Cardiorespiratory effects of abdominal insufflation were evaluated in 8 dogs during isoflurane anesthesia. Each dog was studied 3 times, in 1 of the following orders of insufflation pressures: 10-20-30, 20-30-10, 30-20-10, 10-30-20, 20-10-30, and 30-10-20 mm of Hg. Anesthesia was induced by use of a mask, dogs were intubated, and anesthesia was maintained by isoflurane in 100% oxygen. After instrumentation, baseline values were recorded (time 0), and the abdomen was insufflated with nitrous oxide. Data were recorded at 5, 10, 15, 20, 25, and 30 minutes after insufflation. The abdomen was then desufflated, with recording of data continuing at 35 and 40 minutes. Mean arterial pressure increased at 5 minutes during 20 mm of Hg insufflation pressure, and from 20 to 30 minutes during 30 mm of Hg pressure. Tidal volume decreased from 5 to 30 minutes during 10 and 20 mm of Hg pressures, and from 5 to 40 minutes during 30 mm of Hg pressure. Minute ventilation decreased at 10 and 20 minutes during 20 mm of Hg pressure. End-tidal CO2 concentration increased from 5 to 30 minutes during 20 and 30 mm of Hg pressure. The PaCO2 decreased at 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Values for pH decreased from 10 to 30 minutes during 20 and 30 mm of Hg pressures. The PaO2 decreased from 20 to 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Percentage decrease in tidal volume was greater at 5 and 15 minutes with 30 mm of Hg pressure. Differences in percentage increase in end tidal CO2 concentration were observed among the 3 pressures from 5 to 30 minutes. Although significant, these changes do not preclude use of laparoscopy if insufflation pressure > 20 mm of Hg is avoided.

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.

The influence of the QT, TQ, and ST intervals, and heart score on both cardiac cycle duration (RR) and diastole/systole (D/S) quotient were analyzed during the neonatal (1 day and 5 days) pigs belonging to 2 crossbreeds of different rusticity, Landrace X Belgian White (LBW) and Landrace X Duroc Jersey (LDJ). Our findings indicate that the shortening of the RR interval in 5-day-old pigs of both crossbreeds was determined by different variables in each breed. In LDJ pigs, this shortening was only associated with a shortening of ventricular activation, and in each age group, the systole and the diastole contributed equally to the RR value. The D/S quotient did not differ significantly in 1-day-old vs 5-day-old pigs, and at both ages, the quotient was only determined by the TQ value. In LBW pigs, the RR, QT, TQ, and ST were shortened, but only the shortening of QT was significant as a result of an acceleration of the ventricular recuperation process. Moreover, differences were found between 1-day-old vs 5-day-old pigs with regard to the contribution of the different intervals to the RR duration. In 1-day-old pigs, the RR depended closely on the TQ, whereas in 5-day-old pigs, all intervals contributed significantly to its duration. The D/S quotient was not significantly different in 1-day-old vs 5-day-old pigs, but a different contribution of the variables studied was observed at the 2 ages selected. In 1-day-old pigs, D/S quotient depended on the diastole duration, whereas in 5-day-old pigs, the diastole and systole contributed to its variation.

Quantitative electroencephalography (QEEG) was assessed in 5 dogs anesthetized with 1.6% end-tidal concentration of isoflurane and after subsequent administration of the benzodiazepine midazolam (0.2 mg/kg of body weight, IV). Ventilation was controlled to maintain normocapnia. Effect of the benzodiazepine antagonist, flumazenil (0.04 mg/kg, IV), on QEEG in midazolam-isoflurane-anesthetized dogs was determined. Heart rate, arterial blood pressure, esophageal temperature, arterial pH and blood gas tensions, end-tidal CO2 concentration, and end-tidal isoflurane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG data. Quantitative EEG data were stored on an optical disk for later analysis. Values for absolute power of EEG were determined for delta, theta, alpha, and beta-frequencies. Cardiovascular variables remained stable throughout the study. Midazolam administration was associated with decreased absolute power in all frequencies of EEG at all electrode sites. Administration of flumazenil antagonized midazolam-induced decreased absolute power of EEG in all frequencies at all electrode sites. We conclude that QEEG provides a noninvasive, objective measure of midazolam- and flumazenil-induced changes in cortical activity during isoflurane anesthesia.

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.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1 (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [log(e) detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [log(e) detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). Plasma atrial natriuretic peptide concentration was significantly increased with increasing detomidine concentration (20.4 +/- 3.8 pg/ml at baseline to 33.5 +/- 9.1 at infusion 4). There were few significant changes in respiration rate and arterial blood gas and pH values. We conclude that maintenance of steady-state detomidine plasma concentrations resulted in cardiopulmonary changes that were quantitatively similar to those induced by detomidine bolus administration in horses.

Changes in lateral cecal arterial blood flow, mean internal carotid arterial pressure, and heart rate caused by nasogastric administration of fenoldopam (3, 6, and 9 mg/kg of body weight), a selective agonist of dopaminergic receptors, were recorded in 7 healthy horses. Cecal arterial blood flow was significantly increased within 30 minutes after administration of fenoldopam at all 3 dosages, with the peak increases from baseline (67.8 +/- 17.5 ml/min) being 125 +/- 28, 120 +/- 22, and 153 +/- 32 ml/min for 3, 6, and 9 mg/kg, respectively. Although carotid arterial pressure did not change significantly after administration of fenoldopam at the dosage of 3 mg/kg, administration of fenoldopam at the dosages of 6 and 9 mg/kg significantly reduced carotid arterial pressure from 113 +/- 10 to 88 +/- 3 and 81 +/- 5 mm of Hg, respectively. Intravenous infusion of metoclopramide, a dopaminergic receptor antagonist, at the rate of 0.125 mg/kg/h, blocked the effect of fenoldopam on cecal arterial blood flow and carotid arterial pressure. It was concluded that dopaminergic receptors mediate alterations in local blood flow and systemic pressure in horses.

The effects of exogenous platelet-activating factor (PAF) were determined in anesthetized ponies. Administration of PAF induced a decrease in cardiac index that resulted in systemic hypotension. This was followed by tachycardia, hypertension, and a return of cardiac index to baseline. Pulmonary arterial pressure increased markedly because of pulmonary vasoconstriction. Exogenous PAF also caused leukopenia and thrombocytopenia. The specific PAF receptor antagonist (WEB 2086) blocked all PAF-induced changes. Flunixin meglumine, a cyclooxygenase inhibitor, abolished the pulmonary hypertension and tachycardia, and attenuated the systemic hypotension but did not change the PAF-induced peripheral cellular changes. The PAF antagonist also inhibited platelet aggregation induced by PAF in vitro. The PAF-induced changes are similar to those reported after endotoxin exposure in horses.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs, were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively. Differences for groups IGS, IGX, and IGM could not be calculated because arrhythmias satisfying the ADE criteria were not observed at the maximum infusion rate of 5.0 micrograms/kg/min. Differences among groups IS, IX, and IM were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, IM) or medetomidine (15 micrograms/kg, IM) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either alpha 2-adrenergic receptor agonist.

The role of platelet-activating factor in mediating the cardiovascular and peripheral cellular responses to large-colon ischemia and reperfusion, was explored in anesthetized ponies. A specific platelet. activating factor (PAF) antagonist (WEB 2086) was administered to a group of 6 ponies, and another 6 ponies (controls) were given an equivalent volume of saline solution, prior to 1 hour of large-colon torsion. After correction of the torsion, ponies were monitored during the reperfusion period. Significant (P < 0.05) hypotension and metabolic acidosis developed in afl ponies after correction of colonic torsion, cardiac index increased initially, but then decreased significantly (P < 0.05) over the study period. Mean times between correction of torsion and onset of cardiac failure and death were not different between groups. Significant (P < 0.05) thrombocytopenia developed during the reperfusion period in control ponies, but not in WEB-treated ponies. Blood leukocyte concentration in control ponies was more variable and significantly (P < 0.05) decreased immediately upon reperfusion, compared with that in WEB-treated ponies. We conclude that although the cardiovascular responses to colonic ischemia and reperfusion are not prevented by use of a specific PAF-antagonist, specific peripheral cellular responses are mediated by PAF.