level in 14 NIDDM patients. The log SD of basal CBF correlated with the decrease in CBF during the sitting-to-standing and Valsalva tests in control subjects and during all three tests in NIDDM patients. In NIDDM patients, log mean basal CBF correlated negatively with the log erythrocyte filtration index ([FI] an index of rigidity) and positively with hemoglobin A 1 c = (HbA 1 c ). The log downward slope of CBF during the deep-breathing test correlated negatively with log erythrocyte FI. The log downward slope of CBF during the sitting-to-standing and Valsalva tests correlated positively with total cholesterol and triglycerides, respectively. Basal CBF and the CBF response to these tests did not correlate with retinopathy, nephropathy, peripheral neuropathy, or heart rate variations during these tests. This study suggests that CBF assessment by laser Doppler flowmetry affords an attractive noninvasive way to investigate sympathetic nervous function in diabetic patients. The amplitude of changes in basal CBF and the decrease in CBF during the deep-breathing test show that this is a simple and sensitive procedure for detecting sympathetic nerve dysfunction. Moreover, rheological blood properties and metabolic factors seem to strongly influence resting CBF and vasomotor reflexes.

Priming of eosinophil recruitment in vivo by LPS pretreatment.

Eosinophils are important inflammatory cells in allergic diseases. Recent evidence suggests that priming mechanisms in the blood may be important for effective eosinophil recruitment to sites of allergic inflammation. We have investigated whether priming an inflammatory site could enhance eosinophil recruitment in vivo. Pretreatment of skin sites in the guinea pig with a low dose (30 ng) of LPS, which had little effect on eosinophil accumulation alone, enhanced by up to threefold the 111In-eosinophil accumulation in response to a passive cutaneous anaphylactic reaction and to intradermally injected eosinophil chemoattractants (leukotriene B4, PAF, and C5ades Arg). In contrast, LPS pretreatment did not enhance accumulation of 111In-neutrophils. Priming was seen only with a 1-h pretreatment time and was not associated with an increase in local edema or a change in cutaneous blood flow. It was independent of local protein synthesis, as assessed using cycloheximide, and was unaffected by a PAF antagonist, a 5-lipoxygenase inhibitor, and the IL-1 receptor antagonist. The priming response was, however, reduced by co-injection with the LPS of TNFR-IgG, but not of CD4-IgG. Blockade of CD18 showed this adhesion molecule to be critical for eosinophil accumulation, and LPS-primed sites were inhibited as effectively as nonprimed sites. In conclusion, low dose LPS pretreatment of guinea pig skin sites primes for eosinophil accumulation induced by intradermally injected inflammatory mediators and cutaneous anaphylactic reaction. This may be an important process by which eosinophil recruitment is modulated in vivo.