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Korean Journal of Anesthesiology 1978;11(1):39-48.
DOI: https://doi.org/10.4097/kjae.1978.11.1.39   
The Effect of Halothane-induced Hypotention on the Kidney.
Yong Taek Nam, Hee Jeon Lee, Kwang Won Park, Sang Sup Chung, Jong Woong Doh, Sun Ok Song, Yang Saeng Park
1Department of Anesthesiology, Yonsei University College of Medicine, Seoul, Korea.
2Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Korea.
3Department of Physiology, Yonsei University College of Medicine, Seoul, Korea.
Hypotensive anesthesia is widely used in an operation since 1) it minimizes bleeding and provides a good operation field, 2) it prevents massive hemorrhage in an operation which otherwise involves a large amount of b1ood loss and 3) it is useful in an operation for hypertensive patients. This procedure also involves a number of risks such as delayed awakening, reactionary bleeding, decrease in urine output and tissue hypoxia. The most dangerous complication can be hypoxia especially in the vital organs. 1t is therefore necessary to treat dehydration or blood loss before hypotensive anesthesia is induced. Since hypotensive anesthesia was introduced by Gardner (1947) for an operation of olfactory groove meningioma, various methods of deliberate hypotension have been developed. The most common method of hypotensive anesthesia in the present day is to use drugs, such as trmetaphan, nitroprusside and halothane. The effect of hypotensive anesthesia an various physiological functions of animals have been investigated is the past. Giffiths and Gillies (1948) reported that, in the hypotension induced by sympathectomy, an arterial systolic pressure of 32 mmHg is the minimum to overcome peripheral resistance. Chung (19743 observed in the halothane-induced hypotensive dogs that a systolic pressure of 30mmHg was required to assure adequate cerebral oxygenation. In the present study, we have investigated the effect of halothanie-induced hypotension on the renal function of dogs. The arterial systolic pressure was successively reduced to 60 and 30mmHg for 30min. each, and changes is various renal functions were studied during 100min. of the recovery period. The results are summarized as follows: 1. The systolic blood pressure was completely reeovered 80min. after the cessation of halothane inhalation. 2. Average renal blood flow Cestimated by Cppe) and glomerular filtration rate (estimated by Cg) during the first 20min. of the recovery phase were 26% ind 45% of the control level. However after 100min. of thy recovery period, repal blood flow was recovered to 63% and glomerular filtration rate to 74%of the control leveL 3. Average urine flow during the first 20min. of that recovery phase was approximately 40% of the control. 4. U/P osm. ratio was reduced to 90% the control level during the first 20min. of recovery, but it exceeded the control value after 20min. of recovery. 5. Thero was only 24% of the-tml value in the first 20min. of receavery phese, but there- after it gradually returned to the control level. 6. FEH2O (fractional excretion of N2) was and significantly changed- by halothane inhalation although there was a tendency to slight reduction at the beginning of the recovery phase. 7. FEK was 47% of the control value dqring ghe initial phase of recovery, but it returned to the control level after 40min. of the recovery period. 8. FE, and FEH2O were reduced to 56% and 50% of the control level after the hypotensive period, but returned to 70% and 82% of the control level after 40min. of the recovery period. These results indicate that although the systemic blood pressure completely recovered after halothane-induced hypotension, renal hemodynamics are not completely recovered with 100min. of the recovery period. However renal functions are mostly reversible, suggesting that halathane -induced hypotension did not induce irreversible damage of renal tissue.
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