PubMed Health⌕ Search

Biomedical subjects

F Y Lam

Publications and source records attributed to F Y Lam.

At least 19 recordsLinked to original sources
PubMed2005

Mechanisms of the vasorelaxant effect of Danshen (Salvia miltiorrhiza) in rat knee joints.

The aim of this study is to investigate the mechanisms of the vasorelaxant effect of the crude extract of Salvia miltiorrhiza (family: Labiatae), also known as "Danshen", in rat knee joints. Changes in blood flow of rat knee joints were measured in vivo by a laser Doppler perfusion imager. Topical administration of Danshen onto the exposed knee joint blood vessels produced dose-dependent increases in blood flow. Treatment of the rat knee joint with 2x 1 nmol of atropine, 2x 0.1 nmol of propranolol, or 2x 0.1 nmol of a mixture of pyrilamine plus cimitedine produced no change on the vasodilator response to Danshen. However, significant inhibition of the Danshen-induced vasodilator response was observed in knee joints treated with 2x 100 nmol of N(G)-nitro-L-arginine methyl ester (L-NAME), 2x 100 nmol of flurbiprofen, 2x 10 nmol of the calcitnonin gene-related peptide (CGRP) receptor antagonist CGRP(8-37), and also in knee joints but had been denervated by capsaicin treatment or by surgery. Intravenous administration of low doses of Danshen (2.5 and 6 mg/kg) did not affect the systemic blood pressure but significantly increased knee joint blood flow, whereas, high doses of Danshen (167 and 381 mg/kg) produced hypotension with concurrent decreases in knee joint blood flow. These findings indicate that the knee joint blood vessels are more sensitive to the relaxant effect of Danshen compared to blood vessels in the general circulation. The vasorelaxant effect of Danshen was found to be partly mediated by CGRP released from sensory nerves, and nitric oxide and prostaglandins also played a part. However, there is no evidence to support a role for muscarinic receptors, adrenoceptors, or histamine receptors.

Adrenergic beta-Antagonists↗
PubMed2000

Movement of the endotracheal tube during laparoscopic hernia repair.

BACKGROUND: Laparoscopic surgery is not without its problems, and one of the less known is cephalad displacement of the carina and relative movement of the endotracheal tube in the trachea. The aetiology of this is presumably a consequence of both pneumoperitoneum and the Trendelenburg position frequently adopted during laparoscopic surgery. METHOD: We studied 30 patients undergoing laparoscopic hernia repair utilising 10 degrees of Trendelenburg position and an intra-abdominal inflation pressure of between 12 and 15 mm Hg (mean 13.6 mm Hg). We measured the distance between the tip of the endotracheal tube and the carina using a fibreoptic bronchoscope. RESULT: This distance decreased only slightly, from a mean (SD) of 39.6 (13) mm after intubation, to 38.9 (12.6) mm after adoption of Trendelenburg tilt and pneumoperitoneum. This did not represent a statistically significant change (P=0.09). CONCLUSION: We conclude that the endotracheal tube does not routinely migrate towards the carina when laparoscopic hernia repair is performed under these conditions.

Adult↗
PubMed1996

The effect of meals of differing composition on exercise tolerance in patients with angina pectoris.

In this study we compared different dietary constituents and their effect on the angina threshold. We compared carbohydrate-rich, fat-rich and balanced liquid diets on effort tolerance in 14 patients of mean (range) 61 (41-73) years of age with chronic stable angina. On four different occasions at least 1 week apart, patients had exercise treadmill tests after an overnight fast and then after a rest period of 1 h ingested one of three different approximately isocalorific (about 4000 kJ) liquid drinks of 600 ml consisting mainly of: fat, carbohydrate or a balanced meal with an equal volume of water as control. Meals were given in random order. Analysis of the mean (SD) differences in heart rate between fasting and the post-prandial state for the different meals revealed a significant increase between water and the other meals, fat (+4(6) beats.min-1 P < 0.002), balanced (+9(17) beats.min-1 P < 0.004), and carbohydrate (+10(12) beats.min-1 P < 0.0002). There was no significant difference between the groups as regards systolic or diastolic blood pressure. Cardiac output increased following the meals but decreased after water; however, there was a significant difference between water and balanced meals. Exercise tolerance fell following all the meals but was significantly greater after a balanced (mean (SD) -108(129) s P < 0.01) and carbohydrate meal (-92(52) s P < 0.001). The reduction in exercise duration following a fat meal (-36(53)s) was not significantly different from that following water (-8(43) s) but was significantly smaller than after a carbohydrate meal (P < 0.02). Time to 1 mm of ST depression showed similar changes to that of total exercise duration, being significantly lower after a carbohydrate (mean (SD) -76(77) s P < 0.01) and balanced meal (-76(63) s P < 0.005). Time to 1 mm ST depression, although reduced by a fat meal (-15(84) s) was significantly less than after a carbohydrate meal (P < 0.02). In conclusion, patients with chronic stable angina have impaired effort tolerance and a lower angina threshold after high calorie containing liquid meals. Meals rich in carbohydrate have greater effects than meals where the majority of calories are derived from fat. Patients should be advised to avoid exercise in the first 30 min after eating.

Adult↗
PubMed1996

Characterization of tachykinin receptors mediating plasma extravasation and vasodilatation in normal and acutely inflamed knee joints of the rat.

1. Inflammatory actions of tachykinins in normal rat knee joints were compared with those of animals with acutely inflamed joints induced by intra-articular injection of 2% carrageenan. Plasma protein extravasation in rat knee joints, measured by protein micro-turbidimetry, was induced by intra-articular perfusion of selective tachykinin receptor agonists. Changes in joint blood flow, measured by laser Doppler perfusion imaging, were produced by topical applications of selective tachykinin receptor agonists to the joint capsule. 2. Carrageenan-injected rat knee joints showed significantly higher (P < 0.001) basal plasma extravasation (56 +/- 4 micrograms ml-1, n = 5) than normal rat knee joints (10 +/- 4 micrograms ml-1, n = 6). Intra-articular perfusion of the selective neurokinin1 (NK1) receptor agonist [Sar9, Met(O2)11]-substance P (0.8 nmol min-1) for 60 min elevated the basal plasma extravasation to 90 +/- 17 micrograms ml-1 (n = 6, P < 0.001) in normal joints, and to 150 +/- 14 micrograms ml-1 (n = 5, P < 0.001) in inflamed joints. Perfusion of the selective NK1 receptor antagonist N2-[(4R)-4-hydroxy-1-(1-methyl-1H- indol-3-yl)carbonyl-L-prolyl]-N-methyl-N-phenylmethyl-3-(2-naphthyl)- L-alaninamide (FK888; 0.8 nmol min-1) for 20 min followed by co-perfusion with the NK1 receptor agonist (0.8 nmol min-1) produced complete inhibition of the NK1 receptor agonist-induced plasma extravasation in the two groups of animals (for both groups; n = 3, P < 0.001). 3. Intra-articular perfusion of the selective NK receptor agonist [Nle10]-neurokinin A4-10 (0.8 nmol min-1) and the selective NK3 receptor agonist [MePhe7]-neurokinin B (0.8 nmol min1) produced no increase in plasma extravasation in normal or in inflamed rat knee joints (n = 4 and 11, P > 0.05). 4. Topical bolus applications of the NK1 receptor agonist [Sar9, Met(O2)11]-substance P onto normal joint capsules produced dose-dependent vasodilatation expressed as a voltage increase from control level. The maximum increase in blood flow was 2.05-0.21 V from a basal voltage of 3.42 +/- 0.07 V (n = 13, P < 0.001). To a much lesser extent, administration of the NK2 receptor agonist [Nle10]-neurokinin A4-10 also produced dose-dependent vasodilatation with maximum increase of 0.46 +/- 0.08 V from a basal level of 3.38 +/- 0.1 V (n = 7, P < 0.01). Animals with acutely inflamed joints showed enhanced vasodilator responses to the NK1 and NK2 receptor agonists (for both: P vs non-inflamed joints < 0.001). Thus, the NK1 and NK2 receptor agonists produced maximum increases of 2.56 +/- 0.19 V (basal level = 5.84 +/- 0.07 V; n = 7, P < 0.001) and 1.97 +/- 0.26 V (basal level = 6.31 +/- 0.23 V; n = 11, P < 0.001), respectively. The NK3 receptor agonist [MePhe7]-neurokinin B produced no change in blood flow in normal or in inflamed rat knee joints (n = 7 and 5, P > 0.05). 5. Bolus administration of the NK1 receptor antagonist FK888 (10 pmol) alone followed 5 min later by another dose of 10 pmol FK888 (i.e. total dose of 2 x 10 pmol) applied together with the NK1 receptor selective agonist [Sar9, Met(O2)11]-substance P produced partial, but significant inhibition of the NK1 receptor agonist-induced vasodilatation in both normal (maximum response reduced by 51.9 +/- 5.4%; n = 6, P < 0.001) and inflamed rat knee joints (maximum response reduced by 49.3 +/- 6.1%; n = 5, P < 0.001). The NK2 receptor agonist [Nle10]-neurokinin A4-10-induced vasodilator responses in inflamed joints were not affected by this treatment (n = 6, P > 0.05). However, with two higher doses of FK888 (both 1 nmol), the NK1 and the NK2 receptor agonist-induced vasodilator responses were abolished in the two groups of animals (n = 6-8, P < 0.005). 6. Administration of two doses of the selective NK2 receptor antagonist (S)-N-methyl-N-[4-acetylamino-4-phenylpiperidino)-2-(3,4-dichlorophenyl) -butyl]benzamide (SR48968;...

Animals↗
PubMed1994

Acute joint inflammation--mechanisms and mediators.

1. This review discusses factors contributing to acute joint inflammation, particularly sensory neuropeptides. 2. Mediators known to contribute importantly to the inflammatory process include cytokines, eicosanoids, complement and the kinin systems, histamine and 5-hydroxytryptamine and sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP). 3. The pro-inflammatory neurokinins, SP and CGRP, are present in nerves innervating joints and could significantly contribute to the increased vascular permeability and hyperaemia occurring in acute arthritis. 4. Although perhaps contributing to the pathogenesis of chronic inflammatory joint disease, there is little evidence for involvement of the sympathetic nervous system in acute models of inflammation.

Acute Disease↗
PubMed1994

A comparison of postoperative analgesia following spinal or epidural anaesthesia for caesarean section.

Postoperative analgesia, using a patient-controlled analgesia system, was studied in 32 women after elective Caesarean section performed under either spinal or epidural anaesthesia. Patients who had spinal anaesthesia had significantly higher pain scores and morphine consumption during the first 4 h postoperatively than patients who had epidural anaesthesia. This situation was reversed between 4 to 8 h postoperatively with patients who had had epidurals having significantly higher pain scores despite higher morphine consumption. After 8 h there was little difference in pain scores or morphine use between the two groups. Total morphine consumption in the first 24 h postoperatively was not significantly different between the two groups.

Analgesia, Patient-Controlled↗
PubMed1993

Acute inflammation in the rat knee joint attenuates sympathetic vasoconstriction but enhances neuropeptide-mediated vasodilatation assessed by laser Doppler perfusion imaging.

The effect of sympathetic nerve stimulation and topical application of substance P and calcitonin gene-related peptide on the blood flow of the exposed rat knee joint capsule was investigated. The responses of normal animals were compared to those of animals with acutely inflamed joints induced by intra-articular injection of 2% carrageenan. Laser Doppler perfusion imaging was used to examine the spatial distribution of blood flow in the knee joint capsule. Animals with acute joint inflammation showed markedly reduced vasoconstrictor responses to sympathetic nerve stimulation, but enhanced vasodilator responses to both substance P and calcitonin gene-related peptide when compared to normal. Prior application of either substance P or calcitonin gene-related peptide to the normal joint attenuated sympathetic vasoconstrictor responses. In the acutely inflamed knee, sympathetic vasoconstriction was replaced by a vasodilator response in the presence of neuropeptides. The reduced effectiveness of sympathetically mediated vasoconstriction and enhanced responsiveness to substance P and calcitonin gene-related peptide could contribute to the hyperaemia characteristic of inflamed joints.

Animals↗
PubMed1993

Effects of interactions of naturally-occurring neuropeptides on blood flow in the rat knee joint.

1. Changes of blood flow in the rat knee joint, measured by laser Doppler flowmetry, were produced by topical application of naturally-occurring neuropeptides to the joint capsule. 2. Substance P (SP), neurokinin A (NKA), and neurokinin B (NKB) all produced dose-dependent transient vasodilatation of the rat knee joint microvasculature. NKB showed significantly smaller vasodilator responses compared to SP and NKA which were similar in their potencies. 3. Calcitonin gene-related peptide (CGRP) produced dose-dependent vasodilatation which was more pronounced than that produced by the neurokinins. The rank order of potency was: CGRP > SP = NKA > NKB. The vasodilator effect of CGRP was also more prolonged and this extended phase was abolished by co-administration of SP. 4. Cross-tachyphylaxis was not observed with the different neurokinins, but SP and NKA showed novel antagonistic effects on NKB-induced vasodilatation. 5. Co-administration of 1 nmol of the specific NK1 receptor antagonist, CP-96345, with 1 nmol of each of the neurokinins produced significant inhibition of the vasodilator response to SP but did not affect vasodilator responses to NKA and NKB. Co-administration of CP-96345 with the neurokinins plus superfusion of the rat knee joint with a solution containing 0.1 mM CP-96345 further reduced the vasodilator responses to SP but again the vasodilator responses to NKA and NKB were not significantly altered. 6. The results suggest that multiple neurokinin receptor types may be present in the rat knee joint which could mediate the vasodilator responses of the different neurokinins. Co-release of neuropeptides from sensory nerve endings in the rat knee joint may have inter-regulatory actions on their individual responses on the microvasculature.

Animals↗
PubMed1992

Differences in the axon composition of nerves supplying the rat knee joint following intra-articular injection of capsaicin.

This study was used to examine the ultrastructure of articular nerves supplying the medial aspect of the rat knee joint following injection of capsaicin into the synovial cavity. One week after the intra-articular injection of 0.2 ml of 1% capsaicin solution there was significant reduction in the number of unmyelinated fibres. Two weeks post-injection this appeared to recover and by 4 weeks post-injection no further changes were observed. Myelinated fibres were unaffected by capsaicin injection. This procedure provides an effective means of producing short-term degeneration of unmyelinated fibres innervating the knee joint.

Animals↗
PubMed1992

Acute inflammation enhances substance P-induced plasma protein extravasation in the rat knee joint.

Acute inflammation of the rat knee joint was induced by intra-articular injection of 2% carrageenan. Intra-articular perfusion of the inflamed joint with substance P (SP) exacerbated the inflammatory condition as assessed by the degree of plasma protein extravasation into the synovial cavity. Protein extravasation induced by SP was enhanced and more persistent in the inflamed rat knee compared to normal animals. The time course of the response in the inflamed rat knee was related to SP concentration whilst the persistency of the response was positively correlated with the initial level of joint inflammation.

Animals↗
PubMed1991

Time course of substance P-induced protein extravasation in the rat knee joint measured by micro-turbidimetry.

Intra-articular perfusion of the rat knee joint with substance P (SP) resulted in protein extravasation into the synovial cavity. This response was tested over a range of SP concentrations from 100 pM to 100 microM. The response was dose dependent from 10 nM to 10 microM, with each dose producing a steady rise of the protein content in the fluid aspirated from the synovial cavity for 12-16 min and then fell sharply again over an equivalent period despite continuing perfusion with SP. Concentrations below 10 nM gave rise to very brief increases in protein extravasation whose magnitude differed little over the range of 100 pM to 10 nM but differed significantly from control (saline) perfusion.

Animals↗
PubMed1991

Specific neurokinin receptors mediate plasma extravasation in the rat knee joint.

1 Plasma extravasation in the rat knee joint was induced by intra-articular injection of neurokinins and specific neurokinin receptor agonists. 2 Pronounced plasma extravasation was produced by substance P (SP, 4-185 microM) and to a lesser extent by neurokinin-B (NKB, 83-413 microM), whereas neurokinin-A (NKA, 88-440 microM) and calcitonin gene-related peptide (CGRP, 26-130 microM) had no significant effect. 3 The specific neurokinin1 receptor agonist [Sar9, Met(O2)11]-substance P (NK1 agonist) in doses of 0.4-70 microM appeared to be more potent than SP in eliciting plasma extravasation. The neurokinin2 receptor agonist [Nle10]-neurokinin A4-10 (NK2 agonist) was not effective at 70 microM but produced a small and significant effect at 330 microM, whereas the neurokinin3 receptor agonist [MePhe7]-neurokinin B (NK3 agonist) was without effect at 40 microM or 400 microM. 4 Injections of SP or NKA into the synovial cavity of the rat knee were equally effective in producing marked plasma extravasation in remote sites such as the forelimb and hindlimb paws. 5 Co-administration experiments showed that the effects of SP were synergistic with NKA or the NK1 receptor agonist, but not with CGRP or the NK2 receptor agonist. 6 The rank order of potency was NK1 agonist greater than or equal to SP greater than NKB greater than NK2 agonist suggesting that NK1 receptors mediate plasma extravasation in the rat knee joint.

Animals↗
PubMed1991

Neurogenic component of different models of acute inflammation in the rat knee joint.

This study was performed to investigate whether different models of acute joint inflammation showed a neurogenic component and to establish whether this is mediated through sensory afferent or sympathetic efferent nerve fibres. Intra-articular injection of 2% carrageenan, 20 micrograms substance P, 1% formalin, and 2% urate all produced an inflammatory response. Prior surgical denervation of the joint significantly inhibited this response in the carrageenan and formalin models, but not the others. Pretreatment of the joint with 1% capsaicin (about one week previously) significantly reduced the inflammatory response in all models except formalin. In animals pretreated long term with reserpine (to deplete sympathetic nerve endings of their neurotransmitters) significant reductions occurred in the inflammatory responses to substance P and urate. Intraarticular injection of compound 48/80 produced a marked inflammatory response, which was only significantly reduced by capsaicin pretreatment. These results suggest that both the formalin and carrageenan models of inflammation depend to some extent on the integrity of the sensory innervation of the joint, and thus have a neurogenically mediated component to the inflammatory process they generate. In these models there seems to be little contribution from sympathetic efferent fibres. Each model of inflammation showed a different pattern of response to the pretreatments, suggesting that the mediators of the inflammatory process may differ in each case.

Animals↗
PubMed1990

Mediators of substance P-induced inflammation in the rat knee joint.

Substance P (SP) injected into the synovial cavity of the rat knee resulted in an inflammatory response as measured by plasma protein extravasation into the joint capsule. This response was dose dependent over the range of approximately 4 microM to approximately 200 microM. Part of this inflammatory response was mediated via mast cells as pre-treatment of the animals with a mast cell degranulator (compound 48/80) resulted in a 66% reduction of the response. A direct effect of SP on the vascular receptors may also contribute to the inflammatory response as pre-treatment with the substance P antagonist (SPA) D-Pro4 D-Trp7,9,10 SP4-11 also reduces the inflammatory response. Intra-articular injections of the H1 blocker diphenhydramine or the H2 blocker cimetidine significantly blocked the SP-induced inflammatory response. The 5-hydroxytryptamine (5-HT) antagonist methysergide proved to be even more potent in blocking the SP-induced inflammatory response. No synergistic inhibition was observed with combinations of the different antagonists. Intra-articular injections of 5-HT elicited a much more pronounced inflammatory response than that produced by a 10-fold higher concentration of histamine. The results suggest that SP produces increased vascular permeability partly via direct actions on the blood vessels and partly via mast cells. The inflammatory response occurring via mast cells appears to be mediated by histamine and to a greater extent by 5-HT.

Animals↗
PubMed1989

Capsaicin suppresses substance P-induced joint inflammation in the rat.

Intra-articular injection of 20 micrograms substance P in rat knee joints results in a pronounced inflammatory response. However, prior intra-articular injection of 1% capsaicin solution (1-5 weeks previously) virtually abolishes this response. This is not a neurotoxic effect of capsaicin on nerve fibres as denervation of the knee produces no alteration of the response to injected substance P. The potent effect of capsaicin on substance P-mediated inflammation cannot be attributed to depletion of mast cells by this treatment as the mast cell degranulator compound 48/80 injected into capsaicin pre-treated knees still gives rise to a marked inflammatory response. Compound 48/80 does not activate nerve fibres to cause release of substance P as it is equally effective in eliciting an inflammatory response in the presence of 100 micrograms of the substance P antagonist D-Pro4, D-Trp7,9,10 SP(4-11) in the synovial cavity. The results suggest that capsaicin may act by depleting substance P receptors in joint tissue.

Animals↗