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Korean Journal of Anesthesiology 2003;44(1):103-110.
DOI: https://doi.org/10.4097/kjae.2003.44.1.103   
The Effect of Inhaled Nitric Oxide on Protamine Sulfate-Induced Hypotension in Dogs.
Kyung Yeon Yoo, Cheol Won Jeong, Sang Hyun Kwak, Myung Ha Yoon
Department of Anesthesiology, Chonnam National University Medical School, Gwangju, Korea. kyyoo@chonnam.ac.kr
Protamine sulfate has been found to produce systemic hypotension secondary to acute pulmonary vasoconstriction and subsequent right heart failure in pigs and sheep. Nitric oxide (NO) is a potent pulmonary vasodilator. The present study was aimed to determine whether NO inhalation prevents hypotension in an open-chest canine model.
With IRB approval, 29 mongrel dogs were acutely instrumented during 1.5% enflurane anesthesia. All animals then received protamine 3 mg/kg over 30 s given through right atrium, 5 min after heparin (300 IU/kg, iv). NO inhalation was done for 20 min beginning 10 min before protamine infusion (NO group, n = 10). Control group was without NO inhalation (n = 19), which was retrospectively divided into two groups according to the magnitude of pulmonary arterial pressure (PAP) increase: normal PAP group (increase in PAP less than 6 mmHg, n = 9) and pulmonary hypertensive group (increase in PAP more than 6 mmHg, n = 10). Mean arterial pressure (MAP), PAP, left ventricular end-diastolic pressure (LVEDP), heart rate (HR), and cardiac output and left circumflex (LCX) coronary flow via a Doppler flowmeter were continuously monitored. Calculated parameters included cardiac index (CI), and systemic and pulmonary vascular resistance indices (SVRI and PVRI).
Protamine increased PAP (66 vs 7%) and PVRI (5.1- vs 3.0- fold) more pronouncedly in pulmonary hypertensive than in normal group. However, protamine caused similar reductions of MAP (-40 vs -46%), CI (-60 vs -59%), and LVEDP (-47 vs -53%) in pulmonary hypertensive and normal groups. SVRI showed a biphasic response in both groups, an initial decrease (-15 vs -14%), followed by an increase (48 vs 25%, P<0.05). Continuous inhalation of NO at 80 ppm did not affect the protamine-induced reductions in MAP (-40%), CI (-55%), and LVEDP (-46%) and increases in PAP (45%) and PVRI (4.1-fold). LCX flow increased immediately after the protamine treatment in all groups to a similar magnitude (83-130%), indicating a rapid release of potent vasodilators.
Protamine produces profound hypotension, which may not be causally related to an acute pulmonary vasoconstriction in the dog. It is unlikely that exogenous NO treatment affects hypotension.
Key Words: Dog; hypotension; nitric oxide; protamine sulfate


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