The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

Joji Inamasu, Keiko Sugimoto, Yasuhiro Yamada, Tsukasa Ganaha, Keisuke Ito, Takeya Watabe, Takuro Hayashi, Yoko Kato, Yukio Ozaki, Yuichi Hirose

Research output: Contribution to journalReview article

26 Citations (Scopus)

Abstract

Background Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/ norepinephrine) has been suggested as its principal cause. The objective of this retrospective study is to evaluate the relative contribution of each catecholamine in the pathogenesis of NPE associated with SAH. Methods Records of 63 SAH patients (20 men/43 women) whose plasma catecholamine levels were measured within 48 h of SAH onset were reviewed, and the clinical characteristics and laboratory data of those who developed earlyonset NPE were analyzed thoroughly. Results Seven patients (11 %) were diagnosed with NPE on admission. Demographic comparison revealed that the NPE + group sustained more severe SAH than the NPE- group. Cardiac dysfunction was also significantly more profound in the former, and the great majority of the NPE+ group sustained concomitant cardiac wall motion abnormality. There was no significant difference in the plasma epinephrine levels between NPE+ and NPE- group (324.6±172.8 vs 163.1±257.2 pg/ml, p00.11). By contrast, plasma norepinephrine levels were significantly higher in the NPE+ group (2977.6±2034.5 vs 847.9±535.6 pg/ml, p<0.001). Multivariate regression analysis revealed that increased norepinephrine levels were associated with NPE (OR, 1.003; 95 % CI, 1.002-1.007). Plasma epinephrine and norepinephrine levels were positively correlated (R00.48, p< 0.001). According to receiver operating characteristic curve analysis, the threshold value for plasma norepinephrine predictive of NPE was 2,000 pg/ml, with an area under the curve value of 0.85. Conclusions Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.

Original languageEnglish
Pages (from-to)2179-2184
Number of pages6
JournalActa Neurochirurgica
Volume154
Issue number12
DOIs
Publication statusPublished - 01-12-2012

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Pulmonary Edema
Subarachnoid Hemorrhage
Catecholamines
Norepinephrine
Epinephrine
ROC Curve
Area Under Curve
Multivariate Analysis
Retrospective Studies
Regression Analysis
Demography

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology

Cite this

Inamasu, Joji ; Sugimoto, Keiko ; Yamada, Yasuhiro ; Ganaha, Tsukasa ; Ito, Keisuke ; Watabe, Takeya ; Hayashi, Takuro ; Kato, Yoko ; Ozaki, Yukio ; Hirose, Yuichi. / The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage. In: Acta Neurochirurgica. 2012 ; Vol. 154, No. 12. pp. 2179-2184.
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abstract = "Background Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/ norepinephrine) has been suggested as its principal cause. The objective of this retrospective study is to evaluate the relative contribution of each catecholamine in the pathogenesis of NPE associated with SAH. Methods Records of 63 SAH patients (20 men/43 women) whose plasma catecholamine levels were measured within 48 h of SAH onset were reviewed, and the clinical characteristics and laboratory data of those who developed earlyonset NPE were analyzed thoroughly. Results Seven patients (11 {\%}) were diagnosed with NPE on admission. Demographic comparison revealed that the NPE + group sustained more severe SAH than the NPE- group. Cardiac dysfunction was also significantly more profound in the former, and the great majority of the NPE+ group sustained concomitant cardiac wall motion abnormality. There was no significant difference in the plasma epinephrine levels between NPE+ and NPE- group (324.6±172.8 vs 163.1±257.2 pg/ml, p00.11). By contrast, plasma norepinephrine levels were significantly higher in the NPE+ group (2977.6±2034.5 vs 847.9±535.6 pg/ml, p<0.001). Multivariate regression analysis revealed that increased norepinephrine levels were associated with NPE (OR, 1.003; 95 {\%} CI, 1.002-1.007). Plasma epinephrine and norepinephrine levels were positively correlated (R00.48, p< 0.001). According to receiver operating characteristic curve analysis, the threshold value for plasma norepinephrine predictive of NPE was 2,000 pg/ml, with an area under the curve value of 0.85. Conclusions Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.",
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The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage. / Inamasu, Joji; Sugimoto, Keiko; Yamada, Yasuhiro; Ganaha, Tsukasa; Ito, Keisuke; Watabe, Takeya; Hayashi, Takuro; Kato, Yoko; Ozaki, Yukio; Hirose, Yuichi.

In: Acta Neurochirurgica, Vol. 154, No. 12, 01.12.2012, p. 2179-2184.

Research output: Contribution to journalReview article

TY - JOUR

T1 - The role of catecholamines in the pathogenesis of neurogenic pulmonary edema associated with subarachnoid hemorrhage

AU - Inamasu, Joji

AU - Sugimoto, Keiko

AU - Yamada, Yasuhiro

AU - Ganaha, Tsukasa

AU - Ito, Keisuke

AU - Watabe, Takeya

AU - Hayashi, Takuro

AU - Kato, Yoko

AU - Ozaki, Yukio

AU - Hirose, Yuichi

PY - 2012/12/1

Y1 - 2012/12/1

N2 - Background Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/ norepinephrine) has been suggested as its principal cause. The objective of this retrospective study is to evaluate the relative contribution of each catecholamine in the pathogenesis of NPE associated with SAH. Methods Records of 63 SAH patients (20 men/43 women) whose plasma catecholamine levels were measured within 48 h of SAH onset were reviewed, and the clinical characteristics and laboratory data of those who developed earlyonset NPE were analyzed thoroughly. Results Seven patients (11 %) were diagnosed with NPE on admission. Demographic comparison revealed that the NPE + group sustained more severe SAH than the NPE- group. Cardiac dysfunction was also significantly more profound in the former, and the great majority of the NPE+ group sustained concomitant cardiac wall motion abnormality. There was no significant difference in the plasma epinephrine levels between NPE+ and NPE- group (324.6±172.8 vs 163.1±257.2 pg/ml, p00.11). By contrast, plasma norepinephrine levels were significantly higher in the NPE+ group (2977.6±2034.5 vs 847.9±535.6 pg/ml, p<0.001). Multivariate regression analysis revealed that increased norepinephrine levels were associated with NPE (OR, 1.003; 95 % CI, 1.002-1.007). Plasma epinephrine and norepinephrine levels were positively correlated (R00.48, p< 0.001). According to receiver operating characteristic curve analysis, the threshold value for plasma norepinephrine predictive of NPE was 2,000 pg/ml, with an area under the curve value of 0.85. Conclusions Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.

AB - Background Neurogenic pulmonary edema (NPE) occurs frequently after aneurysmal subarachnoid hemorrhage (SAH), and excessive release of catecholamines (epinephrine/ norepinephrine) has been suggested as its principal cause. The objective of this retrospective study is to evaluate the relative contribution of each catecholamine in the pathogenesis of NPE associated with SAH. Methods Records of 63 SAH patients (20 men/43 women) whose plasma catecholamine levels were measured within 48 h of SAH onset were reviewed, and the clinical characteristics and laboratory data of those who developed earlyonset NPE were analyzed thoroughly. Results Seven patients (11 %) were diagnosed with NPE on admission. Demographic comparison revealed that the NPE + group sustained more severe SAH than the NPE- group. Cardiac dysfunction was also significantly more profound in the former, and the great majority of the NPE+ group sustained concomitant cardiac wall motion abnormality. There was no significant difference in the plasma epinephrine levels between NPE+ and NPE- group (324.6±172.8 vs 163.1±257.2 pg/ml, p00.11). By contrast, plasma norepinephrine levels were significantly higher in the NPE+ group (2977.6±2034.5 vs 847.9±535.6 pg/ml, p<0.001). Multivariate regression analysis revealed that increased norepinephrine levels were associated with NPE (OR, 1.003; 95 % CI, 1.002-1.007). Plasma epinephrine and norepinephrine levels were positively correlated (R00.48, p< 0.001). According to receiver operating characteristic curve analysis, the threshold value for plasma norepinephrine predictive of NPE was 2,000 pg/ml, with an area under the curve value of 0.85. Conclusions Elevated plasma norepinephrine may have more active role in the pathogenesis of SAH-induced NPE compared with epinephrine, although both catecholamines may be involved via multiple signaling pathways.

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