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)
Objective—To determine concentrations of α-tocopherol in serum and CSF of healthy horses following administration of supplemental vitamin E in feed.
Animals—10 healthy adult horses.
Procedures—Horses were allocated to receive supplemental d-α-tocopherol (1,000 U/d [group A; n = 5] or 10,000 U/d [group B; 5]) in feed for 10 days. Blood samples were collected before (baseline), during, and at intervals for 10 days after discontinuation of vitamin E administration for assessment of serum α-tocopherol concentration. Cerebrospinal fluid samples were collected prior to and 24 hours after cessation of vitamin E administration. α-Tocopherol concentrations in serum and CSF samples were analyzed via high-performance liquid chromatography; changes in those values during the treatment period were compared between groups, and the relationship of serum and CSF α-tocopherol concentrations was evaluated.
Results—In both groups, serum α-tocopherol concentration increased significantly from baseline during vitamin E administration; values in group B were significantly greater than those in group A during and after treatment. At the end of vitamin E administration, CSF α-tocopherol concentration was not significantly greater than the baseline value in either group; however, the increase in CSF concentration was significant when the group data were combined and analyzed. Serum and CSF α-tocopherol concentrations were significantly correlated at baseline for all horses, but were not strongly correlated after 10 days of vitamin E administration.
Conclusions and Clinical Relevance—In healthy horses, daily oral administration of supplemental vitamin E in feed resulted in increases in serum and CSF α-tocopherol concentrations.