Jacob Johnsen

Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Standard

Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning. / Hauerslev, Marie; Mørk, Sivagowry Rasalingam; Pryds, Kasper; Contractor, Hussain; Hansen, Jan; Jespersen, Nichlas Riise; Johnsen, Jacob; Heusch, Gerd; Kleinbongard, Petra; Kharbanda, Rajesh; Bøtker, Hans Erik; Schmidt, Michael Rahbek.

I: American Journal of Physiology - Heart and Circulatory Physiology, Bind 315, Nr. 1, 01.07.2018, s. H150-H158.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Hauerslev, M, Mørk, SR, Pryds, K, Contractor, H, Hansen, J, Jespersen, NR, Johnsen, J, Heusch, G, Kleinbongard, P, Kharbanda, R, Bøtker, HE & Schmidt, MR 2018, 'Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning', American Journal of Physiology - Heart and Circulatory Physiology, bind 315, nr. 1, s. H150-H158. https://doi.org/10.1152/ajpheart.00114.2018

APA

Hauerslev, M., Mørk, S. R., Pryds, K., Contractor, H., Hansen, J., Jespersen, N. R., Johnsen, J., Heusch, G., Kleinbongard, P., Kharbanda, R., Bøtker, H. E., & Schmidt, M. R. (2018). Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning. American Journal of Physiology - Heart and Circulatory Physiology, 315(1), H150-H158. https://doi.org/10.1152/ajpheart.00114.2018

CBE

Hauerslev M, Mørk SR, Pryds K, Contractor H, Hansen J, Jespersen NR, Johnsen J, Heusch G, Kleinbongard P, Kharbanda R, Bøtker HE, Schmidt MR. 2018. Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning. American Journal of Physiology - Heart and Circulatory Physiology. 315(1):H150-H158. https://doi.org/10.1152/ajpheart.00114.2018

MLA

Hauerslev, Marie o.a.. "Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning". American Journal of Physiology - Heart and Circulatory Physiology. 2018, 315(1). H150-H158. https://doi.org/10.1152/ajpheart.00114.2018

Vancouver

Author

Hauerslev, Marie ; Mørk, Sivagowry Rasalingam ; Pryds, Kasper ; Contractor, Hussain ; Hansen, Jan ; Jespersen, Nichlas Riise ; Johnsen, Jacob ; Heusch, Gerd ; Kleinbongard, Petra ; Kharbanda, Rajesh ; Bøtker, Hans Erik ; Schmidt, Michael Rahbek. / Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning. I: American Journal of Physiology - Heart and Circulatory Physiology. 2018 ; Bind 315, Nr. 1. s. H150-H158.

Bibtex

@article{1e7f7da19076430eb9668da639fe5dcf,
title = "Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning",
abstract = "Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. Due to overlapping mechanisms this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. We investigated whether long-term GTN treatment modifies the protection by RIC in rat myocardium and human endothelium. We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. In addition to allocated treatment, rats were co-administered with reactive oxygen species (ROS) or nitric oxide (NO) scavengers. Rats and humans were randomized to: 1) control, 2) RIC, 3) GTN, 4) GTN + RIC. In protocols 3 and 4, rats and humans underwent long-term GTN treatment for 7 consecutive days, applied s.c. or 2 hours daily transdermally. In rats, RIC and long-term GTN treatment reduced mean IS (18{plus minus}12%, p=0.007) and (15{plus minus}5%, p=0.002) compared to control (35{plus minus}13%). RIC and long-term GTN treatment in combination did not reduce IS (29{plus minus}12%, p=0.55 vs. control). ROS and NO scavengers both attenuated IS reduction by RIC and long-term GTN treatment. In humans, I/R reduced endothelial function (p=0.01 vs. baseline). Separately, RIC and long-term GTN prevented the reduction in endothelial function caused by I/R; given in combination, prevention was lost. RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO dependent mechanisms. However, when given in combination, RIC and long-term GTN treatment fail to confer protection.",
author = "Marie Hauerslev and M{\o}rk, {Sivagowry Rasalingam} and Kasper Pryds and Hussain Contractor and Jan Hansen and Jespersen, {Nichlas Riise} and Jacob Johnsen and Gerd Heusch and Petra Kleinbongard and Rajesh Kharbanda and B{\o}tker, {Hans Erik} and Schmidt, {Michael Rahbek}",
year = "2018",
month = jul,
day = "1",
doi = "10.1152/ajpheart.00114.2018",
language = "English",
volume = "315",
pages = "H150--H158",
journal = "A J P: Heart and Circulatory Physiology (Online)",
issn = "1522-1539",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning

AU - Hauerslev, Marie

AU - Mørk, Sivagowry Rasalingam

AU - Pryds, Kasper

AU - Contractor, Hussain

AU - Hansen, Jan

AU - Jespersen, Nichlas Riise

AU - Johnsen, Jacob

AU - Heusch, Gerd

AU - Kleinbongard, Petra

AU - Kharbanda, Rajesh

AU - Bøtker, Hans Erik

AU - Schmidt, Michael Rahbek

PY - 2018/7/1

Y1 - 2018/7/1

N2 - Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. Due to overlapping mechanisms this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. We investigated whether long-term GTN treatment modifies the protection by RIC in rat myocardium and human endothelium. We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. In addition to allocated treatment, rats were co-administered with reactive oxygen species (ROS) or nitric oxide (NO) scavengers. Rats and humans were randomized to: 1) control, 2) RIC, 3) GTN, 4) GTN + RIC. In protocols 3 and 4, rats and humans underwent long-term GTN treatment for 7 consecutive days, applied s.c. or 2 hours daily transdermally. In rats, RIC and long-term GTN treatment reduced mean IS (18{plus minus}12%, p=0.007) and (15{plus minus}5%, p=0.002) compared to control (35{plus minus}13%). RIC and long-term GTN treatment in combination did not reduce IS (29{plus minus}12%, p=0.55 vs. control). ROS and NO scavengers both attenuated IS reduction by RIC and long-term GTN treatment. In humans, I/R reduced endothelial function (p=0.01 vs. baseline). Separately, RIC and long-term GTN prevented the reduction in endothelial function caused by I/R; given in combination, prevention was lost. RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO dependent mechanisms. However, when given in combination, RIC and long-term GTN treatment fail to confer protection.

AB - Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. Due to overlapping mechanisms this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. We investigated whether long-term GTN treatment modifies the protection by RIC in rat myocardium and human endothelium. We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. In addition to allocated treatment, rats were co-administered with reactive oxygen species (ROS) or nitric oxide (NO) scavengers. Rats and humans were randomized to: 1) control, 2) RIC, 3) GTN, 4) GTN + RIC. In protocols 3 and 4, rats and humans underwent long-term GTN treatment for 7 consecutive days, applied s.c. or 2 hours daily transdermally. In rats, RIC and long-term GTN treatment reduced mean IS (18{plus minus}12%, p=0.007) and (15{plus minus}5%, p=0.002) compared to control (35{plus minus}13%). RIC and long-term GTN treatment in combination did not reduce IS (29{plus minus}12%, p=0.55 vs. control). ROS and NO scavengers both attenuated IS reduction by RIC and long-term GTN treatment. In humans, I/R reduced endothelial function (p=0.01 vs. baseline). Separately, RIC and long-term GTN prevented the reduction in endothelial function caused by I/R; given in combination, prevention was lost. RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO dependent mechanisms. However, when given in combination, RIC and long-term GTN treatment fail to confer protection.

U2 - 10.1152/ajpheart.00114.2018

DO - 10.1152/ajpheart.00114.2018

M3 - Journal article

C2 - 29569958

VL - 315

SP - H150-H158

JO - A J P: Heart and Circulatory Physiology (Online)

JF - A J P: Heart and Circulatory Physiology (Online)

SN - 1522-1539

IS - 1

ER -