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S M Cobbe - One of the best experts on this subject based on the ideXlab platform.

  • increase in plasma beta endorphins precedes vasodepressor syncope
    Heart, 1994
    Co-Authors: D R Wallbridge, H E Macintyre, C E Gray, M Denvir, Keith G Oldroyd, Alan P Rae, S M Cobbe
    Abstract:

    BACKGROUND--Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS--To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS--24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING--Tertiary referral centre. METHODS--Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS--Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION--An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

  • Increase in plasma beta endorphins precedes vasodepressor syncope.
    British heart journal, 1994
    Co-Authors: D R Wallbridge, H E Macintyre, C E Gray, M Denvir, Keith G Oldroyd, Alan P Rae, S M Cobbe
    Abstract:

    Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. 24 patients undergoing tilt testing for investigation of unexplained syncope. Tertiary referral centre. Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

Virgilio Gallai - One of the best experts on this subject based on the ideXlab platform.

  • study of pressure pain and cellular concentration of neurotransmitters related to nociception in episodic tension type headache patients
    Headache, 1997
    Co-Authors: Giovanni Mazzotta, Paola Sarchielli, Alessandro Gaggioli, Virgilio Gallai
    Abstract:

    : The pressure pain threshold of 30 patients affected by tension-type headache was assessed and the values compared with those of a group of 30 age-matched control subjects. In the patient group, pressure pain threshold values were related to the blood cell concentration of some neurotransmitters which are considered to be involved in the genesis and modulation of pain (Beta-Endorphin levels in peripheral blood mononuclear cells [PBMCs], substance P and serotonin concentrations in platelets). The pressure pain threshold was significantly lower in tension-type headache patients than in control subjects (P < 0.0006). Significantly lower levels of Beta-Endorphins in PBMCs and substance P in platelets, as well as significantly higher levels of serotonin in platelets were found in tension-type headache patients compared to the control subjects (P < 0.0001). A significant positive correlation was found between pressure pain threshold values and Beta-Endorphin levels in both control and patient groups (P < 0.0001). On the contrary, a statistically significant negative correlation was evident between pressure pain threshold values and substance P levels in platelets in both patients and control subjects (P < 0.01 and P < 0.001, respectively). In both groups, there was a negative correlation between Beta-Endorphins in PBMCs and substance P in platelets (patients P < 0.02, controls P < 0.001). The findings of altered Beta-Endorphin levels in blood mononuclear cells and substance P levels in platelets could be the peripheral biochemical reflection of the low pressure pain threshold values in tension-type headache patients, and support the hypothesis of an impairment of the antinociceptive systems in this form of headache.

  • Study of Pressure Pain and Cellular Concentration of Neurotransmitters Related to Nociception in Episodic Tension‐Type Headache Patients
    Headache, 1997
    Co-Authors: Giovanni Mazzotta, Paola Sarchielli, Alessandro Gaggioli, Virgilio Gallai
    Abstract:

    The pressure pain threshold of 30 patients affected by tension-type headache was assessed and the values compared with those of a group of 30 age-matched control subjects. In the patient group, pressure pain threshold values were related to the blood cell concentration of some neurotransmitters which are considered to be involved in the genesis and modulation of pain (Beta-Endorphin levels in peripheral blood mononuclear cells [PBMCs], substance P and serotonin concentrations in platelets). The pressure pain threshold was significantly lower in tension-type headache patients than in control subjects (P < 0.0006). Significantly lower levels of Beta-Endorphins in PBMCs and substance P in platelets, as well as significantly higher levels of serotonin in platelets were found in tension-type headache patients compared to the control subjects (P < 0.0001). A significant positive correlation was found between pressure pain threshold values and Beta-Endorphin levels in both control and patient groups (P < 0.0001). On the contrary, a statistically significant negative correlation was evident between pressure pain threshold values and substance P levels in platelets in both patients and control subjects (P < 0.01 and P < 0.001, respectively). In both groups, there was a negative correlation between Beta-Endorphins in PBMCs and substance P in platelets (patients P < 0.02, controls P < 0.001). The findings of altered Beta-Endorphin levels in blood mononuclear cells and substance P levels in platelets could be the peripheral biochemical reflection of the low pressure pain threshold values in tension-type headache patients, and support the hypothesis of an impairment of the antinociceptive systems in this form of headache.

D R Wallbridge - One of the best experts on this subject based on the ideXlab platform.

  • increase in plasma beta endorphins precedes vasodepressor syncope
    Heart, 1994
    Co-Authors: D R Wallbridge, H E Macintyre, C E Gray, M Denvir, Keith G Oldroyd, Alan P Rae, S M Cobbe
    Abstract:

    BACKGROUND--Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS--To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS--24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING--Tertiary referral centre. METHODS--Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS--Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION--An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

  • Increase in plasma beta endorphins precedes vasodepressor syncope.
    British heart journal, 1994
    Co-Authors: D R Wallbridge, H E Macintyre, C E Gray, M Denvir, Keith G Oldroyd, Alan P Rae, S M Cobbe
    Abstract:

    Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. 24 patients undergoing tilt testing for investigation of unexplained syncope. Tertiary referral centre. Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

Giovanni Mazzotta - One of the best experts on this subject based on the ideXlab platform.

  • study of pressure pain and cellular concentration of neurotransmitters related to nociception in episodic tension type headache patients
    Headache, 1997
    Co-Authors: Giovanni Mazzotta, Paola Sarchielli, Alessandro Gaggioli, Virgilio Gallai
    Abstract:

    : The pressure pain threshold of 30 patients affected by tension-type headache was assessed and the values compared with those of a group of 30 age-matched control subjects. In the patient group, pressure pain threshold values were related to the blood cell concentration of some neurotransmitters which are considered to be involved in the genesis and modulation of pain (Beta-Endorphin levels in peripheral blood mononuclear cells [PBMCs], substance P and serotonin concentrations in platelets). The pressure pain threshold was significantly lower in tension-type headache patients than in control subjects (P < 0.0006). Significantly lower levels of Beta-Endorphins in PBMCs and substance P in platelets, as well as significantly higher levels of serotonin in platelets were found in tension-type headache patients compared to the control subjects (P < 0.0001). A significant positive correlation was found between pressure pain threshold values and Beta-Endorphin levels in both control and patient groups (P < 0.0001). On the contrary, a statistically significant negative correlation was evident between pressure pain threshold values and substance P levels in platelets in both patients and control subjects (P < 0.01 and P < 0.001, respectively). In both groups, there was a negative correlation between Beta-Endorphins in PBMCs and substance P in platelets (patients P < 0.02, controls P < 0.001). The findings of altered Beta-Endorphin levels in blood mononuclear cells and substance P levels in platelets could be the peripheral biochemical reflection of the low pressure pain threshold values in tension-type headache patients, and support the hypothesis of an impairment of the antinociceptive systems in this form of headache.

  • Study of Pressure Pain and Cellular Concentration of Neurotransmitters Related to Nociception in Episodic Tension‐Type Headache Patients
    Headache, 1997
    Co-Authors: Giovanni Mazzotta, Paola Sarchielli, Alessandro Gaggioli, Virgilio Gallai
    Abstract:

    The pressure pain threshold of 30 patients affected by tension-type headache was assessed and the values compared with those of a group of 30 age-matched control subjects. In the patient group, pressure pain threshold values were related to the blood cell concentration of some neurotransmitters which are considered to be involved in the genesis and modulation of pain (Beta-Endorphin levels in peripheral blood mononuclear cells [PBMCs], substance P and serotonin concentrations in platelets). The pressure pain threshold was significantly lower in tension-type headache patients than in control subjects (P < 0.0006). Significantly lower levels of Beta-Endorphins in PBMCs and substance P in platelets, as well as significantly higher levels of serotonin in platelets were found in tension-type headache patients compared to the control subjects (P < 0.0001). A significant positive correlation was found between pressure pain threshold values and Beta-Endorphin levels in both control and patient groups (P < 0.0001). On the contrary, a statistically significant negative correlation was evident between pressure pain threshold values and substance P levels in platelets in both patients and control subjects (P < 0.01 and P < 0.001, respectively). In both groups, there was a negative correlation between Beta-Endorphins in PBMCs and substance P in platelets (patients P < 0.02, controls P < 0.001). The findings of altered Beta-Endorphin levels in blood mononuclear cells and substance P levels in platelets could be the peripheral biochemical reflection of the low pressure pain threshold values in tension-type headache patients, and support the hypothesis of an impairment of the antinociceptive systems in this form of headache.

G Flik - One of the best experts on this subject based on the ideXlab platform.

  • identification of beta endorphins in the pituitary gland and blood plasma of the common carp cyprinus carpio
    Journal of Endocrinology, 2001
    Co-Authors: E H Van Den Burg, Juriaan R Metz, R J Arends, Bart Devreese, Isabel Vandenberghe, J Van Beeumen, S Wendelaar E Bonga, G Flik
    Abstract:

    Carp Beta-Endorphin is posttranslationally modified by N-terminal acetylation and C-terminal cleavage. These processes determine the biological activity of the Beta-Endorphins. Forms of Beta-Endorphin were identified in the pars intermedia and the pars distalis of the pituitary gland of the common carp (Cyprinus carpio), as well as the forms released in vitro and into the blood. After separation and quantitation by high performance liquid chromatography (HPLC) coupled with radioimmunoassay, the Beta-Endorphin immunoreactive products were identified by electrospray ionisation mass spectrometry and peptide sequencing. The release of Beta-Endorphins by the pituitary gland was studied after stimulation with corticotrophin-releasing factor (CRF) in vitro. In the pars intermedia, eight N-acetylated truncated forms were identified. Full length N-acetyl Beta-Endorphin(1-33) coeluted with N-acetyl Beta-Endorphin(1-29) and these forms together amounted to over 50% of total immunoreactivity. These products were partially processed to N-acetyl betaendorphin(1-15) (30.8% of total immunoreactivity) and N-acetyl Beta-Endorphin(1-10) (3.1%) via two different cleavage pathways. The acetylated carp homologues of mammalian alpha- and gamma-endorphin were also found. N-acetyl Beta-Endorphin(1-15) and (1-29) and/or (1-33) were the major products to be released in vitro, and were the only acetylated Beta-Endorphins found in blood plasma, although never together. CRF stimulated the release of opioid Beta-Endorphin from the pars distalis. This non-acetylated Beta-Endorphin represents the full length peptide and is the most abundant form in plasma.