Objective—To quantitate the effects of desflurane
and mode of ventilation on cardiovascular and respiratory
functions and identify changes in selected clinicopathologic
variables and serum fluoride values
associated with desflurane anesthesia in horses.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized on 2 occasions:
first, to determine the minimum alveolar concentration
(MAC) of desflurane in O2 and second, to
characterize cardiopulmonary and clinicopathologic
responses to 1×, 1.5×, and 1.75× desflurane MAC during
both controlled and spontaneous ventilation.
Results—Mean ± SEM MAC of desflurane in horses
was 8.06 ± 0.41%; inhalation of desflurane did not
appear to cause airway irritation. During spontaneous
ventilation, mean PaCO2 was 69 mm Hg.
Arterial blood pressure, stroke volume, and cardiac
output decreased as the dose of desflurane
increased. Conditions of intermittent positive pressure
ventilation and eucapnia resulted in further cardiovascular
depression. Horses recovered quickly
from anesthesia with little transient or no clinicopathologic
evidence of adverse effects. Serum fluoride
concentration before and after administration of
desflurane was below the limit of detection of
0.05 ppm (2.63µM/L).
Conclusions and Clinical Relevance—Results indicate
that desflurane, like other inhalation anesthetics,
causes profound hypoventilation in horses. The
magnitude of cardiovascular depression is related to
dose and mode of ventilation; cardiovascular depression
is less severe at doses of 1× to 1.5× MAC, compared
with known effects of other inhalation anesthetics
under similar conditions. Desflurane is not
metabolized to an important degree and does not
appear to prominently influence renal function or
hepatic cellular integrity or function. ( Am J Vet Res 2005;66:669–677)
Objective—To quantitate effects of dose of sevoflurane
and mode of ventilation on cardiovascular and
respiratory function in horses and identify changes in
serum biochemical values associated with sevoflurane
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized twice: first, to
determine the minimum alveolar concentration (MAC)
of sevoflurane and second, to characterize cardiopulmonary
and serum biochemical responses of horses
to 1.0, 1.5, and 1.75 MAC multiples of sevoflurane during
controlled and spontaneous ventilation.
Results—Mean (± SEM) MAC of sevoflurane was
2.84 ± 0.16%. Cardiovascular performance during
anesthesia decreased as sevoflurane dose
increased; the magnitude of cardiovascular depression
was more severe during mechanical ventilation,
compared with spontaneous ventilation.
Serum inorganic fluoride concentration increased to
a peak of 50.8 ± 7.1 µmol/L at the end of anesthesia.
Serum creatinine concentration and sorbitol
dehydrogenase activity reached their greatest values
(2.0 ± 0.8 mg/dL and 10.2 ± 1.8 U/L, respectively)
at 1 hour after anesthesia and then returned
to baseline by 1 day after anesthesia. Serum creatine
kinase, aspartate aminotransferase, and alkaline
phosphatase activities reached peak values by
the first (ie, creatine kinase) or second (ie, aspartate
aminotransferase and alkaline phosphatase) day
Conclusions and Clinical Relevance—Sevoflurane
causes dose-related cardiopulmonary depression,
and mode of ventilation further impacts the magnitude
of this depression. Except for serum inorganic
fluoride concentration, quantitative alterations in
serum biochemical indices of liver- and muscle-cell
disruption and kidney function were considered clinically
unremarkable and similar to results from comparable
studies of other inhalation anesthetics. (Am J Vet Res 2005;66:606–614)