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Nitric Oxide Impairs the Recovery from Hemorrhagic Hypotension in Conscious Rats

Park, Yoon-Yub   (Department of Physiology, School of Medicine, Catholic University of Taegu-HyosungUU0013933  ); Lee, Young-Man   (Department of Physiology, School of Medicine, Catholic University of Taegu-HyosungUU0013933  );
  • 초록

    The role of nitric oxide (NO) in the hemorrhagic hypotension was examined using a NO synthase inhibitor, $N^{\omega}-nitro-L-arginine$ methyl ester (L-NAME), in conscious rats. The rats were bled at a constant rate (2 ml/kg/min) through a femoral arterial catheter until the mean arterial pressure (MAP) was reduced by 50 mmHg. We studied the responses to hemorrhage under normal condition (Control) and after the pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6, NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME produced a sustained increase in MAP and decrease in heart rate (HR). During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated groups than in Control group, but the control group showed same response to NOX1.6. HR greatly increased in NOX groups. The recovery from hemorrhagic hypotension was slowed in the control group, which was not treated with L-NAME. In comparison with the control group, NOX8 and NOX1.6-treated groups registered a significant recovery in MAP during the 15 min recovery period, but NOX40 brought about only a slight increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced significant bradycardic responses before and after hemorrhage and significant depressor response only after hemorrhagic hypotension regardless of pretreatment with L-NAME. These data suggest that the role of NO in blood pressure regulation is greater after hemorrhagic hypotension than basal condition, but the effect of NO can be detrimental to the recovery from hemorrhagic hypotension. In addition, the bradycardic response of L-arginine provides indirect evidence that NO may inhibit sympathetic activity, especially after hemorrhagic hypotension.


  • 주제어

    hemorrhagic hypotension .   nitric oxide .   L-NAME .   L-arginine.  

 저자의 다른 논문

  • Park, Yoon-Yub (8)

    1. 1998 "Effect of the Inhibition of Platelet Activating Factor on Oxidative Lung Injury Induced by Interleukin-$1\;{\alpha}$" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2 (4): 479~491    
    2. 1998 "Effect of the Inhibition of PLA2 on Oxidative Lung Injury Induced by $Interleukin-1{\alpha}$" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2 (5): 617~628    
    3. 1999 "Effect of the Inhibition of Phospholipase $A_2$ in Generation of Free Radicals in Intestinal Ischemia/Reperfusion Induced Acute Lung Injury" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 3 (3): 263~273    
    4. 1999 "PAF Contributes to Intestinal Ischemia/Reperfusion-Induced Acute Lung Injury through Neutrophilic Oxidative Stress" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 3 (4): 405~414    
    5. 2000 "호중구의 Respiratory Burst에 미치는 PLA2 및 PAF와 영향 : In vitro에서의 호중구의 산소기 생성 및 Apoptosis에 관한 연구" 결핵 및 호흡기 질환 = Tuberculosis and respiratory diseases 48 (6): 887~897    
    6. 2009 "Ischemia/reperfusion Lung Injury Increases Serum Ferritin and Heme Oxygenase-1 in Rats" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 13 (3): 181~187    
    7. 2010 "Role of the PLA2-Activated Neutrophilic Oxidative Stress in Oleic Acid-Induced Acute Lung Injury" Tuberculosis and respiratory diseases : TRD = 결핵 및 호흡기 질환 68 (2): 55~61    
    8. 2010 "The Intracisternal Administration of MEK Inhibitor Attenuates Mechanical and Cold Allodynia in a Rat Model of Compression of the Trigeminal Ganglion" International journal of oral biology : official journal of the Korean Academy of Oral Biology and the UCLA Dental Research Institute 35 (3): 75~81    

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