Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model

Takeshi Adachi, Shingo Hori, Koji Miyazaki, Masahiro Nakagawa, Soshin Inoue, Yozo Ohnishi, Hiroe Nakazawa, Naoki Aikawa, Satoshi Ogawa

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

In hemorrhagic shock (HS), nitric oxide synthase (NOS) inhibitor is known to increase blood pressure and prolong survival time. On the other hand, NOS inhibitor decreases coronary flow and worsens myocardial ischemia. Therefore, we hypothesized that the beneficial effect of NOS inhibitor is attributable to the increased coronary perfusion pressure and that it outcompetes the coronary vasodilating effects of nitric oxide. To investigate the direct effect of NOS inhibitor on the regulation of coronary circulation and the induction of myocardial ischemia in HS, we used a canine model at a constant aortic pressure of 40 mmHg with an aortic reservoir. In seven dogs, intravenous administration of Nω-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg) at 10 min after induction of HS increased both systemic and coronary vascular resistances and further increased the serum catecholamine concentration at 10 min after L-NAME. In another 14 dogs, the beating hearts were rapidly cross-sectioned (120 ms) and freeze clamped (-190°C) by a specially developed sampling device after 10 min of HS. Transmurally distributed myocardial ischemia was visualized by the enhanced reduced nicotinamide adenine dinucleotide fluorescence, which was significantly increased with L-NAME (n = 7). Chemical analysis revealed a decrease in the myocardial ATP concentration with L-NAME in the subendocardial ischemic region in HS. In conclusion, with the use of an aortic reservoir to keep the aortic pressure constant in HS, NOS blockade significantly worsened myocardial ischemia by decreasing coronary flow and augmenting the serum catecholamine concentration.

Original languageEnglish
Pages (from-to)204-209
Number of pages6
JournalShock
Volume9
Issue number3
Publication statusPublished - 1998 Mar

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Hemorrhagic Shock
Myocardial Ischemia
Nitric Oxide
Nitric Oxide Synthase
NG-Nitroarginine Methyl Ester
Pressure
Catecholamines
Arterial Pressure
Dogs
Coronary Circulation
Serum
Intravenous Administration
Vascular Resistance
NAD
Canidae
Perfusion
Adenosine Triphosphate
Fluorescence
Blood Pressure
Equipment and Supplies

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Adachi, T., Hori, S., Miyazaki, K., Nakagawa, M., Inoue, S., Ohnishi, Y., ... Ogawa, S. (1998). Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model. Shock, 9(3), 204-209.

Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model. / Adachi, Takeshi; Hori, Shingo; Miyazaki, Koji; Nakagawa, Masahiro; Inoue, Soshin; Ohnishi, Yozo; Nakazawa, Hiroe; Aikawa, Naoki; Ogawa, Satoshi.

In: Shock, Vol. 9, No. 3, 03.1998, p. 204-209.

Research output: Contribution to journalArticle

Adachi, T, Hori, S, Miyazaki, K, Nakagawa, M, Inoue, S, Ohnishi, Y, Nakazawa, H, Aikawa, N & Ogawa, S 1998, 'Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model', Shock, vol. 9, no. 3, pp. 204-209.
Adachi T, Hori S, Miyazaki K, Nakagawa M, Inoue S, Ohnishi Y et al. Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model. Shock. 1998 Mar;9(3):204-209.
Adachi, Takeshi ; Hori, Shingo ; Miyazaki, Koji ; Nakagawa, Masahiro ; Inoue, Soshin ; Ohnishi, Yozo ; Nakazawa, Hiroe ; Aikawa, Naoki ; Ogawa, Satoshi. / Inhibition of nitric oxide synthesis aggravates myocardial ischemia in hemorrhagic shock in constant pressure model. In: Shock. 1998 ; Vol. 9, No. 3. pp. 204-209.
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