To maintain the adequate cerebral blood flow ana tissue perfusion to the vital organs is crucial during hypotensive anesthesia. Enflurane maintains the myocardial contractility better than halothane because of increased beta-sympathetic activity and inhibition of aortic baroreceptor activity, and sodium nitroprnsside(SNP) that commonly used as a vasodilator during hypotensive anesthesia also has the tendency to increase the heart rate and to maintain the cardiac output. Therefore induced hypotensive anesthesia using enflurane with SNP seems to be different from the halothane with SNP anesthesia in terms hemodynamic changes.
The purpose of this study was to investigate whether enflurane anesthesia with SNP used in induced hypotension has the similar effects as has been described in halothane anesthesia with SNP.
In fifteen mongrel dogs with supine position, anesthesia was induced using 15mg/kg of thiopental sodium, and then endotracheal intubation was performed without succinylcholine. Heart rate, cardiac output, central venous pressure, pulmonary capillary wedge pressure and pulmonary artery mean pressure were measured and stroke volume, systemic vascular resistance and pulmonary vascular resistance were calculated during IPPV with 100% oxygen(Ⅰ), 30 minutes after anesthesia with 2.0% enflurane-100%O₂(Ⅱ), one minute after enflurane-O₂ anesthesia with 2.0㎍/kg/min SNP(Ⅲ), three minutes after(Ⅳ), and five minutes after enflurane-O₂-SNP anesthesia(Ⅴ).
The results were as follows:
1. Heart rate was decreased significantly from 162±7.0/min in Ⅰ to 146±5.7/min in Ⅴ, which was reduced by 9.9% (P<0.05).
2. Mean arterial pressure was decreased progressively from 105.7±5.70mmHg in Ⅰ to 56.1±6.90mmHg in Ⅴ, which was reduced very significantly by 46.9%(P<0.005).
3. Cardiac output was decreased significantly from 2.05±0.41 ℓ/min in Ⅰ to 1.65±0.12 ℓ/min Ⅴ, which was reduced by 19.5%(P<0.05).
4. Pulmonary capillary wedge pressure was 3.7±0.42mmHg in Ⅰ, but it was increased to 4.5±0.56mmHg in Ⅱ and to 4.0±0.73mmHg in Ⅲ. Level of Ⅲ was maintained in Ⅳ an4 Ⅴ.
5. Systemic vascular resistance was decreased significantly from 62.7±14.36mmHg/ℓ/min in Ⅰ to 32.7±2.38mmHg/ℓ/min in Ⅴ, which was reduced by 47.8%(p<0.01).
It is concluded that enflurane anesthesia has the tendency to maintain cardiac output and SNP also has the same effect on cardiac output although it decrease MAP, but enflurane anesthesia with SNP infusion brings about marked decrease in arterial pressure and moderate decrease in cardiac output.
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