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

Najafipour, Hamid; Ferrell, W.R.

doi:10.1113/expphysiol.1995.sp003841

Cited by 30 publications

(35 citation statements)

References 18 publications

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“…Using the 133 Xe clearance technique, Dick and colleagues (1971) obtained evidence for a contribution from both á_ and â_adrenergic mechanisms to the regulation of blood flow in normal and diseased human articular vascular beds. Our previous study showed a significant reduction in the efficacy of the sympathetic nervous system in regulating blood flow to the inflamed joint (Najafipour & Ferrell, 1995), a possible explanation for the significantly higher blood flow observed in this condition. Further investigations revealed that although prostaglandins have a role to play in the regulation of basal blood flow to the inflamed joint but they do not appear to play a significant role in the modulation of sympathetic vasoconstriction responses (Najafipour & Ferrell, 1994).…”

mentioning

confidence: 73%

“…Alterations in blood flow (and also blood pressure) are expressed as the percentage change from control values measured immmediately before each test procedure. The biological zero values were measured as described previously (Najafipour & Ferrell, 1995) and subtracted from the flow values before calculation of percentage changes in blood flow. Mean arterial pressure was calculated by adding one-third of pulse pressure to the diastolic pressure.…”

Section: Methodsmentioning

confidence: 99%

“…Mean arterial pressure was calculated by adding one-third of pulse pressure to the diastolic pressure. The posterior articular nerve (PAN) was dissected after removal of the medial belly of the gastrocnemious muscle, as described before (Najafipour & Ferrell, 1995), and stimulated. The stimulus parameters were: width 1 ms, voltage 10 V, frequency 30 Hz, and duration 1 min; we have shown that these parameters give rise to maximal vasoconstrictor response in inflamed joints (Najafipour & Ferrell, 1995).…”

Section: Methodsmentioning

confidence: 99%

“…The posterior articular nerve (PAN) was dissected after removal of the medial belly of the gastrocnemious muscle, as described before (Najafipour & Ferrell, 1995), and stimulated. The stimulus parameters were: width 1 ms, voltage 10 V, frequency 30 Hz, and duration 1 min; we have shown that these parameters give rise to maximal vasoconstrictor response in inflamed joints (Najafipour & Ferrell, 1995). Acute knee joint inflammation was produced by intra-articular injection of 1 ml of a 2% solution (wÏv) of carrageenan (Sigma, UK) in distilled water into the joint space through the anterior region (mid-patellar tendon) 24 h before the experiment during a short period of anaesthesia induced with 2% halothane in the Oµ-N2O mixture.…”

Section: Methodsmentioning

confidence: 99%

“…A high correlation has been found between synovial POµ and synovial blood flow in both normal and acutely inflamed rabbit knee joints (Najafipour & Ferrell, 1995), suggesting the importance of joint blood flow regulatory mechanisms in supplying oxygen and other nutrients to the synovial tissues. Using the 133 Xe clearance technique, Dick and colleagues (1971) obtained evidence for a contribution from both á_ and â_adrenergic mechanisms to the regulation of blood flow in normal and diseased human articular vascular beds.…”

mentioning

confidence: 94%

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Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

Najafipour

2000

Experimental Physiology

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Experiments were performed to investigate the nature of α‐ and β‐adrenoceptors in blood vessels supplying the posterior capsule of the acutely inflamed rabbit knee joint, and results were compared to findings from previous experiments on the normal joint, to assess any alteration which may occur in the adrenoceptor profile due to the inflammation process. Electrical stimulation of the posterior articular nerve resulted in vasoconstriction which was reversed to vasodilatation by phentolamine and yohimbine. The dose‐response curves to close intra‐arterial injection of α‐adrenoceptor agonists showed a rank‐order potency of: adrenaline = phenylephrine = clonidine. The adrenaline dose‐response curve was shifted to the right by administration of antagonists with a rank‐order potency of: phentolamine = yohimbine = prazosin. At this stage of the experiments there was an equal response of α1‐ and α2‐adrenoceptors in blood vessels of the acutely 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 by about 50% by atenolol. The dose‐response curves to close intra‐arterial injection of β‐adrenoceptor agonists showed a rank‐order potency of: isoprenaline > salbutamol = dobutamine. The isoprenaline dose‐response curve was shifted to the right by administration of antagonists with a rank‐order potency of: propranolol > atenolol. These experiments also showed an almost equal response of β1‐ and β2‐adrenoceptors in blood vessels of the acutely inflamed rabbit knee joint. Overall, compared to previous experiments on the normal joint in which α2‐ and β1‐adrenoceptor responses predominated, acute inflammation resulted in a shift from α2‐ towards α1‐ and from β1‐ towards β2‐adrenoceptor responses.

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mentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 94%

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Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

Najafipour

2000

Experimental Physiology

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Factors influencing the oxygen concentration gradient from the synovial surface of articular cartilage to the cartilage–bone interface: A modeling study

Zhou¹,

Cui²,

Urban³

2004

Arthritis & Rheumatism

241

222

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Objective. There is very little information on the gradients of oxygen concentration from the synovial surface to the subchondral bone in articular cartilage. Cartilage is usually regarded as hypoxic, even though cellular metabolism is inhibited at low oxygen concentrations. We therefore measured rates of cellular consumption of oxygen and used these rates to calculate oxygen tension profiles across articular cartilage.Methods. The rate of oxygen consumption by bovine articular chondrocytes was measured in vitro, either in intact cartilage slices or in isolated chondrocytes. The oxygen tension profile across articular cartilage was predicted by solving a 1-dimensional reactiondiffusion equation. The effect of synovial fluid oxygen concentration, cell density, cartilage thickness, and influx of oxygen from the subchondral bone on the oxygen profile in the tissue was examined.Results. Oxygen consumption rates were relatively independent of oxygen tension at high oxygen tensions (5-21%), where they were ϳ10 nmoles/10 6 cells/hour for both isolated chondrocytes and for cartilage slices. Below 5% oxygen, the rate fell in an oxygen tension-dependent manner. Analysis showed that the oxygen profile across cartilage fell steeply in all but the thinnest cartilage samples but only fell to ϳ1% for low oxygen tensions in synovial fluid, with no supply from the subchondral bone. Conclusion.The oxygen tension in normal cartilage is not likely to fall to 1% except under abnormal conditions. Oxygen tensions within cartilage are strongly affected by a number of factors, including oxygen concentrations in synovial fluid, cartilage thickness, cell density, and cellular oxygen consumption rates. Supply from the subchondral bone may be of particular importance.

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Emerging role of metabolic signaling in synovial joint remodeling and osteoarthritis

June

Liu‐Bryan

Long

et al. 2016

Journal Orthopaedic Research

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Obesity and associated metabolic diseases collectively referred to as the metabolic syndrome increase the risk of skeletal and synovial joint diseases, including osteoarthritis (OA). The relationship between obesity and musculoskeletal diseases is complex, involving biomechanical, dietary, genetic, inflammatory, and metabolic factors. Recent findings illustrate how changes in cellular metabolism and metabolic signaling pathways alter skeletal development, remodeling, and homeostasis, especially in response to biomechanical and inflammatory stressors. Consequently, a better understanding of the energy metabolism of diarthrodial joint cells and tissues, including bone, cartilage, and synovium, may lead to new strategies to treat or prevent synovial joint diseases such as OA. This rationale was the basis of a workshop presented at the 2016 Annual ORS Meeting in Orlando, FL on the emerging role of metabolic signaling in synovial joint remodeling and OA. The topics we covered included (i) the relationship between metabolic syndrome and OA in clinical and pre-clinical studies, (ii) the effect of biomechanical loading on chondrocyte metabolism, (iii) the effect of Wnt signaling on osteoblast carbohydrate and amino acid metabolism with respect to bone anabolism, and (iv) the role of AMP-activated protein kinase in chondrocyte energetic and biomechanical stress responses in the context of cartilage injury, aging, and OA. Although challenges exist for measuring in vivo changes in synovial joint tissue metabolism, the findings presented herein provide multiple lines of evidence to support a central role for disrupted cellular energy metabolism in the pathogenesis of OA.

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

Cited by 30 publications

References 18 publications

Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

Factors influencing the oxygen concentration gradient from the synovial surface of articular cartilage to the cartilage–bone interface: A modeling study

Emerging role of metabolic signaling in synovial joint remodeling and osteoarthritis

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