Inhibition of endothelium-derived relaxing factor enhances myocardial stunning in conscious dogs

Naoyuki Hasebe, You Tang Shen, Stephen Vatner

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

Background. Impaired endothelial-dependent vascular responses after coronary artery occlusion (CAO) and reperfusion (CAR) have been investigated extensively. However, it is not known whether impaired endogenous endothelium-derived relaxing factor production affects postischemic myocardial dysfunction, ie, myocardial stunning. Methods and Results. Eight dogs were instrumented with an intracoronary catheter and an hydraulic occluder on the left circumflex coronary artery. The effects of a 10-minute CAO randomized with and without intracoronary administration of NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor, were compared in the same conscious dogs. Postischemic regional contractile dysfunction in subendocardial and subepicardial as well as transmural wall thickening was measured with ultrasonic dimension crystals, and myocardial blood flow was measured with radioactive microspheres. Intracoronary infusion of L-NA did not affect systemic hemodynamics, and transmural myocardial blood flow was reduced slightly (-8%), but significantly, only in the left circumflex territory. The recovery of wall thickening was significantly delayed in the presence of L-NA compared with the absence of L-NA, eg, at 30-minute CAR, not only in the subendocardium (-76±9% versus -49±9%) but also in the subepicardium (-52±8% versus -29±7%). During CAO, blood flow was decreased identically in both conditions, and during CAR, the differences in blood flow were minor (7%). Conclusions. Inhibition of NO synthesis enhanced myocardial stunning transmurally in conscious dogs, potentially independent of its effects on blood flow.

Original languageEnglish (US)
Pages (from-to)2862-2871
Number of pages10
JournalCirculation
Volume88
Issue number6
DOIs
StatePublished - Jan 1 1993
Externally publishedYes

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Myocardial Stunning
Endothelium-Dependent Relaxing Factors
Dogs
Coronary Occlusion
Coronary Vessels
Reperfusion
Nitric Oxide
Myocardial Reperfusion
Nitroarginine
Microspheres
Ultrasonics
Blood Vessels
Catheters
Hemodynamics

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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title = "Inhibition of endothelium-derived relaxing factor enhances myocardial stunning in conscious dogs",
abstract = "Background. Impaired endothelial-dependent vascular responses after coronary artery occlusion (CAO) and reperfusion (CAR) have been investigated extensively. However, it is not known whether impaired endogenous endothelium-derived relaxing factor production affects postischemic myocardial dysfunction, ie, myocardial stunning. Methods and Results. Eight dogs were instrumented with an intracoronary catheter and an hydraulic occluder on the left circumflex coronary artery. The effects of a 10-minute CAO randomized with and without intracoronary administration of NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor, were compared in the same conscious dogs. Postischemic regional contractile dysfunction in subendocardial and subepicardial as well as transmural wall thickening was measured with ultrasonic dimension crystals, and myocardial blood flow was measured with radioactive microspheres. Intracoronary infusion of L-NA did not affect systemic hemodynamics, and transmural myocardial blood flow was reduced slightly (-8{\%}), but significantly, only in the left circumflex territory. The recovery of wall thickening was significantly delayed in the presence of L-NA compared with the absence of L-NA, eg, at 30-minute CAR, not only in the subendocardium (-76±9{\%} versus -49±9{\%}) but also in the subepicardium (-52±8{\%} versus -29±7{\%}). During CAO, blood flow was decreased identically in both conditions, and during CAR, the differences in blood flow were minor (7{\%}). Conclusions. Inhibition of NO synthesis enhanced myocardial stunning transmurally in conscious dogs, potentially independent of its effects on blood flow.",
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Inhibition of endothelium-derived relaxing factor enhances myocardial stunning in conscious dogs. / Hasebe, Naoyuki; Shen, You Tang; Vatner, Stephen.

In: Circulation, Vol. 88, No. 6, 01.01.1993, p. 2862-2871.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inhibition of endothelium-derived relaxing factor enhances myocardial stunning in conscious dogs

AU - Hasebe, Naoyuki

AU - Shen, You Tang

AU - Vatner, Stephen

PY - 1993/1/1

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N2 - Background. Impaired endothelial-dependent vascular responses after coronary artery occlusion (CAO) and reperfusion (CAR) have been investigated extensively. However, it is not known whether impaired endogenous endothelium-derived relaxing factor production affects postischemic myocardial dysfunction, ie, myocardial stunning. Methods and Results. Eight dogs were instrumented with an intracoronary catheter and an hydraulic occluder on the left circumflex coronary artery. The effects of a 10-minute CAO randomized with and without intracoronary administration of NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor, were compared in the same conscious dogs. Postischemic regional contractile dysfunction in subendocardial and subepicardial as well as transmural wall thickening was measured with ultrasonic dimension crystals, and myocardial blood flow was measured with radioactive microspheres. Intracoronary infusion of L-NA did not affect systemic hemodynamics, and transmural myocardial blood flow was reduced slightly (-8%), but significantly, only in the left circumflex territory. The recovery of wall thickening was significantly delayed in the presence of L-NA compared with the absence of L-NA, eg, at 30-minute CAR, not only in the subendocardium (-76±9% versus -49±9%) but also in the subepicardium (-52±8% versus -29±7%). During CAO, blood flow was decreased identically in both conditions, and during CAR, the differences in blood flow were minor (7%). Conclusions. Inhibition of NO synthesis enhanced myocardial stunning transmurally in conscious dogs, potentially independent of its effects on blood flow.

AB - Background. Impaired endothelial-dependent vascular responses after coronary artery occlusion (CAO) and reperfusion (CAR) have been investigated extensively. However, it is not known whether impaired endogenous endothelium-derived relaxing factor production affects postischemic myocardial dysfunction, ie, myocardial stunning. Methods and Results. Eight dogs were instrumented with an intracoronary catheter and an hydraulic occluder on the left circumflex coronary artery. The effects of a 10-minute CAO randomized with and without intracoronary administration of NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor, were compared in the same conscious dogs. Postischemic regional contractile dysfunction in subendocardial and subepicardial as well as transmural wall thickening was measured with ultrasonic dimension crystals, and myocardial blood flow was measured with radioactive microspheres. Intracoronary infusion of L-NA did not affect systemic hemodynamics, and transmural myocardial blood flow was reduced slightly (-8%), but significantly, only in the left circumflex territory. The recovery of wall thickening was significantly delayed in the presence of L-NA compared with the absence of L-NA, eg, at 30-minute CAR, not only in the subendocardium (-76±9% versus -49±9%) but also in the subepicardium (-52±8% versus -29±7%). During CAO, blood flow was decreased identically in both conditions, and during CAR, the differences in blood flow were minor (7%). Conclusions. Inhibition of NO synthesis enhanced myocardial stunning transmurally in conscious dogs, potentially independent of its effects on blood flow.

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