OBJECTIVE To evaluate the mRNA expression of T helper (Th)1, Th2, and Th17 cell–associated inflammatory mediators in cells of bronchoalveolar lavage fluid samples collected from healthy horses exposed to hyperbaric oxygen (HBO) and to monitor blood oxygen concentration during and following HBO therapy. ANIMALS 8 healthy horses. PROCEDURES In a randomized controlled crossover design study, each horse was exposed (beginning day 1) to 100% oxygen at a maximum of 3 atmospheres absolute (304 kPa) daily for 10 days or ambient air at atmospheric pressure in the HBO chamber for an equivalent amount of time (control). Bronchoalveolar lavage fluid samples were collected on days 0 and 10. After validation of candidate reference genes, relative mRNA expressions of various innate inflammatory, Th1 cell–derived, Th2 cell–derived (including eotaxin-2), Th17 cell–derived, and regulatory cytokines were measured by quantitative PCR assays. For 3 horses, arterial blood samples were collected for blood gas analysis during a separate HBO session. RESULTS The optimal combination of reference genes was glyceraldehyde-3-phosphate dehydrogenase, hypoxanthine ribosyltransferase, and ribosomal protein L32. Compared with day 0 findings, expression of eotaxin-2 mRNA was significantly lower (0.12-fold reduction) and the percentage of neutrophils in bronchoalveolar lavage fluid samples was significantly lower on day 10 when horses received HBO therapy. Values of Pao2 rapidly increased (> 800 mm Hg) but immediately decreased to pretreatment values when HBO sessions ended. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that HBO therapy does not increase mRNA expression of inflammatory cytokines, but reduces eotaxin-2 mRNA transcription. The Pao2 increase was transient with no cumulative effects of HBO.

OBJECTIVE To determine effects of anesthesia on plasma concentrations and pulsatility of ACTH in samples obtained from the cavernous sinus and jugular vein of horses. ANIMALS 6 clinically normal adult horses. PROCEDURES Catheters were placed in a jugular vein and into the cavernous sinus via a superficial facial vein. The following morning (day 1), cavernous sinus blood samples were collected every 5 minutes for 1 hour (collection of first sample = time 0) and jugular venous blood samples were collected at 0, 30, and 60 minutes. On day 2, horses were sedated with xylazine hydrochloride and anesthesia was induced with propofol mixed with ketamine hydrochloride. Horses were positioned in dorsal recumbency. Anesthesia was maintained with isoflurane in oxygen and a continuous rate infusion of butorphanol tartrate. One hour after anesthesia was induced, the blood sample protocol was repeated. Plasma ACTH concentrations were quantified by use of a commercially available sandwich assay. Generalized estimating equations that controlled for horse and an expressly automated deconvolution algorithm were used to determine effects of anesthesia on plasma ACTH concentrations and pulsatility, respectively. RESULTS Anesthesia significantly reduced the plasma ACTH concentration in blood samples collected from the cavernous sinus. CONCLUSIONS AND CLINICAL RELEVANCE Mean plasma ACTH concentrations in samples collected from the cavernous sinus of anesthetized horses were reduced. Determining the success of partial ablation of the pituitary gland in situ for treatment of pituitary pars intermedia dysfunction may require that effects of anesthesia be included in interpretation of plasma ACTH concentrations in cavernous sinus blood.

OBJECTIVE To determine the effects of acepromazine maleate premedication on cardiovascular function before and after infusion of dobutamine hydrochloride for 30 minutes in isoflurane-anesthetized horses. ANIMALS 6 healthy adult horses. PROCEDURES Each horse was anesthetized once following premedication with acepromazine (0.02 mg/kg, IV) administered 30 minutes prior to anesthetic induction (ACP+ treatment) and once without premedication (ACP– treatment). Anesthesia was induced with IV administration of xylazine hydrochloride (0.8 mg/kg), ketamine hydrochloride (2.2 mg/kg), and diazepam (0.08 mg/kg). Horses were positioned in right lateral recumbency, and anesthesia was maintained via inhalation of isoflurane delivered in oxygen. End-tidal isoflurane concentration was adjusted to achieve a target mean arterial blood pressure of 60 mm Hg (interquartile range [25th to 75th percentile], 57 to 63 mm Hg) for at least 15 minutes. Cardiac index, oxygen delivery index, and femoral arterial blood flow indices were determined 60 minutes after anesthetic induction (baseline). Dobutamine was then infused to achieve a target mean arterial blood pressure of 80 mm Hg (interquartile range, 76 to 80 mm Hg). Data collection was repeated 30 minutes after the start of dobutamine infusion for comparison with baseline values. RESULTS Complete data sets were available from 5 of the 6 horses. Dobutamine administration resulted in significant increases in oxygen delivery and femoral arterial blood flow indices but no significant change in cardiac index for each treatment. However, at baseline or 30 minutes after the start of dobutamine infusion, findings for the ACP+ and ACP– treatments did not differ. CONCLUSIONS AND CLINICAL RELEVANCE In isoflurane-anesthetized horses, dobutamine administration increased oxygen delivery and femoral arterial blood flow indices, but these changes were unaffected by premedication with acepromazine.

OBJECTIVE To investigate the effects of isoflurane anesthesia administered at 2 multiples of the minimum alveolar concentration (MAC) on tissue perfusion in dogs. ANIMALS 8 healthy young adult Beagles. PROCEDURES A randomized crossover design was used. Dogs were anesthetized with isoflurane at 1.5 or 2.0 times the MAC for 2 hours, a 7-day washout period was provided, and dogs were reanesthetized with the alternate treatment. Various physiologic variables were monitored before anesthesia (baseline), at 20-minute intervals during anesthesia, and after anesthetic recovery. Variable values were compared between MAC multiples by means of repeated-measures ANOVA, with the Tukey test used for multiple comparisons. RESULTS During anesthesia, mean arterial blood pressure, cardiac output, and mixed venous oxygen saturation were significantly greater when isoflurane was administered at 1.5 versus 2.0 times the MAC. Cardiac output gradually increased during anesthesia at 1.5 times but not at 2.0 times the MAC. Arterial blood lactate concentration did not differ between MAC multiples at any point; however, this concentration decreased with increasing anesthetic duration at both MAC multiples. Oxygen delivery differed between MAC multiples, and oxygen consumption differed from baseline during anesthesia at 2.0 times the MAC. Oxygen extraction was higher at 2.0 versus 1.5 times the MAC. Heart rate differed between MAC multiples only after anesthetic recovery. CONCLUSIONS AND CLINICAL RELEVANCE Isoflurane anesthesia impaired tissue perfusion in dogs, but these changes would not be clinically relevant with oxygen delivery at 100%. Peripheral tissue perfusion was maintained or improved with time.

OBJECTIVE To assess the effect of anesthetic induction with a benzodiazepine plus ketamine or propofol on hypothermia in dogs undergoing ovariohysterectomy without heat support. ANIMALS 23 adult sexually intact female dogs undergoing ovariohysterectomy. PROCEDURES Baseline rectal temperature, heart rate, and respiratory rate were recorded prior to premedication with buprenorphine (0.02 mg/kg, IM) and acepromazine (0.05 mg/kg, IM). Anesthesia was induced with midazolam or diazepam (0.25 mg/kg, IV) plus ketamine (5 mg/kg, IV; n = 11) or propofol (4 mg/kg, IV; 12) and maintained with isoflurane in oxygen. Rectal temperature was measured at hospital intake, prior to premedication, immediately after anesthetic induction, and every 5 minutes after anesthetic induction. Esophageal temperature was measured every 5 minutes during anesthesia, beginning 30 minutes after anesthetic induction. After anesthesia, dogs were covered with a warm-air blanket and rectal temperature was measured every 10 minutes until normothermia (37°C) was achieved. RESULTS Dogs in both treatment groups had lower rectal temperatures within 5 minutes after anesthetic induction and throughout anesthesia. Compared with dogs that received a benzodiazepine plus ketamine, dogs that received a benzodiazepine plus propofol had significantly lower rectal temperatures and the interval from discontinuation of anesthesia to achievement of normothermia was significantly longer. CONCLUSIONS AND CLINICAL RELEVANCE Dogs in which anesthesia was induced with a benzodiazepine plus propofol or ketamine became hypothermic; the extent of hypothermia was more profound for the propofol combination. Dogs should be provided with adequate heat support after induction of anesthesia, particularly when a propofol-benzodiazepine combination is administered.