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FRI0366 A pilot study on ischemia and reperfusion injury during a raynaud's attack: sequential assessment of redox stress parameters in a unique cooling and rewarming experiment

FRI0366 A pilot study on ischemia and reperfusion injury during a raynaud's attack: sequential assessment of redox stress parameters in a unique cooling and rewarming experiment
FRI0366 A pilot study on ischemia and reperfusion injury during a raynaud's attack: sequential assessment of redox stress parameters in a unique cooling and rewarming experiment
Background: Oxidative stress plays a role in systemic sclerosis (SSc), but the molecular mechanisms involved are incompletely understood. During an attack of Raynaud's phenomenon (RP) a period of ischemia (I), followed by reperfusion (R) occurs frequently, associated with the severity of vasculopathy. [1] Only in secondary RP digital ulcers develop. We hypothesized that I/R injury may play a role in the pathogenesis and could offer new therapeutic targets.

Objectives: To explore the course of oxidative stress in patients with SSc compared with primary RP and healthy controls.

Methods: A total of 30 patients were included: 10 with limited cutaneous SSc (age: 57 (53–61) yr, male/female 5/5), 10 with primary RP (age: 54 (41–58), 2/8), and 10 healthy controls (age: 25 (22–25), 3/7). A standardized cooling experiment was performed and digital perfusion was assessed in all 5 fingers using photo-electric plethysmography: at baseline (T=0) the dominant hand was submerged in water at 33°C, followed by cooling in steps of 3°C every 4 minutes, until 6°C or when pain became intolerable (T=1). Recording was continued 10 (T=2) and 30 (T=3) minutes of rewarming to ambient temperature (23°C). Blood was drawn from ipsilateral cubital vein at T0, 1, 2 and 3, markers for tissue injury (lactate, LDH, creatinine phosphokinase (CPK) [routine methods]), redox status (free thiols corrected for total protein) and nitric oxide (NO) activity (NO2–, NO3–, RXNO) were measured in plasma. [1–3] Numbers are in median (IQR).

Results: Baseline free thiols were significantly decreased in RP vs. controls (5.18 (4.79–5.63) vs 5.87 (5.41–5.99) umol/g, p=0.013), with no differences in lactate, LDH, CPK, and NO activity. Raynaud's attack was induced in all RP patients but not in controls. Median duration of hypoperfusion was greater in SSc vs. PRP (30 (27–35) vs. 12 (9–14) min, p=0.010), with a considerably longer recovery time (8 (4–10) vs. 0 (0–1) min, p=0.006). No changes were observed in lactate, LDH, and CPK levels. A rise in free thiols occurred at recovery (T4) in all 3 groups (figure 1). The concentrations of NO-related products did not change during cooling or recovery. No association was detected between the extent of I/R and plasma parameters.
0003-4967
625-626
Van Roon, A. M.
8caab310-5af8-4b8b-b44c-f90aefa13281
Abdulle, A. Eman
9b1327da-4063-445c-abcf-d2a27a932be1
van Roon, A. M.
8caab310-5af8-4b8b-b44c-f90aefa13281
Lefrandt, J. D.
e6e9bcf5-b6f4-4c47-84dc-dd01889bd410
Smit, A.J.
dacc2abc-a1fa-4851-a095-40248251fc61
Bootsma, H.
68e80d3d-657b-4c7c-9690-77f3af70c0b6
Fernandez, B.O.
9890aabc-1fe6-4530-a51e-31182e537131
Minnion, M.
ab23b32b-9f8e-4876-aaf5-99cb6a725a2f
Feelisch, M.
8c1b9965-8614-4e85-b2c6-458a2e17eafd
van Goor, H.
fadc9a49-233e-40c3-9e05-8713ffbc02e5
Mulder, D.J.
5bc391e2-d754-431b-bef9-083c17cb5304
Van Roon, A. M.
8caab310-5af8-4b8b-b44c-f90aefa13281
Abdulle, A. Eman
9b1327da-4063-445c-abcf-d2a27a932be1
van Roon, A. M.
8caab310-5af8-4b8b-b44c-f90aefa13281
Lefrandt, J. D.
e6e9bcf5-b6f4-4c47-84dc-dd01889bd410
Smit, A.J.
dacc2abc-a1fa-4851-a095-40248251fc61
Bootsma, H.
68e80d3d-657b-4c7c-9690-77f3af70c0b6
Fernandez, B.O.
9890aabc-1fe6-4530-a51e-31182e537131
Minnion, M.
ab23b32b-9f8e-4876-aaf5-99cb6a725a2f
Feelisch, M.
8c1b9965-8614-4e85-b2c6-458a2e17eafd
van Goor, H.
fadc9a49-233e-40c3-9e05-8713ffbc02e5
Mulder, D.J.
5bc391e2-d754-431b-bef9-083c17cb5304

Van Roon, A. M., Abdulle, A. Eman, van Roon, A. M., Lefrandt, J. D., Smit, A.J., Bootsma, H., Fernandez, B.O., Minnion, M., Feelisch, M., van Goor, H. and Mulder, D.J. (2017) FRI0366 A pilot study on ischemia and reperfusion injury during a raynaud's attack: sequential assessment of redox stress parameters in a unique cooling and rewarming experiment. Annals of the Rheumatic Diseases, 76 (2), 625-626. (doi:10.1136/annrheumdis-2017-eular.5972).

Record type: Article

Abstract

Background: Oxidative stress plays a role in systemic sclerosis (SSc), but the molecular mechanisms involved are incompletely understood. During an attack of Raynaud's phenomenon (RP) a period of ischemia (I), followed by reperfusion (R) occurs frequently, associated with the severity of vasculopathy. [1] Only in secondary RP digital ulcers develop. We hypothesized that I/R injury may play a role in the pathogenesis and could offer new therapeutic targets.

Objectives: To explore the course of oxidative stress in patients with SSc compared with primary RP and healthy controls.

Methods: A total of 30 patients were included: 10 with limited cutaneous SSc (age: 57 (53–61) yr, male/female 5/5), 10 with primary RP (age: 54 (41–58), 2/8), and 10 healthy controls (age: 25 (22–25), 3/7). A standardized cooling experiment was performed and digital perfusion was assessed in all 5 fingers using photo-electric plethysmography: at baseline (T=0) the dominant hand was submerged in water at 33°C, followed by cooling in steps of 3°C every 4 minutes, until 6°C or when pain became intolerable (T=1). Recording was continued 10 (T=2) and 30 (T=3) minutes of rewarming to ambient temperature (23°C). Blood was drawn from ipsilateral cubital vein at T0, 1, 2 and 3, markers for tissue injury (lactate, LDH, creatinine phosphokinase (CPK) [routine methods]), redox status (free thiols corrected for total protein) and nitric oxide (NO) activity (NO2–, NO3–, RXNO) were measured in plasma. [1–3] Numbers are in median (IQR).

Results: Baseline free thiols were significantly decreased in RP vs. controls (5.18 (4.79–5.63) vs 5.87 (5.41–5.99) umol/g, p=0.013), with no differences in lactate, LDH, CPK, and NO activity. Raynaud's attack was induced in all RP patients but not in controls. Median duration of hypoperfusion was greater in SSc vs. PRP (30 (27–35) vs. 12 (9–14) min, p=0.010), with a considerably longer recovery time (8 (4–10) vs. 0 (0–1) min, p=0.006). No changes were observed in lactate, LDH, and CPK levels. A rise in free thiols occurred at recovery (T4) in all 3 groups (figure 1). The concentrations of NO-related products did not change during cooling or recovery. No association was detected between the extent of I/R and plasma parameters.

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More information

Published date: 15 June 2017
Additional Information: Annual European Congress of Rheumatology, Madrid, SPAIN, JUN 14-17, 2017

Identifiers

Local EPrints ID: 447309
URI: http://eprints.soton.ac.uk/id/eprint/447309
ISSN: 0003-4967
PURE UUID: 1f4e1d97-9927-4f15-9d06-620b3725c6ff
ORCID for B.O. Fernandez: ORCID iD orcid.org/0000-0001-6337-0381
ORCID for M. Feelisch: ORCID iD orcid.org/0000-0003-2320-1158

Catalogue record

Date deposited: 09 Mar 2021 17:31
Last modified: 10 Mar 2021 02:43

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Contributors

Author: A. M. Van Roon
Author: A. Eman Abdulle
Author: A. M. van Roon
Author: J. D. Lefrandt
Author: A.J. Smit
Author: H. Bootsma
Author: B.O. Fernandez ORCID iD
Author: M. Minnion
Author: M. Feelisch ORCID iD
Author: H. van Goor
Author: D.J. Mulder

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