The efficacy of ECT in mixed affective states.

ECT is efficacious in the treatment of both the depressed and manic phases of bipolar disorder. While ECT is believed to be equally efficacious in the treatment of mixed affective states, to our knowledge there are no empirical studies on this issue. A chart review study was conducted to compare treatment response and clinical course in three groups of patients who received ECT in a general hospital service: bipolar depressed (n = 38), bipolar manic (n = 5), and bipolar mixed (n = 10), diagnosed by DSM-IV criteria. All three groups showed robust response rates, but the number of days of hospitalization was significantly longer in the mixed group (mean 30, SD 19.0 days) compared with the depressed group (mean 19.0, SD 10.9 days, t = 2.4, p < 0.03). There was a trend for the number of ECT treatments to be greater in the mixed compared with the depressed group. These findings indicate that patients with mixed affective states do respond well to a course of ECT, but the longer hospital stays and greater number of ECT treatments suggest that they may be more difficult to treat with ECT than patients with pure bipolar depression or bipolar mania.

Evaluation of two applanation tonometers in cats.

Comparisons of the MacKay-Marg and Tono-Pen applanation tonometers in open and closed in vitro systems were made for the eyes of cats. Both instruments significantly underestimated intraocular pressure (IOP) vs direct manometry (P less than 0.001), but in readily predictable manner, with high coefficients of determination (r2 = 0.99). For tonometer 1 (MacKay-Marg), calculated actual IOP = 1.36 x (MacKay-Marg measurement) - 1.67 mm of Hg; and for tonometer 2 (Tono-Pen), calculated actual IOP = 1.37 x (Tono-Pen measurement) + 0.8 mm of HG, using measurements from 11 enucleated eyes. In vivo comparisons were initially made in 81 clinically normal eyes (n = 41 cats) by applying the Tono-Pen first followed by the MacKay-Marg. Compared with the MacKay-Marg, the Tono-Pen significantly (P less than 0.001) underestimated IOP in these cats. When the order of tonometer applanation was subsequently reversed in 73 clinically normal eyes (n = 37 cats) the Tono-Pen again significantly (P less than 0.001) underestimated IOP, compared with the MacKay-Marg. Alterations in tonometer order did not result in significant differences in measured IOP for the MacKay-Marg when compared with itself, but Tono-Pen measurements were significantly (P less than 0.05) less when its use followed, rather than preceded, that of the MacKay-Marg. Mean (+/- SD) IOP in clinically normal cats when each tonometer was used first was 22.6 +/- 4.0 mm of Hg (range, 14 to 32 mm of Hg) for the MacKay-Marg and 19.7 +/- 5.6 mm of Hg (9 to 31 mm of Hg) for the Tono-Pen.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of two applanation tonometers in horses.

Comparisons were made of measurements obtained in horses, using 2 applanation tonometers in vivo and in vitro. In vitro comparisons indicated that although neither instrument accurately recorded intraocular pressure (IOP), compared with manometric measurements, results of both instruments indicated linear digression from manometric IOP values that could readily be corrected, thereby accurately estimating IOP in horses. For tonometer 1 (MacKay-Marg), calculated actual IOP = 1.48 - 0.9 mm of Hg; and for tonometer 2 (Tono-Pen), calculated actual IOP = 1.38 + 2.3 mm of Hg. The coefficients of determination (r2) values were markedly high (0.99 for both equations). In vivo comparisons in clinically normal horses did not reveal significant differences in measured IOP between the 2 instruments, and IOP was not altered from baseline after auriculopalpebral nerve block. Mean (+/- SD) IOP in clinically normal horses was 23.5 +/- 6.10 mm of Hg and 23.3 +/- 6.89 mm of Hg, for tonometers 1 and 2, respectively.

Cardiovascular effects of vasopressors in halothane-anesthetized dogs before and after hemorrhage.

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.

Cardiovascular effects of vasopressors in isoflurane-anesthetized dogs before and after hemorrhage.

Exogenously administered vasopressors (sympathomimetics) were evaluated in isoflurane-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 isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, 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. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increased to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Induction of equine postanesthetic myositis after halothane-induced hypotension.

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during, and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Although the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.

Prevalence of ocular microorganisms in hospitalized and stabled horses.

Microorganisms from normal eyes of hospitalized and stabled horses were identified, and the frequency of isolation was compared between the 2 groups. Using standard techniques, swab specimens from both eyes of 22 hospitalized horses and both eyes of 18 stabled horses were cultured for aerobic bacteria and fungi. Ninety-six aerobic bacteria and 57 fungi were isolated. The predominant bacterial isolates were gram-positive organisms, most of which belonged to the genera Corynebacterium, Bacillus, Staphylococcus, and Streptomyces. Gram-negative organisms comprised less than one-fourth of the bacterial isolates, with the genera Neisseria, Moraxella, and Acinetobacter being the most commonly isolated. Environmental fungi Cladosporium and Alternaria accounted for half of all fungal isolates. In only 5 horses were fungi isolated without accompanying isolation of bacteria. The frequency of isolation of fungi was higher (P less than 0.01) in stabled horses. For bacteria, the frequency of isolation was higher (P less than 0.08) in male horses. Results of susceptibility testing were recorded as the percentage of all isolates susceptible to a given antimicrobic drug. Bacterial isolates were highly susceptible (greater than or equal to 90%) to neomycin, polymixin B, gentamicin, and chloramphenicol. Overall, filamentous fungi had highest susceptibility to natamycin (97%). Miconazole was highly efficacious (100% susceptibility) against Fusarium and Aspergillus.

Reduction of the ventricular arrhythmogenic dose of epinephrine by ketamine administration in halothane-anesthetized cats.

The effect of ketamine administration on the ventricular arrhythmogenic dose of epinephrine (VADE) was studied in 4 halothane-anesthetized cats. Each cat was anesthetized 4 times, 1 week apart, with halothane (end-tidal concentration, 1.5%) and with halothane (end-tidal concentration, 1.5%) combined with ketamine infusion (50, 100, and 200 micrograms/kg of body weight/min). Epinephrine was infused in progressively increasing doses. The VADE (micrograms/kg) was calculated as the product of infusion rate of epinephrine and time of infusion necessary to induce 4 or more ventricular premature depolarizations within 15 s. The mean (+/- SD) VADE during halothane anesthesia was 1.1 (+/- 0.30) micrograms/kg. Ketamine infusion significantly (P less than 0.01) lowered the VADE independently of dose. The dose of epinephrine (micrograms/kg) that induced an ECG change in P-wave configuration was calculated similarly. Less epinephrine was necessary to induce a change in P-wave configuration than was necessary to induce 4 or more ventricular premature depolarizations within 15 s. Blood samples were collected after 4 hours of ketamine infusion and again immediately after determination of the VADE for analysis of plasma ketamine and norketamine concentrations by use of gas chromatography. Plasma ketamine and norketamine concentrations after a 4-hour infusion and immediately after determination of the VADE were similar for any given ketamine infusion rate, indicating that steady-state plasma concentrations had been reached for each infusion rate. Blood pressure and heart rate were measured immediately before (base line) and immediately after infusion of the VADE. Ketamine infusion significantly (P less than 005) lowered base-line blood pressure, but not heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Density and distribution of canine conjunctival goblet cells.

Conjunctival goblet cells (GCs) were quantitated to establish baseline values for density and distribution of these cells in healthy canine eyes. From each of 18 sites, tissue was collected, sectioned at 2 micron, and stained with periodic acid Schiff stain. Within each sampling site, 500 epithelial cells (GCs, squamous, polygonal, and basal epithelial cells) were counted and the ratio of GCs to total epithelial cells was computed as an index of goblet cell density or goblet cell index (GCI). A heterogenous distribution of canine conjunctival goblets cells was demonstrated. Lower nasal fornix (LNf) and adjacent sites, lower middle fornix (LMf) and lower nasal tarsal (LNt), had the highest mean densities of goblet cells. In contrast, GCs were essentially absent from the upper and lower bulbar areas. Remaining sites had intermediate GCIs. Sex differences in GCIs were noted for LNf and LNt sites. Mean tear film breakup times (BUTs) were determined, and, for normal beagle dogs, were 19.38 (+/- 4.80 secs) OS and 19.96 (+/- 5.01 secs) OD. The similarities between canine and human conjunctival goblet cell distributions support the use of the dog for studying the conjunctival mucous system.

Dental dolorimetry for the evaluation of an analgesic agent in the horse.

A monopolar electrode was implanted surgically in the canine tooth dentine layer to evaluate pain threshold responses of horses. A constant-current stimulator was used to deliver a known electrical current to the tooth pulp nerve. A single stimulus of 2-ms duration, repeated at greater than or equal to 20-s intervals, was used to elicit a head lift response. The lowest current level that produced 3 positive head lift responses was recorded as the pain threshold of the horse. The testing technique, dental dolorimetry, was easily performed. Tooth pulp pain thresholds (TPPT) were established on 8 nonmedicated adult male horses. Electrodes were nonreactive and remained functional for up to 98 days. Base-line TPPT values were consistent with repeated measurements on the same day and measurements on subsequent test days. The quantity of electrical current necessary to elicit the TPPT was increased after administration of xylazine HCl as a test analgesic.

Comparative analgesia of xylazine, xylazine/morphine, xylazine/butorphanol, and xylazine/nalbuphine in the horse, using dental dolorimetry.

Xylazine, morphine, butorphanol, and nalbuphine were evaluated in 5 adult male horses, using dental dolorimetry. Comparisons were made at 30, 60, and 100 minutes after IV drug administration. Peak analgesia and the time to develop peak analgesia also were compared. Xylazine induced a marked increase in the tooth pulp pain threshold measurements as did the xylazine/narcotic combinations. Statistical differences were not detectable between these treatments. Xylazine and xylazine/butorphanol were better analgesics than was butorphanol alone at 30 and 60 minutes. Xylazine resulted in peak analgesia faster than did butorphanol or the combination of xylazine/butorphanol. Additive analgesic effects were not detected with the combined treatments.

Ketamine and the arrhythmogenic dose of epinephrine in cats anesthetized with halothane and isoflurane.

Epinephrine-induced arrhythmias were studied in 4 cats (group A), using a 4 X 4 Latin square design. Each cat was anesthetized 4 times, 1 week apart, with halothane (1.5% end expired), isoflurane (2.0% end expired), and halothane or isoflurane preceded by ketamine administered IM (8.8 mg/kg). Lead II of the ECG and femoral artery pressure were recorded. Epinephrine was infused in progressively doubled rates (initial rate = 0.125 micrograms/kg/min) for a maximum of 2.5 minutes or until at least 4 ventricular premature depolarizations occurred within 15 s of each other. The arrhythmogenic dose of epinephrine (ADE; micrograms/kg) was calculated as the product of infusion rate and time to arrhythmia. The ADE (means +/- SD) during anesthesia with halothane alone and with ketamine-halothane anesthesia were 1.33 +/- 0.65 and 1.37 +/- 0.59 micrograms/kg, respectively; during anesthesia with isoflurane alone and ketamine-isoflurane anesthesia, the ADE were 9.34 +/- 1.29 and 16.16 +/- 3.63 micrograms/kg, respectively. The ADE was significantly greater (P less than 0.05) during isoflurane anesthesia and ketamine-isoflurane anesthesia than during halothane anesthesia. The percentages of change in systolic blood pressure (means +/- SD) at the ADE during halothane, ketamine-halothane, isoflurane, and ketamine-isoflurane were 31 +/- 34, 41 +/- 17, 127 +/- 27, and 148 +/- 57, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Epinephrine-induced ventricular arrhythmias in dogs anesthetized with halothane: potentiation by thiamylal and thiopental.

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.