Objective-To assess the accuracy of isoflurane, halothane, and sevoflurane vaporizers during high oxygen flow and at maximum dial settings at room temperature and to test sevoflurane vaporizers similarly during heating and at low-fill states. Sample-5 isoflurane, 5 halothane, and 5 sevoflurane vaporizers. Procedures-Vaporizers were tested at an oxygen flow of 10 L/min and maximum dial settings for 15 minutes under various conditions. All 3 vaporizer types were filled and tested at room temperature (21 degrees to 23 degrees C). Filled sevoflurane vaporizers were wrapped with circulating hot water (42 degrees C) blankets for 2 hours and tested similarly, and near-empty sevoflurane vaporizers were tested similarly at room temperature. During each 15-minute test period, anesthetic agent concentration was measured at the common gas outlet with a portable refractometer and temperature of the vaporizer wall was measured with a thermistor. Results-For each vaporizer type, anesthetic agent concentrations and vaporizer wall temperatures decreased during the 15-minute test period. Accuracy of isoflurane and halothane vaporizers remained within the recommended 20% (plus or minus) deviation from dial settings. Heated and room-temperature sevoflurane vaporizers were accurate to within 23% and 11.7% (plus or minus) of dial settings, respectively. Sevoflurane vaporizers at low-fill states performed similarly to vaporizers at full-fill states. Conclusions and Clinical Relevance-Under these study conditions, the isoflurane and halothane vaporizer models tested were accurate but the sevoflurane vaporizers were not. Sevoflurane vaporizer accuracy was not affected by fill state but may be improved with vaporizer heating; measurements of inspired anesthetic agent concentrations should be obtained during the use of heated vaporizers.

To study behavioral and cardiopulmonary characteristics of horses recovering from inhalation anesthesia, 6 nonmedicated horses were anesthetized under laboratory conditions on 3 different days, with either halothane or isoflurane in O2. Anesthesia was maintained at constant dose (1.5 times the minimum alveolar concentration [MAC]) of halothane in O2 for 1 hour (H1), halothane in O2 for 3 hours (H3), or isoflurane in O2 for 3 hours (13). The order of exposure was set up as a pair of Latin squares to account for horse and trial effects. Circulatory (arterial blood pressure and heart rate) and respiratory (frequency, PaCO2, PaO, pHa) variables were monitored during anesthesia and for as long as possible during the recovery period. End-tidal percentage of the inhaled agent was measured every 15 seconds by automated mass spectrometry, then by hand-sampling after horses started moving. Times of recovery events, including movement of the eyelids, ears, head, and limbs, head lift, chewing, swallowing, first sternal posture and stand attempts, and the number of sternal posture and stand attempts, were recorded. The washout curve or the ET ratio (end-tidal percentage of the inhaled agent at time t to end-tidal percentage of the inhaled agent at the time the anesthesia circuit was disconnected from the tracheal tube) plotted against time was similar for HI and H3. The slower, then faster (compared with halothane groups) washout curve of isoflurane was explainable by changes in respiratory frequency as horses awakened and by lower blood/gas solubility of isoflurane. The respiratory depressant effects of isoflurane were marked and were more progressive than those for halothane at the same 1.5 MAC dose. During the first 15 minutes of recovery, respiratory frequency for group-13 horses increased significantly (P < 0.05), compared with that for the halothane groups. For all groups, arterial blood pressure increased throughout the early recovery period and heart rate remained constant. Preanesthesia temperament of horses and the inhalation agent used did not influence the time of the early recovery events (movement of eyelids, ears, head, and limbs), except for head lift. For events that occurred at anesthetic end-tidal percentage < 0.20, or when horses were awake, temperament was the only factor that significantly influenced the nature of the recovery (chewing P = 0.04, extubation P = 0.001, first stand attempt P = 0.008, and standing P = 0.005). The quality of the recoveries did not differ significantly among groups (H1, H3, I3) or horses; however 5 of 6 horses recovering from the H1 exposure had ideal recovery. During recovery, the anesthetic end-tidal percentage did not differ significantly among groups. However, when concentrations were compared on the basis of anesthetic potency (ie, MAC multiple) a significantly (P < 0.05) lower MAC multiple of isoflurane was measured for the events ear movement, limb movement, head lift, and first attempt to sternal posture, compared with that for horses given halothane, indicating that isoflurane may be a more-potent sedative than halothane in these horses.

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the ADD. These results indicate that atropine may lower the arrhythmogenic threshold for dobutamine in halothane-anesthetized horses.

Platelet aggregation and adenosine triphosphate (ATP) release were measured by use of the impedance method in blood samples obtained from 25 adult female Beagles before and after sedation with acepromazine (0.13 mg/kg of body weight) and atropine (0.05 mg/kg), and during general anesthesia. General anesthesia was induced by IV administration of thiamylal (average dosage, 2.1 mg/kg, range, 1.2 to 4.2 mg/kg) and was maintained with halothane in oxygen. Samples of jugular venous blood were obtained from each dog, using citrate as anticoagulant. Platelet count was done on each sample. Platelet aggregation and ATP released from the aggregating platelets were measured within 2.5 hours of sample collection, using a whole-blood aggregometer. Adenosine diphosphate (ADP) or collagen was used as aggregating agent. For each aggregating agent, platelet aggregation and ATP release were measured over 6 minutes. After sedation with acepromazine and atropine, significant (P < 0.01) reduction was observed in platelet count (from median values of 341,000 cells/microliter to 283,000 cells/microliter) and in the ability of platelets to aggregate in response to ADP (from 14.0 to 7.0 Ohms). During the same period, maximal release of ATP in response to collagen also was reduced (from 5.56 micromoles to 4.57 micromoles; P < 0.01); however, this difference ceased to be significant when ATP release was normalized for platelet count. During general anesthesia and surgery (200 minutes after sedation), platelet count and aggregation responses to ADP and collagen had returned to presedation values. None of the dogs in this study appeared to have hemostasis problems during surgery. In conclusion, sedation with acepromazine and atropine induces measurable inhibition of ADP-induced platelet aggregation that resolves during subsequent general anesthesia and surgery. Transient inhibition of platelet aggregation is not manifested by a change in gross hemostasis during surgery.

Dynamic baroreflex sensitivity for increasing arterial pressure (DBSI) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (less than or equal to 2 minutes) pressure changes in the horse. Anesthesia was induced with IV administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (SAP) was increased a minimum of 30 mm of Hg in response to an IV bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the R-R interval/SAP relationship. During dynamic increases in SAP, a significant correlation between R-R interval and SAP was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between R-R interval and sap were > 0.80 in 5 of 8 horses. Mean (+/- SD) DBSI was 4.8 +/- 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between R-R interval and SAP was observed in only 3 of 6 awake horses during dynamic increases in SAP. Lack of correlation between R-R interval and SAP in 3 of 6 awake horses indicated that rapidly increasing SAP with an IV phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (+/- SD) DBSI (3 horses) was 7.3 +/- 3.3 ms/mm of Hg in awake horses.

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (MH) had calcium extrusion activity higher than unaffected swine. Cytoplasmic concentration of ionized calcium was determined by use of dual emission spectrofluorometry and measurement of the ratio of free to calcium-bound form of the fluorescent calcium dye indo-1. Net calcium accumulation and unidirectional calcium extrusion rate were dependent on intracellular calcium concentration. Calcium extrusion from calcium-loaded lymphocytes was monitored while calcium influx was inhibited by suspending the cells in calcium-free medium with a calcium chelator. Net calcium accumulation of untreated lymphocytes was monitored in calcium-replete medium. A novel method of calculation of ionized calcium was used. This method confirmed our previous findings of lower ionized calcium concentration (86 +/- 40 and 370 +/- 216 nmol/L; P < 0.01) and slower rates of calcium accumulation (39 +/- 16 and 127 +/- 52 nmol/L/min) in untreated lymphocytes from MH-susceptible swine compared with controls. These changes were attributable to calcium extrusion activity two- to three-fold higher in lymphocytes of MH-susceptible swine (154 +/- 36 and 408 +/- 47 nmol/L/min at 175 nmol/L; 972 +/- 111 and 1,690 +/- 505 nmol/L/min at 425 nmol/L). These data were compatible with our model of higher calcium extrusion activity being a compensatory adaptation of MH-susceptible swine lymphocytes to their hypersensitivity to stimuli that increase cytoplasmic calcium concentration.

Programmed electrical stimulation techniques were used to evaluate the effects of halothane and isoflurane on induction of atrial fibrillation in anesthetized dogs. Experiments were performed in 16 dogs anesthetized with alpha-chloralose. Critically timed premature stimuli were applied to the right atrial appendage and Bachmann bundle to determine the atrial fibrillation threshold, defined as the minimal current required to induce rapid, irregular atrial electrical activity of at least 8 seconds' duration. Atrial fibrillation thresholds were determined at baseline (0.0% inhalational anesthetic), 0.5 minimal alveolar concentration (MAC), and 1.0 MAC of halothane (n = 8) and isoflurane (n = 8). In the absence of inhalation anesthetic, it was significantly (P < 0.01) easier to induce atrial fibrillation at the Bachmann bundle vs the right atrial appendage. Atrial fibrillation threshold at the Bachmann bundle was not affected by increasing concentrations of halothane, but was increased by 1.0 MAC of isoflurane (P < 0.05). It was concluded that at 1.0 MAC isoflurane, but not halothane, has antifibrillatory effects in atrial tissue.

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR. Methoxamine significantly decreased CI, SVR, and HR, whereas SVR and SAP were increased significantly. After hemorrhage, the only variables that had a significant change in the absolute magnitude of the response to a drug, relative to the response before hemorrhage, were a significantly reduced ability of dobutamine and methoxamine to increase SAP, and a significantly decreased ability of methoxamine to decrease CI. We concluded that dobutamine and epinephrine provide beneficial short-term support of the cardiovascular system in the halothane-anesthetized dog during acute hypovolemia.

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P < 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P < 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P < 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P < 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P < 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses. Steady-state infusions of phenylephrine in anesthetized horses resulted in arrhythmia development, with premature atrial and ventricular complexes seen in halothane-anesthetized horses and increased heart rate and atrial premature complexes seen less frequently in isoflurane-anesthetized horses. Dynamic BS was 25.0 +/- 4.5 and 20.1 +/- 2.8 ms/mm of Hg for decreasing and increasing SAP, respectively, in awake horses. The R-R interval and SAP were linearly correlated during dynamic decreases in SAP in 7 of 9 halothane and 8 of 10 isoflurane anesthesia periods. Baroreflex sensitivity decreased to 15.0 +/- 6.8 and 13.3 +/- 3.5 ms/mm of Hg during anesthesia with low MAC of halothane and isoflurane, respectively. High MAC of halothane and isoflurane significantly (P < 0.05) decreased BS during dynamic decreases in SAP in 7.8 +/- 1.8 and 7.2 +/- 1.3 ms/mm of Hg, respectively. There were no significant differences in BS depression between halothane and isoflurane.

Atracurium (0.4 mg/ml in isotonic NaCl solution) was administered by IV infusion to 7 healthy adult horses for 2 hours. Over the 2-hour period, a 95 to 99% reduction of train-of-four hoof-twitch response was maintained by 0.17 +/- 0.01 mg of atracurium/kg of body weight/h, for a total of 161 +/- 6 mg of atracurium (mean +/- SEM) for horses 1 to 4, 6, and 7. Horse 5, a mare in estrus, required 0.49 mg of atracurium/kg/h to maintain comparable relaxation. Hoof-twitch recovery time from 10 to 75% of baseline strength was 19.8 +/- 2.5 minutes for all horses. The 10 to 75% recovery time for horse 5 was 18 minutes. Recovery time from discontinuation of halothane until standing was 86 +/- 14 minutes (range, 55 to 165 minutes). Horse 5 had a 165-minute recovery. Regarding recovery from anesthesia, 3 recoveries were rated as excellent, 1 recovery good, and 2 recoveries as fair. Horse 5 laid quietly until she stood with 1 strong, smooth effort.