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Biomedical subjects

W R Ferrell

Publications and source records attributed to W R Ferrell.

At least 19 recordsLinked to original sources
PubMed2001

Expression of constitutive but not inducible cyclooxygenase maintains articular perfusion in the rat knee.

Experiments were performed in the normal rat knee joint to investigate the role of different isoforms of cyclooxygenase (COX) in the regulation of basal joint blood flow. Laser Doppler imaging (LDI) was used to measure articular perfusion, and reverse transcriptase polymerase chain reaction (RT-PCR) for the detection of COX-1 and COX-2 mRNA in joint tissue. Intravenous infusion of indomethacin (a non-selective inhibitor of COX; 0.34 nmol min(-1)) over 40 min produced a time dependent increase in articular vascular resistance (maximum 22.5 % at 40 min; P < 0.0001, one-way ANOVA) whereas vehicle over a similar time period had no effect in a control group. An equimolar concentration of a highly selective inhibitor for COX-2, SC-236, was administered in a further group of rats but this did not increase articular vascular resistance. While there was no significant difference between the response to vehicle and SC-236 (two-way ANOVA; P = 0.686, n = 6) the response to indomethacin was significantly greater than vehicle or SC-236 (two-way Anova; P < 0.0001, n = 6). COX-1, but not COX-2, was detectable by RT-PCR in all joint tissue samples examined (n = 4). The results of this study indicate that prostaglandins (PGs) play an important role in the maintenance of basal perfusion in the rat knee joint, with COX-1 being the physiologically relevant isoform. Experimental Physiology (2001) 86.2, 191-197.

Animals↗
PubMed2001

Metacarpophalangeal joints in rheumatoid arthritis: laser Doppler imaging--initial experience.

Laser Doppler imaging is a noninvasive method yielding a spatial perfusion map. With use of a near-infrared laser, elevated perfusion associated with the metacarpophalangeal joints was detectable in patients with active rheumatoid arthritis. Findings at laser Doppler imaging correlated with pain scores and synovitis detected at ultrasonography, whereas the power Doppler sign (red pixels inside the active green box) did not. Laser Doppler imaging has the potential to help assess soft-tissue inflammation.

Adult↗
PubMed2000

Novel use of laser Doppler imaging for investigating epicondylitis.

OBJECTIVE: This investigation evaluated a novel form of tissue perfusion measurement, laser Doppler imaging (LDI), in a case of lateral epicondylitis to establish if it might have applications in assessing soft tissue lesions. LDI was used in conjunction with ultrasonography to provide information about tissue oedema as well as the power Doppler signal as an alternative method of assessing blood flow. METHODS: A laser Doppler imager with a near-infrared (NIR) laser source was used to improve tissue penetration and yield measurements of perfusion (flux) from structures under the skin. Skin temperature over the lateral epicondylar region was also measured. Ultrasonography was used in both grey-scale and power Doppler modes. LDI, temperature measurements and ultrasonographic data were obtained before treatment and serially after local injection of methylprednisolone. RESULTS: Before treatment there was increased perfusion and skin temperature and the presence of a power Doppler sign associated with the right lateral epicondyle as well as oedema at the extensor origin. None of these was present at the asymptomatic contralateral epicondylar region. Twenty-four hours after methylprednisolone administration, both perfusion and skin temperature had increased, and they declined over the subsequent 48 h. Although skin temperature had declined to normal (referenced to the contralateral epicondyle) by the third day after injection, it took until the eleventh day after injection for perfusion to normalize. CONCLUSIONS: LDI using an NIR laser source appears to be an effective non-invasive method for the examination of inflammatory responses in soft tissue, with greater sensitivity than thermally based methods. In addition, LDI was found to correlate with power Doppler ultrasonography.

Anti-Inflammatory Agents↗
PubMed1999

Neurogenic origin of articular hyperemia in early degenerative joint disease.

It has been speculated that joint instability resulting from anterior cruciate ligament (ACL) rupture could be exacerbated by changes in vasomotor activity in the remaining supporting structures. In this study, the effect of ACL transection on medial collateral ligament (MCL) basal perfusion and its responsiveness to calcitonin gene-related peptide (CGRP) and sympathetic adrenergic influences was examined. Using urethan-anesthetized rabbits, we tested the effects of CGRP and its antagonist CGRP-(8-37) by topical application of these agents to the exposed knee while sympathetic influences were tested by electrically stimulating the saphenous nerve. It was found that MCL basal perfusion was elevated in ACL-sectioned joints; however, this effect was abrogated by prior resection of the articular nerve supply. At the doses tested, the normal vasodilator response to CGRP was abolished in ACL-sectioned joints, whereas the response to CGRP-(8-37) was attenuated. Even under the influence of increased constrictor tone, MCL and capsule blood vessels still showed substantially reduced responses to exogenous CGRP administration. By contrast, nerve-mediated constrictor responses were mostly unaffected by joint instability. This study suggests that posttraumatic knee joint hyperemia is neurogenically mediated, possibly by increased secretion of CGRP.

Animals↗
PubMed1998

Repetitive activity alters perfusion of proximal interphalangeal joints of the human hand.

OBJECTIVE: To examine whether competitive volleyball players show any difference in perfusion of their proximal interphalangeal (PIP) joints compared with a healthy group of subjects. Also to assess the viability of a dual wavelength laser Doppler imager (LDI) in making these measurements. SETTING: Physiology laboratory. PARTICIPANTS: Ten active volleyball players who had experienced repetitive finger joint injury and 12 age- and sex-matched normal control subjects. MAIN OUTCOME MEASURES: Using a modified LDI incorporating a near- infrared (850 nm) laser as well as a standard red (633 nm) laser, scans were performed over the dorsum of the hands of the volleyball players and the control group. RESULTS: Higher perfusion values were obtained with the 850-nm laser than with the red 633-nm laser. When referenced to adjacent skin blood flow, perfusion over PIP joints of volleyball players was found to be significantly higher than that in control subjects (p=0.00012; n=10-12). CONCLUSIONS: The higher perfusion values obtained using the 850-nm laser suggest that the longer wavelength laser is measuring perfusion in a greater volume of tissue, which could include subcutaneous structures. Volleyball players have significantly higher perfusion over the PIP joints, which is unlikely to be due to differences in skin perfusion over the two regions but is more likely to be related to hyperemia of the underlying PIP joints. The reason for increased PIP perfusion is not clear; it may represent ongoing tissue inflammation due to repeated injury, or it could be an adaptive response to the stresses placed on these joints by this type of repetitive activity. CLINICAL RELEVANCE: Near-infrared laser Doppler imaging has the potential to provide a noninvasive clinical assessment of finger joint injuries.

Adult↗
PubMed1997

Spatial variation in sympathetic influences on the vasculature of the synovium and medial collateral ligament of the rabbit knee joint.

1. Laser Doppler perfusion imaging was used to assess the role of the sympathetic nervous system in the control of blood flow to the medial collateral ligament and capsule (synovium and overlying fibrous tissues) of the rabbit knee joint. 2. Electrical stimulation of the saphenous nerve (width 1 ms; amplitude 20V; 1-30 Hz) produced a frequency-dependent vasoconstriction of knee joint vasculature. The response was maximal at 30 Hz and gave the greatest fall in perfusion at the femoral insertion of the ligament (by 33.8 +/- 7.4%, mean +/- S.E.M.; n = 5-6) and the smallest decrease at the tibial insertion of the ligament (by 10.6 +/- 2.9%). 3. Topical application of phentolamine (10(-6) mol) had no significant effect on basal knee joint blood flow. However, it abolished the nerve-mediated constrictor responses in all regions of the medial collateral ligament and synovium at all frequencies. 4. Topical administration of adrenaline (10(-14) to 10(-7) mol) caused a dose-dependent decrease in knee joint blood flow with the highest dose producing > 75% reduction in perfusion at all areas. 5. There was no evidence of a reactive hyperaemia in the 5 min following a 5 min period of femoral artery occlusion. Artificial manipulation of arterial blood pressure by intravenous infusion or withdrawal of blood caused a proportional change in ligament and synovial blood flow. These observations may indicate a lack of autoregulation in the joint and its exclusion from baroreflex modulation. 6. These results suggest a potential role for the sympathetic nervous system in the control of knee joint blood flow. Neuromodulation of ligament perfusion appears to predominate at the femoral insertion and this could prove to have functional significance.

Adrenergic alpha-Agonists↗
PubMed1997

Tachykinin regulation of basal synovial blood flow.

1. Experiments were performed to investigate the role of endogenously released tachykinins in the regulation of blood flow to the rat knee joint. Synovial perfusion was assessed by laser Doppler perfusion imaging, which permitted spatial measurement of relative changes in perfusion from control (pre drug administration), expressed as the percentage change. Most experiments were performed on the exposed medial aspect of the knee joint capsule. 2. Neither the selective tachykinin NK1 receptor antagonist, FK888, nor the selective tachykinin NK2 receptor antagonist, SR48968, significantly influenced synovial blood flow at doses of 10(-12), 10(-10) and 10(-8) mol. However, topical co-administration of these agents produced significant dose-dependent reductions in basal synovial perfusion of 6.3 +/- 4.6 and 12.0 +/- 3.4 and 19.9 +/- 2.6%, respectively; n = 29. The non-selective tachykinin NK1/NK2 receptor antagonist, FK224, also produced significant (at 10(-10) and 10(-8) mol), but less potent, reductions in perfusion of 5.3 +/- 4.0, 8.4 +/- 2.2 and 5.9 +/- 2.8%, respectively; n = 25. 3. Topical administration of the alpha 1-, alpha 2-adrenoceptor antagonist phenoxybenzamine elicited a 31.3 +/- 6.2% increase in blood flow which was substantially reduced to 10.4 +/- 3.8% by co-administration of the FK888 and SR48968 (both at 10(-8) mol; n = 8-13), suggesting that normally there is sympathetic vasoconstrictor "tone' which is opposed by the vasodilator action of endogenous tachykinins. 4. One week after surgical interruption of the nerve supply to the knee joint, co-administration of FK888 and SR48968 (both at 10(-8) mol) now produced slight vasodilatation (6.7 +/- 4.6%; n = 9) which did not differ significantly from vehicle treatment. Depletion of tachykinins from sensory nerve fibres by systemic capsaicin administration also resulted in abolition of the vasoconstrictor effect of FK888 and SR48968 (both at 10(-8) mol), with these agents only producing a slight vasodilatation (2.5 +/- 5.3%; n = 6). 5. By use of a near infra-red laser source it was possible to image knee joint perfusion transcutaneously, the overlying skin being left intact. In this more physiological situation, close intra-arterial injection of the combination of FK888 and SR48968 (both at 10(-8) mol) again elicited vasoconstriction (48.8 +/- 16.2% reduction in blood flow; n = 4). 6. These results indicate that endogenous tachykinins may be continuously released from sensory fibers innervating the joint. Basal release of tachykinins could therefore be an important physiological influence opposing sympathetic vasoconstrictor tone.

Administration, Topical↗
PubMed1997

Modulation of synovial blood flow by the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP(8-37).

1. The effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP(8-37) on blood flow in the knee joint of the anaesthetized rat was investigated. 2. Synovial blood flow in both exposed and intact, skin-covered knees was measured by laser Doppler perfusion imaging. 3. Topical application of CGRP(8-37) caused a dose-dependent fall in synovial blood flow in the exposed knee joint of the rat. At low (1.5 nmol) doses of CGRP(8-37) there was no significant effect on synovial blood flow. In rats treated with 7.5 nmol CGRP(8-37) there was a fall in synovial blood flow (maximum effect at 10 min: -28.8 +/- 4.6%; n=7), which returned to resting levels within 30 min. The highest dose (15 nmol) of antagonist used in this study caused a marked (maximum at 10 min: -35.6 +/- 9.3%; n=8), and prolonged (up to 30 min) fall in blood flow. 4. Ten days after surgical denervation, CGRP(9-37) (15 nmol, topical) had no significant effect on blood flow in the rat exposed knee joint (change in flux at 10 min: -5.1+/-3.6%; n=4). This suggests that CGRP(8-37) acts selectively to antagonize the actions of a neurally derived product, probably CGRP, on the rat synovial vasculature. 5. In skin-covered knee joints, intra-articular injection of CGRP(8-37) (15 nmol; bolus) elicited a significant fall in synovial blood flow (maximum effect at 10 min: -15.5 +/- 5.8%; n=6). 6. CGRP (0.01, 0.1 or 1.0 nmol; topical) caused a dose-dependent increase in exposed knee joint blood flow, which was attenuated by co-administration of 1.5 nmol CGRP(8-37). For example, 1 nmol CGRP elicited a peak increase in flux at 10 min of 94.7 +/- 31.8% (n=8) and 28.8 +/- 8.9% (n=7) in the absence and presence of CGRP(8-37), respectively. The vasodilator responses induced by acetylcholine (ACh) (10 nmol, topical; n=4-5) or sodium nitroprusside (SNP) (10 nmol, topical; n=4-5) were unaltered in the presence of CGRP(8-37) (1.5 nmol, topical). 7. Thus, the CGRP receptor antagonist CGRP(8-37) elicits vasoconstriction in the rat synovium. This suggests that the endogenous, basal release of CGRP may play a physiological role in the regulation of blood flow in the rat knee joint.

Animals↗
PubMed1997

Spatial heterogeneity of the effects of calcitonin gene-related peptide (CGRP) on the microvasculature of ligaments in the rabbit knee joint.

1. Experiments were performed in anaesthetized rabbits to examine the effects of calcitonin gene-related peptide (CGRP) and the CGRP antagonist CGRP8-37 on blood flow to the medial collateral ligament of the knee joint. 2. Topical application of CGRP (10(-13) to 10(-9) mol) to the exposed external surface of eight knee joints resulted in dose-dependent dilatation of vessels in both the ligament and the joint capsule. The magnitude of this response varied significantly in different regions of the medial collateral ligament, with the 10(-9) mol dose of CGRP giving the maximum response (101.5 +/- 25.3% increase) at the femoral insertion site of the medial collateral ligament and lowest (23.1 +/- 8.8%) at the tibial insertion site. 3. Topical application of CGRP8-37 (0.1, 1 and 10 nmol) produced dose-dependent constriction of vessels in the ligament and the joint capsule in five knees, with a trend towards the greatest effect occurring at the femoral insertion site (45.8 +/- 8.1% reduction in blood flow). With the 10 nmol dose, the vasoconstrictor response at the femoral insertion site differed significantly (P<0.05) from the responses obtained at the tibial insertion and joint capsule sites. 4. Topical application of CGRP8-37 (0.1, 1 and 10 nmol) to four chronically denervated knees produced substantially smaller vasoconstrictor responses at all sites. At the femoral insertion site, where 10 nmol CGRP8-37 normally produces a 45.8 +/- 8.1% reduction in blood flow (n=8), ten days following denervation this response was reduced to 6.5 +/- 6.1%, this difference being significant (P=0.01). 5. Adrenaline was applied topically to augment blood vessel tone, in order to establish how effectively co-administration of CGRP would offset this increase in tone. Adrenaline (10(-10) mol) produced vasoconstriction at all sites (n=6). In the capsule this vasoconstriction was virtually abolished when CGRP (10(-9) mol) was co-administered with adrenaline but in the ligament vasodilatation occurred at all sites. This vasodilatation was significantly greater at the femoral insertion site compared to the tibial insertion and mid ligament sites (P<0.05 for both) and the capsule (P<0.01). 6. Topical application of substance P (10(-10) or 10(-9) mol) failed to elicit dilatation of ligament blood vessels. 7. These results suggest that endogenous CGRP may play an important role in regulating blood flow to different structures in and around the knee joint.

Animals↗
PubMed1996

Inhibition of nitric oxide production during electrical stimulation of the nerves supplying the rat knee joint.

A rôle for nitric oxide in the regulation of knee joint blood flow in the male anaesthetised rat was investigated using laser Doppler perfusion imaging. Intravenous infusion of the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) at a rate of 0.1 and 1 mg/kg per h caused an initial, but transient, rise in vascular resistance by about 15%. Mean arterial blood pressure was by and large unaffected by both dose of inhibitor during these first 5 min of infusion. The effect of an alternative nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) was also investigated. When 10 mg/kg per h of this drug was infused intravenously, there was a negligible effect on joint vascular resistance for the first 40 min but it then fell by about 15% over the next 20 min of infusion; mean arterial pressure gradually rose throughout administration. Electrical stimulation of the saphenous nerve in control animals elicited a frequency-dependent constriction of articular blood vessels over the range 5-30 Hz. Nerve stimulation at lower frequencies had little effect on joint capsular perfusion. When the nerve was stimulated over the same range of frequencies but in the presence of L-NAME it was found that the frequency response profile was unaffected. However, intravenous infusion of the less potent inhibitor L-NMMA caused a greater vasoconstrictor response to nerve stimulation over all but the lowest frequency tested. The results of these experiments indicate that endogenous nitric oxide may be produced in only very small amounts by the vascular bed of the rat knee joint. This differs markedly from the findings of a previous study in the rabbit knee joint where L-NAME administration resulted in a large and sustained increase in vascular resistance, suggesting substantial and continuous NO release. A unique isoform of the enzyme may possibly occur in the terminals of the nerves supplying the joint whose enzymatic activity is only inhibited by L-NMMA and not L-NAME.

Animals↗
PubMed1996

Evaluation of laser Doppler imaging to measure blood flow in knee ligaments of adult rabbits.

Laser Doppler imaging (LDI) is investigated as a novel method for in vivo ligament tissue blood flow determination. LDI output signal is obtained from surgically exposed rabbit medial collateral ligaments (MCL). The LDI signal is compared with simultaneously determined, coloured microsphere (CM)-derived standardised MCL blood flow. Correlation of LDI output with the CM flow data and a linear regression of 17 data points in nine rabbits (joint injured to provoke an acute vascular response in the tissues) indicate that LDI provides a reasonable estimate of MCL blood flow, at least over the ranges assessed. If properly calibrated, and given enough tissue-specific data points, LDI may have advantages over conventional, but more invasive, techniques. The potential clinical application of LDI technology to joint injury and arthritis research is discussed.

Animals↗
PubMed1996

Laser Doppler perfusion imaging of skin blood flow using red and near-infrared sources.

At present, scanning laser Doppler imaging uses a 633-nm helium-neon laser (RED) as the only light source, but this restricts its ability to measure blood flow (i) at darkly pigmented skin and (ii) from deeper or subdermal structures. Because near-infrared (NIR) light is known to penetrate deeper into tissue and to be less absorbed than RED, two imagers were adapted to include a NIR laser diode source (one of 830 nm for UK studies; one of 780 nm for leprosy field trials) in parallel with the existing RED source. In human hands representing a range of skin pigmentations, RED scans were unobtainable at the darkest areas of skin, but intact NIR scans could be collected in all cases. In experiments at the rat knee and the dorsal human hand, NIR and RED values were similar on normal skin. Over underlying vessels, however, NIR values greatly exceeded RED values, an effect abolished by occlusion. Similarly, in patients with leprosy and in healthy controls in Spain, fingerpulp NIR values exceeded RED values to the greatest degree when thermoregulatory flow was highest, i.e., when the deeper-lying arteriovenous anastomoses were open. Over areas of experimental inflammation, NIR gave higher values and also exhibited a greater degree of spatial heterogeneity than RED. We conclude that some current limitations of laser Doppler imaging technology can be overcome by the use of NIR laser diode sources.

Adult↗
PubMed1996

The action of knee joint afferents and the concomitant influence of cutaneous (sural) afferents on the discharge of triceps surae gamma-motoneurones in the cat.

Electrical stimulation of group II joint afferents of the posterior articular nerve (PAN) to the knee evoked short-latency facilitation and/or inhibition of the background discharge of gastrocnemius-soleus (GS) gamma-motoneurones in decerebrated spinal cats. The latencies of these responses were consistent with mediation via segmental oligosynaptic spinal pathways. In addition, a longer-latency facilitation was frequently observed. Mechanical non-noxious stimulation of the skin within the field of innervation of the sural nerve, on the lateral aspect of the heel, suppressed the short-latency facilitation, but not the inhibition or long-latency facilitation. Brief mechanical indentation of the posterior aspect of the knee joint capsule could elicit facilitation or inhibition of gamma-motoneurones. Facilitation, but not inhibition, was blocked by anaesthesia or section of the PAN. Both actions could be suppressed by mechanical stimulation of the heel. We conclude that GS gamma-motoneurones receive both facilitatory and inhibitory segmental inputs from group II articular afferents arising in the knee joint. Cutaneous afferents from the sural field exert a selective inhibitory influence over the facilitation of fusimotor discharge by articular afferents.

Animals↗
PubMed1995

The effect of the hypermobility syndrome on knee joint proprioception.

Proprioceptive sensory feedback is utilized by the central nervous system for conscious appreciation of the position and movement of the body and limbs. In patients with the hypermobility syndrome (HMS), it has been suggested that there is alteration of proprioceptive acuity. Proprioceptive performance of the knee joint was investigated in 10 female subjects who suffered from HMS using a threshold detection paradigm (accurate determination of the onset and direction of knee joint displacement at constant angular velocity). Compared to age- and sex-matched controls, HMS subjects showed significantly higher detection levels at starting knee flexion angles of 30 degrees P < 0.001) and 5 degrees (P < 0.001). Control subjects showed no significant difference in threshold acuity between the sexes (at 5 degrees P = 0.63, at 30 degrees P = 0.48). The increased acuity in proprioception observed towards full extension in the control population (P < 0.001) was absent in the HMS subjects (P = 0.596). Findings reported here suggest that HMS subjects have poorer proprioceptive feedback than controls. Reduced sensory feedback may lead to biomechanically unsound limb positions being adopted. Such a mechanism may allow acceleration of degenerative joint conditions, and may account for the increased prevalence of such conditions seen with HMS subjects.

Adult↗
PubMed1995

Comparison of synovial PO2 and sympathetic vasoconstrictor responses in normal and acutely inflamed rabbit knee joints.

Experiments were performed to assess the effect of acute inflammation of the rabbit knee joint on the partial pressure of oxygen in synovial fluid (Ps,O2) and nerve-mediated vasoconstrictor responses of articular blood vessels. With the hypodermic needle oxygen electrode sited within the synovial cavity in the posterior region of the knee joint, mean (+/- S.E.M.). Ps,O2 was 37.4 +/- 3.6 mmHg (n = 10) in the inflamed group, which differed significantly (P < 0.05) from that occurring in the normal group from a different series (48.2 +/- 3.1 mmHg; n = 18). Ps,O2 was found to decrease with increasing depth of penetration of the oxygen electrode into the joint cavity of the inflamed knee, as in the normal knee. The lowest values were observed close to articular cartilage. Absolute blood flow was measured using radiolabelled microspheres whilst relative changes in blood flow were assessed using laser Doppler flowmetry. The former technique showed that the inflamed joints had a significantly higher blood flow. Electrical stimulation of the posterior articular nerve (PAN) of the knee resulted in vasoconstriction of knee joint blood vessels, which was accompanied by a reduction in Ps,O2. The frequency-response and voltage-response profiles to electrical stimulation of the PAN, although differing in magnitude, showed a high degree of correlation between blood flow and Ps,O2. The frequency-response profile to electrical stimulation of the PAN shifted to the right in inflamed joints compared with normal joints, suggesting a reduction in the efficacy of the sympathetic nervous system in regulating blood flow to the inflamed joints. Although the inflamed joint had a higher blood flow, Ps,O2 was lower compared with the normal joint. The results of this study show significantly altered blood flow, Ps,O2 and nerve-mediated constrictor responses in the acutely inflamed joint. These are related to the inflammatory response and may contribute to the pathogenesis of arthritis.

Adrenergic Fibers↗
PubMed1995

Neuropeptidergic and autonomic control of the vasculature of the rat knee joint revealed by laser Doppler perfusion imaging.

An imaging technique (laser Doppler perfusion imaging, LDI), based on measurement of backscattered Doppler-broadened laser radiation, was used to provide two-dimensional images of perfusion in the exposed rat knee joint capsule. In control animals, frequency-dependent constriction of knee joint blood vessels occurred during electrical stimulation of sympathetic nerve fibres whilst dose-dependent vasodilatation of these vessels was elicited by direct application of the sensory neuropeptide substance P (SP) to the capsule. Intra-articular injection of the neurotoxic agent capsaicin did not affect vasoconstrictor responses when tested 5-7 days later, but substantially reduced dilator responses to SP. These findings indicate that capsaicin is selectively neurotoxic for sensory unmyelinated fibres but not sympathetic postganglionic fibres and is also capable of modifying receptor-mediated effects of SP. LDI is a useful method for mapping tissue perfusion, particularly in structures such as joints where the spatial distribution of blood flow is heterogeneous.

Animals↗
PubMed1995

Prolonged alteration of vasoconstrictor and vasodilator responses in rat knee joints by adjuvant monoarthritis.

Both neurogenic influences and the regulatory neuropeptide substance P (SP) have been implicated in the development of joint inflammation. Using the laser Doppler perfusion imaging technique to quantify relative changes in joint blood flow, the effects of nerve stimulation and topical SP application were examined in normal and chronically inflamed rat knee joints. Synovial inflammation was induced by unilateral intra-articular injection of Freund's complete adjuvant and experiments were carried out 1 week and 3 weeks later. Normal knees showed a frequency-dependent vasoconstriction in response to saphenous nerve stimulation over the range of 5-30 Hz and a dose-dependent vasodilation in response to SP administration. These vasoactive responses were completely abolished in the chronically inflamed knee joint, the abolition persisting throughout the investigation. Since articular cartilage is critically dependent on synovial fluid formation for its nutrition, loss of neurovascular control of the synovial microcirculation could contribute to the degenerative changes that commonly accompany chronic inflammatory joint diseases.

Animals↗