Physiologic responses and plasma endothelin-1 concentrations associated with abrupt cessation of nitric oxide inhalation in isoflurane-anesthetized horses

Tamara L. Grubb Riverview Animal Clinic, 2002 Schultheis Rd, Uniontown, WA 99179.

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Marieann Högman Department of Medical Cell Biology: Integrative Physiology, Uppsala University, Uppsala, SE-751 05 Sweden.
Centre for Research and Development, Uppsala University/County Council of Gävleborg, Gävle, Sweden.

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Anna Edner Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, S-750 07 Sweden.

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Jan H. M. Frendin Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, S-750 07 Sweden.

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Erkki Heinonen Datex-Ohmeda, Kuortaneenkatu 2, 00510 Helsinki, Finland.

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Laís M. Malavasi Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, S-750 07 Sweden.

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Claes G. Frostell Department of Anaesthesia and Intensive Care, Karolinska Institute, Stockholm, S-171 77 Sweden.

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Anneli Ryden Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, S-750 07 Sweden.

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Kjell Alving Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, S-171 77 Sweden.

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Görel C. Nyman Department of Clinical Physiology, University Hospital, Uppsala, S-75 185 Sweden.

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Abstract

Objective—To assess physiologic responses and plasma endothelin (ET)-1 concentrations associated with abrupt cessation of nitric oxide (NO) inhalation in isoflurane-anesthetized horses.

Animals—6 healthy adult Standardbreds.

Procedures—Horses were anesthetized with isoflurane in oxygen and placed in dorsal recumbency. Nitric oxide was pulsed into the respiratory tract for 2.5 hours, and then administration was abruptly discontinued. Just prior to commencement and at cessation of NO administration, and at intervals during a 30-minute period following cessation of NO inhalation, several variables including PaO2, mean pulmonary artery pressure, venous admixture or pulmonary shunt fraction (Qs/Qt), and plasma ET-1 concentration were recorded or calculated.

Results—After cessation of NO inhalation, PaO2 decreased slowly but significantly (172.7 ± 29.8 mm Hg to 84.6 ± 10.9 mm Hg) and Qs/Qt increased slowly but significantly (25 ± 2% to 40 ± 3%) over a 30-minute period. Mean pulmonary artery pressure increased slightly (14.0 ± 1.3 mm Hg to 16.8 ± 1 mm Hg) over the same time period. No change in serum ET-1 concentration was detected, and other variables did not change or underwent minor changes.

Conclusions and Clinical Relevance—The improvement in arterial oxygenation during pulsed inhalation of NO to healthy isoflurane-anesthetized horses decreased only gradually during a 30-minute period following cessation of NO inhalation, and serum ET-1 concentration was not affected. Because a rapid rebound response did not develop, inhalation of NO might be clinically useful in the treatment of hypoxemia in healthy isoflurane-anesthetized horses.

Abstract

Objective—To assess physiologic responses and plasma endothelin (ET)-1 concentrations associated with abrupt cessation of nitric oxide (NO) inhalation in isoflurane-anesthetized horses.

Animals—6 healthy adult Standardbreds.

Procedures—Horses were anesthetized with isoflurane in oxygen and placed in dorsal recumbency. Nitric oxide was pulsed into the respiratory tract for 2.5 hours, and then administration was abruptly discontinued. Just prior to commencement and at cessation of NO administration, and at intervals during a 30-minute period following cessation of NO inhalation, several variables including PaO2, mean pulmonary artery pressure, venous admixture or pulmonary shunt fraction (Qs/Qt), and plasma ET-1 concentration were recorded or calculated.

Results—After cessation of NO inhalation, PaO2 decreased slowly but significantly (172.7 ± 29.8 mm Hg to 84.6 ± 10.9 mm Hg) and Qs/Qt increased slowly but significantly (25 ± 2% to 40 ± 3%) over a 30-minute period. Mean pulmonary artery pressure increased slightly (14.0 ± 1.3 mm Hg to 16.8 ± 1 mm Hg) over the same time period. No change in serum ET-1 concentration was detected, and other variables did not change or underwent minor changes.

Conclusions and Clinical Relevance—The improvement in arterial oxygenation during pulsed inhalation of NO to healthy isoflurane-anesthetized horses decreased only gradually during a 30-minute period following cessation of NO inhalation, and serum ET-1 concentration was not affected. Because a rapid rebound response did not develop, inhalation of NO might be clinically useful in the treatment of hypoxemia in healthy isoflurane-anesthetized horses.

Contributor Notes

Supported in part by grants from the AGA Gas Foundation.

Presented as an abstract at the World Congress of Veterinary Anesthesia, Knoxville, Tenn, September 2003.

The authors thank Karin Thulin and Kristina Karlström for laboratory assistance.

Address correspondence to Dr. Grubb.
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