Lateral exploration of fistulas developing after total ear canal ablations: 10 cases (1989-1993).

A lateral approach was used successfully in seven of 10 dogs to resolve fistulas which developed after total ear canal ablations and bulla osteotomies. The approach facilitated identification and removal of horizontal ear canal remnants in four of the 10 cases. Facial nerve function was worsened temporarily by lateral exploration in two cases. Seven cases had no fistula recurrence during follow-up, which ranged from 12 to 72 months. Three cases each had fistula recurrence one-to-two months after fistula exploration.

Circumcostal cloacapexy in a python.

A chronic cloacal prolapse in an Indian python was repaired by modification of a cloacapexy technique. After isolation of the cloaca, stay sutures were placed through the lumen of the cloaca and through the musculature of the body wall, incorporating a rib within the pexy.

Retained caseous yolk sac in a Burmese python (Python molurus bivittatus).

Retained yolk sacs are common in the domestic chicken and account for considerable morbidity and mortality during late embryonic development and within the first 10 days of life. What is believed to be the first recorded instance of a retained caseous yolk sac and its successful surgical removal from a Burmese python (Python molurus bivittatus) is reported. The snake experienced no post-operative complications and continues to be well 16 mo following surgery.

Echocardiography and surgery in a dog with left atrial rupture and hemopericardium.

Endocardial splitting and left atrial rupture were diagnosed in a dog with mitral regurgitation that experienced the sudden onset of collapsing episodes, weakness, depression, labored breathing, and weak pulses. Thoracic radiographs showed a rounded cardiac silhouette with prominent left atrium consistent with hemopericardium due to left atrial rupture. Two-dimensional echocardiography confirmed the presence of severe mitral valve disease, pericardial fluid, and a laminated blood clot caudal to the left ventricle. A sterile emergency thoracotomy was performed, the hemopericardium and blood clot were removed, and the rupture site in the left atrium was repaired with reinforced sutures. The dog recovered from surgery but died the next day, presumably from a ventricular arrhythmia.

Studies on the permeability of potassium ions across the dura and arachnoid mater of the rat spinal cord.

A combined impounder-surface K+ electrode was developed to measure change in K+ ion concentration of the cerebrospinal fluid (CSF) across the dura and arachnoid maters. To determine whether K+ permeability of the rat dura and arachnoid maters is due to an intrinsic permeability, a study was conducted using an atraumatic laminectomy model. Dorsal laminectomy was performed at T7-8, T12, and L1. Artificial CSF containing 4.2 mM, 24.2 mM, or 54.2 mM of K+ was administered by anterograde subdural infusion into the subarachnoid space from the proximal laminectomy site (T7-8), with effluent overflow at the distal laminectomy site (L1). K+ concentration on the dorsal aspect of the central laminectomy site (T12) was measured. It was found that changes in K+ concentrations of the infused solution were detected by the epidural surface electrode. This suggests that the intact rat spinal cord dura and arachnoid maters may be permeable to K+ in this laminectomy model. This study supports the use of the combined impounder-K+ electrode for measuring changes in K+ ion concentration of the CSF that can result from spinal cord trauma and ischemia.

Effects of membrane acting-drugs on plasmodium species and sickle cell erythrocytes.

The effects of several membrane-acting drugs on malaria and sickle cell anemia was studied. In the initial experiments, propranolol and W-7 were shown to increase red cell density. In vitro, these drugs inhibited the growth of P. falciparum. However, in vivo experiments using the murine malarial parasite, P. vinckei, demonstrated little, if any, anti-parasite activity with the doses of drugs employed. Subsequently, prostaglandin oligomeric derivatives were found to inhibit the growth of P. falciparum in vitro and P. vinckei in vivo. Since prostaglandin oligomers inhibited the formation of dense, dehydrated cells (irreversible sickle cells), they may also have therapeutic efficacy in sickle cell anemia.

Chlorpromazine protects rat spinal cord against contusion injury.

The protective effect of chlorpromazine on rat spinal cord injury was investigated using a dynamic impact model. A 10 g weight was dropped 5 cm on an impounder placed on the exposed spinal cord at the T-11 level. Changes in potassium concentration on the epidural surface of the injured spinal cord were measured using a combined impounder-K+ electrode assembly. Recovery of motor performance was estimated using the modified Tarlov score. In the injury control (no treatment) group, the recovery was slow. Animals were still paralyzed 4 weeks after injury and none of them could walk; the Tarlov score was 1.88 +/- 0.78 (S.D.). In contrast, the chlorpromazine-treated group (20 mg/kg i.p. 30 min prior to injury) recovered significantly in 4 weeks. Animals could either support body weight or walk with some deficit; the Tarlov score was 4.0 +/- 0.35. Chlorpromazine inhibited potassium efflux from the spinal cord after contusion. Possible mechanisms of protection of neural cells by chlorpromazine are discussed.

Charybdotoxin improves motor recovery of the rat after spinal cord injury.

Charybdotoxin, a highly specific inhibitor of calcium-activated potassium efflux, was found to protect rat spinal cord against dynamic impact injury. In a control (nontreated) group, a weight drop of 10 gram X 5 cm on the T-11 segment of the rat spinal cord paralyzed hindlimbs, and recovery was slow. After 4 weeks, Tarlov scores (a behavioral index) were 1 to 2; the hind legs could not support body weight. In contrast, with animals pretreated 30 minutes prior to the injury by 0.12 mg charybdotoxin/kg (IP), Tarlov scores increased to 3.5-4.5 by three weeks after injury; animals could walk with some deficit. A possible mechanism for the protective effect of this drug is discussed.

Abnormal membrane properties of the sarcoplasmic reticulum of pigs susceptible to malignant hyperthermia: modes of action of halothane, caffeine, dantrolene, and two other drugs.

The role of sarcoplasmic reticulum (SR) in malignant hyperthermia (MH) was studied using the heavy microsomal fraction prepared from semitendinosus muscles of both normal and genetically MH-susceptible pigs. In the presence of ATP, SR was loaded with 70 nmol Ca2+/mg SR protein. Under these conditions, MH-SR demonstrated Ca2+-induced Ca2+ release (Ca-ICaR) and halothane-induced Ca2+ release (halothane-ICaR; halothane concentrations as low as 10 microM). Normal SR did not demonstrate these release phenomena. Dantrolene inhibited the halothane-ICaR, but did not inhibit the Ca-ICaR. Ruthenium red and tetracaine inhibited both types of Ca2+ release. From the measurement of passive Ca2+ efflux, it was shown that dantrolene did not affect the Ca2+ permeability of the SR itself, but suppressed only the halothane-induced increment of the permeability. The membrane order parameter of the SR, as measured by the spin-probe EPR technique, indicated that halothane disordered the lipid bilayer of MH-SR to a greater extent than it did of normal SR. This halothane disordering effect on MH-SR was antagonized by dantrolene. Ruthenium red and tetracaine did not antagonize the halothane disordering effect. These results raise the possibility that halothane could disturb the structure of the lipoprotein complex in MH-SR in such a way that it could open the Ca2+-release channels. The Ca2+ thus released further opens the channel through the Ca-ICaR mechanism in a positive feedback fashion, thus triggering the MH syndrome. The efficacy of dantrolene in ameliorating the MH syndrome might be related to the inhibition of this halothane effect.

Nitrendipine, nifedipine and verapamil inhibit the in vitro formation of irreversibly sickled cells.

Nitrendipine, nifedipine and verapamil inhibit the in vitro formation of irreversibly sickled cells. Using a method of forming both dehydrated cells and irreversibly sickled cells in vitro by repeated cycles of sickling and unsickling, the effects of several drugs in inhibiting the formation of these cells were studied. Drugs known as Ca2+ channel antagonists, such as nitrendipine, nifedipine and verapamil were found to inhibit these reactions. Other types of calcium channel blockers, such as lanthanum and zinc, did not inhibit the formation of these cells. The potency of drugs to inhibit irreversibly sickled cell formation was related to the potency of inhibition of calmodulin-activated phosphodiesterase.