Studies on the Sympathetic Control of Normal and Diseased Synovial Blood Vessels: The Effect of <i>α</i> and <i>β</i> Receptor Stimulation and Inhibition, Monitored by the 133Xenon Clearance Technique

Dick, W C; Jubb, R. W.; Buchanan, W. Watson; Williamson, John; Whaley, K; Porter, Barbara J.

doi:10.1042/cs0400197

Cited by 22 publications

(7 citation statements)

References 13 publications

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“…This discrepancy may be due to different substances being used to induce inflammation and/or the longer time course of inflammation (24 h) in this study. Our results are more in agreement with the findings of Dick, Jubb, Buchanan, Williamson, Whaley & Porter (1971), in which they observed loss of constrictor tone of blood vessels in chronically inflamed human joints. Although highly correlated with blood flow, the proportionality of change in P3°2 compared with blood flow was dissimilar (Fig.…”

Section: Discussionsupporting

confidence: 93%

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

Najafipour

Ferrell²

1995

Experimental Physiology

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SUMMARYExperiments were performed to assess the effect of acute inflammation of the rabbit knee joint on the partial pressure of oxygen in synovial fluid (P0o) 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.) P 02 was 37-4 + 3-6 mmHg (n = 10) in the inflamed group, which differed significantly (P < 0.05) from that occumng in the normal group from a different series (48.2 + 3-1 mmHg; n = 18). P O, 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 P80°2. 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 P 02 . 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, P0 2 was lower compared with the normal joint. The results of this study show significantly altered blood flow, P 02 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.

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Section: Discussionsupporting

confidence: 93%

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

Najafipour

Ferrell²

1995

Experimental Physiology

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“…Previous investigations have revealed the role of the sympathetic nervous system in normal and inflamed knee JBF regulation [6,8,22] showing a significant reduction in constrictor response to nerve stimulation by the process of inflammation. Bloodvessel response to saphenous nerve stimulation in the rat was also shown to be reduced in chronically inflamed knee joints [15].…”

Section: Discussionmentioning

confidence: 99%

“…A high correlation has been found between synovial fluid PO 2 and synovial blood flow in both normal and acutely inflamed rabbit knee joints [22], suggesting the importance of joint blood flow (JBF) regulatory mechanisms in supplying oxygen and other nutrients to the synovial tissues. Using the 133 Xe clearance technique, Dick et al [6] obtained evidence for a contribution from both α-and β-adrenergic mechanisms to the regulation of blood flow in normal and diseased human articular vascular beds. Our previous studies showed a significant reduction in the efficacy of the sympathetic nervous system in regulating blood flow to the inflamed joint [22], which may account for the significantly higher blood flow observed in this condition.…”

Section: Introductionmentioning

confidence: 98%

Alteration in α- and β- adrenoceptor profile of rabbit-knee-joint blood vessels due to chronic inflammation

Najafipour

Niazmand

2006

Pflugers Arch - Eur J Physiol

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Experiments were performed to investigate the nature of alpha- and beta-adrenoceptors in blood vessels supplying the posterior capsule of the chronically inflamed rabbit knee joint, and results were compared to the finding from previous experiments on the normal and acutely inflamed joint to assess any alteration which may occur in the adrenoceptor profile due to the chronic inflammation process. Electrical stimulation of the posterior articular nerve resulted in vasoconstriction that was completely blocked by phentolamine. This constrictor response was almost equally inhibited by prazosin and yohimbine. The dose-response curves to close intraarterial injection of alpha-adrenoceptor agonists showed a rank-order potency of adrenaline = clonidine = phenylephrine. The adrenaline dose-response curve was shifted to the right by administration of alpha-antagonists with a rank-order potency of phentolamine = prazosin = yohimbine. At this stage of experiments, there was an equal response of alpha(1)- and alpha(2)- adrenoceptors in blood vessels of the chronically inflamed rabbit knee joint. In another group of animals, the neurally mediated vasodilatation, which appeared after administration of phentolamine, was completely blocked by propranolol and was reduced significantly by ICI118551, but the effect of atenolol was not significant. The dose-response curve to close intraarterial injection of beta-adrenoceptor agonists showed a rank-order potency of: isoprenaline > salbutamol > dobutamine. The isoprenaline dose-response curve was shifted to the right by administration of beta-antagonists with rank-order potency of propranolol > ICI118551 > atenolol. These experiments showed a greater beta(2)-adrenoceptor response than beta(1)-adrenoceptor response in chronically inflamed rabbit-knee-joint blood vessels. Overall, compared to previous experiments on normal joint in which alpha(2)- and beta(1)-adrenoceptor responses predominated, and in acutely inflamed joint in which an equal alpha(1)/alpha(2) and beta(1)/beta(2) response was shown, in chronically inflamed joint the sympathetic constriction response was returned toward normal. No more alpha-adrenoceptor shift had happened, and the shift of beta(1) to beta(2) response continued.

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“…Intra-articular administration of isoprenaline results in a marked increase in the clearance rate of 133 Xe from diarthrodial joints (Dick et al 1971a). In contrast, the clearance rate is markedly decreased, when norepinephrine is administered.…”

Section: Synovial Vascular Bedmentioning

confidence: 98%

Hemodynamics of the juvenile knee

Bünger

1987

Acta Orthopaedica Scandinavica

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Studies on the Sympathetic Control of Normal and Diseased Synovial Blood Vessels: The Effect of α and β Receptor Stimulation and Inhibition, Monitored by the 133Xenon Clearance Technique

Cited by 22 publications

References 13 publications

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

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

Alteration in α- and β- adrenoceptor profile of rabbit-knee-joint blood vessels due to chronic inflammation

Hemodynamics of the juvenile knee

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