A previous study on canine babesiosis showed low serum tonicity in affected dogs, which may result from syndrome of inappropriate antidiuretic hormone secretion (SIADH). This endocrine disorder was recognised in human malaria which is considered a disease with similar pathogenesis to canine babesiosis. The aim of this study was to investigate the occurrence of SIADH in babesiosis-afflicted dogs.

OBJECTIVE To investigate use of the plethysmographic variability index (PVI) and perfusion index (PI) for evaluating changes in arterial blood pressure in anesthetized tigers (Panthera tigris). ANIMALS 8 adult tigers. PROCEDURES Each tiger was anesthetized once with a combination of ketamine, midazolam, medetomidine, and isoflurane. Anesthetic monitoring included assessment of PI, PVI, direct blood pressure measurements, anesthetic gas concentrations, esophageal temperature, and results of capnography and ECG. Mean arterial blood pressure (MAP) was maintained for at least 20 minutes at each of the following blood pressure conditions: hypotensive (MAP = 50 ± 5 mm Hg), normotensive (MAP = 70 ± 5 mm Hg), and hypertensive (MAP = 90 ± 5 mm Hg). Arterial blood gas analysis was performed at the beginning of anesthesia and at each blood pressure condition. RESULTS Mean ± SD PI values were 1.82 ± 2.38%, 1.17 ± 0.77%, and 1.71 ± 1.51% and mean PVI values were 16.00 ± 5.07%, 10.44 ± 3.55%, and 8.17 ± 3.49% for hypotensive, normotensive, and hypertensive conditions, respectively. The PI values did not differ significantly among blood pressure conditions. The PVI value for the hypotensive condition differed significantly from values for the normotensive and hypertensive conditions. The PVI values were significantly correlated with MAP (r = −0.657). The OR of hypotension to nonhypotension for PVI values ≥ 18% was 43.6. CONCLUSIONS AND CLINICAL RELEVANCE PVI was a clinically applicable variable determined by use of noninvasive methods in anesthetized tigers. Values of PVI ≥ 18% may indicate hypotension.

OBJECTIVE To evaluate the efficacy of each of 3 incremental doses of MK-467 for alleviation of dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats. ANIMALS 6 healthy adult domestic shorthair cats. PROCEDURES Each cat was anesthetized with isoflurane and received a target-controlled infusion of dexmedetomidine estimated to maintain the plasma dexmedetomidine concentration at 10 ng/mL throughout the experiment. Heart rate (HR) and direct arterial pressures were measured at baseline (isoflurane administration only), during dexmedetomidine infusion, and before and after IV administration of each of 3 serially increasing doses (15, 30, and 60 μg/kg) of MK-467. Cardiac index (CI) and systemic vascular resistance (SVR) were recorded at baseline, during dexmedetomidine infusion, and at the mean arterial pressure nadir after administration of the 30- and 60-μg/kg doses of MK-467. RESULTS Compared with baseline values, the dexmedetomidine infusion significantly decreased HR and increased arterial pressures. Each dose of MK-467 caused a significant decrease in arterial pressures and a significant, albeit clinically irrelevant, increase in HR (≤ 10%). Following administration of the 30- and 60-μg/kg doses of MK-467, all cats developed clinical hypotension (mean arterial pressure, < 60 mm Hg) even though CI and SVR returned to baseline values. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated administration of small doses of MK-467 to isoflurane-anesthetized cats receiving dexmedetomidine restored CI and SVR, but caused a substantial decrease in arterial pressures and only a marginal increase in HR. Therefore, caution should be used when MK-467 is administered to alleviate dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats.

We investigated vascular access ports for feline blood donation. Eight cats were anesthetized for conventional blood collection by jugular venipuncture at the beginning and end of the study. In-between conventional collections, vascular access ports were used for collection with or without sedation every 6 to 8 wk for 6 mo. Ports remained functional except for one catheter breakage, but intermittent occlusions occurred. Systolic blood pressure was lower during conventional collection. Behavioral abnormalities occurred during 3 port collections. Packed red cells prepared from collected blood were stored at 4°C for 25 d and assessed for quality pre- and post-storage. With both collection methods, pH and glucose level declined, and potassium level, lactate dehydrogenase activity and osmotic fragility increased. There were no differences between methods in pre-storage albumin and HCO3− levels, and pre and post-storage hematocrit, lactate dehydrogenase activity, and glucose and potassium levels. Pre-storage pH and pCO2 were higher with conventional collection, and pre- and post-storage osmotic fragility were greater with port collection. One port became infected, but all cultures of packed red cells were negative. Tissue inflammation was evident at port removal. In a second study of conventional collection in 6 cats, use of acepromazine in premedication did not exacerbate hypotension. The use of vascular access ports for feline blood donation is feasible, is associated with less hypotension, and may simplify donation, but red cell quality may decrease, and effects on donors must be considered.

A study was undertaken to determine the pressor and toxic effects of etoposide, an antineoplastic agent, when administered IV in 0.9% sodium chloride solution (0.4 mg of etoposide/ml) over a 30-minute period to dogs at a dosage of 40 mg/m2 of body surface. On day 1, 6 adult German Shorthaired Pointers were anesthetized with halothane, and blood pressures were measured via a femoral artery catheter before, during, and after the etoposide was administered. Systolic, diastolic, and mean blood pressures of each dog increased significantly (P less than 0.01) within 30 minutes after initiation of etoposide infusion. On day 3, when the dogs were not anesthetized, etoposide was again administered to each dog, using the same dosage. Each dog developed a moderate to severe cutaneous reaction characterized by moderate to severe pruritus, urticaria, and swelling of the head and extremities that began during the second infusion of etoposide. These same cutaneous reactions were seen on day 30, when etoposide was administered to 3 of the previously treated dogs and 2 previously untreated Beagles. We concluded that the administration of the commercial preparation of etoposide is likely to cause a significant reduction in blood pressure of anesthetized dogs, and that the drug is likely to induce a moderate to severe cutaneous reaction when administered to unanesthetized dogs.

OBJECTIVE To determine the minimum alveolar concentration of desflurane (MACDES) and effects on cardiovascular variables in positive-pressure ventilated sheep. ANIMALS 13 adult female sheep. PROCEDURES Anesthesia was induced with desflurane. After a 30-minute equilibration at an end-tidal concentration of desflurane (etDES) of 10.5%, an electrical stimulus (5 Hz/ms and 50 mA) was applied for 1 minute or until gross purposeful movement occurred. The etDES was then changed by 0.5% (modified up-down method), depending on whether a positive motor response had been elicited, and stimulation was repeated. The MACDES was the etDES midway between a positive and negative response. After MACDES was determined, etDES was increased to 1.3 and 1.6 MACDES. Animals were allowed to equilibrate for 15 minutes, and cardiovascular, blood gas, acid-base, and hematologic variables were measured. Times to induction of anesthesia, extubation, attainment of sternal position, and standing and duration of anesthesia were recorded. RESULTS Mean ± SD MACDES was 9.81 ± 0.79%. Times to intubation, extubation, and standing were 4.81 ± 2.21 minutes, 14.09 ± 4.05 minutes, and 32.4 ± 12.5 minutes, respectively. Duration of anesthesia was 226 ± 22 minutes. Heart rate increased significantly at induction of anesthesia but otherwise remained at preanesthetic rates. Arterial blood pressures progressively decreased with increasing etDES; pressures increased slightly only in response to noxious stimulation. CONCLUSIONS AND CLINICAL RELEVANCE The MACDES determined here compared favorably with that determined for other sheep populations and indicated similar anesthetic potency as in other species. Desflurane caused dose-dependent arterial hypotension, which indicated the need for careful blood pressure monitoring.

OBJECTIVE To determine the cardiopulmonary effects of progressively increasing infusion rates of dopamine hydrochloride and phenylephrine hydrochloride in healthy adult New Zealand White rabbits anesthetized with isoflurane. ANIMALS 6 New Zealand White rabbits. (Oryctolagus cuniculus). PROCEDURES Each rabbit was anesthetized on 2 occasions (≥ 2 weeks apart) with isoflurane in oxygen at 1.5 times the published isoflurane minimum alveolar concentration of 2.07%. Carotid artery and pulmonary artery catheters were placed. During each anesthetic episode, each rabbit received 5 progressively increasing doses of either dopamine (5, 10, 15, 20, or 30 μg/kg/min) or phenylephrine (0.125, 0.25, 0.5, 1.0, and 2.0 μg/kg/min). Blood gas and cardiopulmonary measurements were obtained after a 20-minute equilibration period prior to administration of the first drug dose (baseline) and after each subsequent dose administration. RESULTS Dopamine increased stroke index at the highest infusion rate of 30 μg/kg/min; however, cardiac output and mean arterial blood pressure remained unchanged from baseline values. Administration of phenylephrine at a rate of 2 μg/kg/min increased mean arterial blood pressure to 62 mm Hg from the baseline value of 45 mm Hg. This was a result of an increase in systemic vascular resistance with a concomitant decrease in heart rate and no change in cardiac output. Blood lactate concentration increased with time when rabbits received either treatment. CONCLUSIONS AND CLINICAL RELEVANCE Within the dose range of 5 to 30 μg/kg/min, dopamine was not an effective treatment for isoflurane-induced hypotension in rabbits and phenylephrine was only minimally effective at a dose of 2 μg/kg/min.

Objective: To determine cardiopulmonary effects of incremental doses of dopamine and phenylephrine during isoflurane-induced hypotension in cats with hypertrophic cardiomyopathy (HCM). Animals: 6 adult cats with severe naturally occurring HCM. Procedures: Each cat was anesthetized twice (once for dopamine treatment and once for phenylephrine treatment; treatment order was randomized). Hypotension was induced by increasing isoflurane concentration. Cardiopulmonary data, including measurement of plasma concentration of cardiac troponin I (cTnI), were obtained before anesthesia, 20 minutes after onset of hypotension, and 20 minutes after each incremental infusion of dopamine (2.5, 5, and 10 μg/kg/min) or phenylephrine (0.25, 0.5, and 1 μg/kg/min). Results: Mean ± SD end-tidal isoflurane concentration for dopamine and phenylephrine was 2.44 ± 0.05% and 2.48 ± 0.04%, respectively. Cardiac index and tissue oxygen delivery were significantly increased after administration of dopamine, compared with results after administration of phenylephrine. Systemic vascular resistance index was significantly increased after administration of phenylephrine, compared with results after administration of dopamine. Oxygen consumption remained unchanged for both treatments. Systemic and pulmonary arterial blood pressures were increased after administration of both dopamine and phenylephrine. Acid-base status and blood lactate concentration did not change and were not different between treatments. The cTnI concentration increased during anesthesia and infusion of dopamine and phenylephrine but did not differ significantly between treatments. Conclusions and Clinical Relevance: Dopamine and phenylephrine induced dose-dependent increases in systemic and pulmonary blood pressure, but only dopamine resulted in increased cardiac output. Hypotension and infusions of dopamine and phenylephrine caused significant increases in cTnI concentrations.

A controlled study of the cardiovascular responses in horses anesthetized with acepromazine (0.05 mg/kg of body weight, IV), guaifenesin (100 mg/kg, IV), thiamylal (5.0 mg/kg, IV), and halothane in O2 (1.2 to 1.4% end-expired concentration) was performed to determine whether hypotension could be prevented by use of various treatments. Six horses were given 5 treatments in a randomized sequence: no treatment (control), methoxamine (0.04 mg/kg IV), lactated Ringer solution (20.0 ml/kg, IV), 7.5% hypertonic saline solution (4.0 ml/kg, IV), or constant infusion of dobutamine (5.0 mg/kg/min, IV) during anesthesia. Heart rate, ECG, blood pressure, central venous pressure, cardiac output, blood gas analysis, PCV, and plasma total protein concentration were measured during the study. Compared with the control value, an increase in blood pressure during halothane administration was observed after administration of lactated Ringer solution, hypertonic saline solution, or dobutamine (P < 0.05). The improved blood pressure response to hypertonic saline solution and dobutamine was related to an increase in cardiac output, which was statistically significant (P < 0.05) Other statistically significant differences in cardiopulmonary responses among treatments were not observed during anesthesia. The PCV was increased in response to dobutamine infusion, and plasma total protein concentration was reduced in response to administration of hypertonic saline or lactated Ringer solution.

OBJECTIVE To evaluate the cardiovascular effects of atipamezole administered at half the volume or the same volume as dexmedetomidine to isoflurane-anesthetized cats. ANIMALS 6 adult (1 to 2 years old) domestic shorthair cats (body weight, 3 to 6 kg). PROCEDURES Each cat was anesthetized with isoflurane and rocuronium 3 times; there was a 1-week washout period between successive anesthetic procedures. For each anesthetic procedure, dexmedetomidine (5 μg/kg) was administered IV. Five minutes after dexmedetomidine was administered, atipamezole (25 or 50 μg/kg) or saline (0.9% NaCl) solution was administered IM. Pulse rate, mean arterial blood pressure (MAP), cardiac output (CO), and systemic vascular resistance (SVR) were measured during anesthesia before dexmedetomidine administration (baseline), after dexmedetomidine administration, and 15, 30, 60, and 120 minutes after administration of atipamezole or saline solution. Pulse rate and MAP were also recorded when MAP was at its lowest value. Hemodynamic variables were compared among treatments at baseline, after dexmedetomidine administration, and after administration of atipamezole or saline solution. Effects of treatment and time on all variables were assessed with mixed-effects models. RESULTS Both doses of atipamezole resulted in a significantly lower MAP than did saline solution. Pulse rate, CO, and SVR were not significantly different among treatments after atipamezole or saline solution were administered. CONCLUSIONS AND CLINICAL RELEVANCE Atipamezole administered IM at half the volume or the same volume as dexmedetomidine was ineffective at increasing pulse rate or CO in anesthetized cats that received dexmedetomidine. However, atipamezole caused short-lasting but severe arterial hypotension.