Facial swelling associated with impaction of the deciduous and permanent maxillary fourth premolars in a dog with patent ductus arteriosus.

A three-year-old Labrador retriever was referred for decreased appetite, a painful swelling in the region of the maxillary right fourth premolar, and a heart murmur indicative of patent ductus arteriosus (PDA) diagnosed 1.5-weeks prior to presentation. Oral examination and intraoral dental radiographs showed impaction of the maxillary right fourth premolar surrounded by reactive alveolar bone. Necrotic bone, remnants of the deciduous maxillary right fourth premolar, and the impacted permanent maxillary right fourth premolar were removed following surgical exploration of the area. The PDA was repaired without complication 2-weeks following oral surgery. The extraction site was healing appropriately, and the dog's inappetence and painful facial swelling had resolved.

Exercise potentiation of lung injury following inhalation of a pneumoedematogenic gas: perfluoroisobutylene.

Exercise performed after exposure to various pneumoedematogenic gases can increase the severity of pulmonary edema beyond that which occurs when exposure is followed by rest. The present study was performed to investigate the potential relationship between a preexisting breach in the lung's permeability status following exposure to an edematogenic gas (perfluoroisobutylene, PFIB) and the potentiating effects of postexposure exercise. Rats were exposed to a concentration of PFIB (100 mg/M3 for 10 min) that results in a unique postexposure latency period (approximately 8 h) prior to the occurrence of overt pulmonary edema. The study examined how exercise performed during and after the latency period affects the severity of the injurious response to this toxic gas. The initial results indicated that exercise performed during the post-PFIB exposure latency period does not potentiate the injurious response, as judged by conventional lung gravimetric and histopathological criteria, but when overt pulmonary edema was preexistent, exercise had a potentiating effect. Changes in lavageable protein were assessed as a more sensitive indicator of permeability changes that may occur during the latency period following PFIB exposure, and the study examined how exercise performed early during the latency period affects this index of pulmonary edema. The study also assessed whether PFIB-induced damage to lung cells is enhanced by exercise during the latency period by measuring lavageable lactate dehydrogenase activity. The results from these latter experiments suggest that a preexisting enhancement in lung permeability is not an absolute requirement for exercise to potentiate the pulmonary edematous response in lungs that are undergoing insidious injury, and that postexposure exercise does not enhance the cell-killing effects of PFIB as a mechanism underlying the exercise potentiating response. Conceivably, the ability of exercise to increase lavageable protein in the absence of a preexisting increase in lung permeability may be due to hyperventilation- and/or pulmonary hypertension-associated intercellular junctional changes that may occur during exercise. Additionally, it remains possible that exercise during PFIB-induced insideous lung injury results in an enhancement in the rate of transcellular transport of blood proteins onto the alveolar surface.

Use of permethrin as a miticide in the African hedgehog (Atelerix albiventris).

The African hedgehog, Atelerix albiventris (also known as Erinaceous albiventris; 1,2) has recently undergone an increase in popularity as an exotic pet. This popularity (Beatrix Potter not withstanding) is due in part to the small size of the African hedgehog (adults are 4-6 in in length, weighing approximately 1 lb), its lack of hibernation or aestivation if reared under controlled light and temperature, and its general good nature and accommodation to handling.

Relative acute toxicities of hydrogen fluoride, hydrogen chloride, and hydrogen bromide in nose- and pseudo-mouth-breathing rats.

Hydrogen fluoride (HF), hydrogen bromide (HBr), and hydrogen chloride (HCl) gases can be generated during the pyrolysis of a variety of materials and they may be encountered in numerous industrial settings. Although injury to the respiratory tract has been characterized following the inhalation of halide gases via the nasal route, essentially no experimental information is currently available about their injurious effects when they are inhaled during mouth breathing. In this study, we simulated mouth breathing by using a pseudo-mouth-breathing (MB) rat model in order to: (1) characterize the profiles and magnitudes of respiratory tract injury that result from the acute inhalation of relatively high mass concentrations of the above halides when the upper airway is bypassed, and (2) assess the relative toxicities of HF, HBr, and HCl when inhaled by way of either the nasal or the oral pathways. Tracheal tubes connected to mouthpieces were inserted into temporarily anesthetized rats, i.e., mouth breathers. Awake rats were placed into whole body flow plethysmographs for pulmonary ventilation studies while they were exposed either to air or to 1300 ppm of HF, HBr, or HCl for 30 min. Similarly pretreated rats were also exposed but without the mouthpiece, i.e., nose breathers (NB). The animals were euthanized 24 hr after exposure for histopathologic analyses of their upper and lower respiratory tracts and for lung gravimetric measurements. Tissue injury following NB exposure to the halides was confined to the nasal region, e.g., epithelial and submucosal necrosis, accumulations of inflammatory cells, exudates, and the extravasation of erythrocytes. MB exposure caused higher mortality rates and major tissue disruption in the trachea, including epithelial, submucosal, glandular, and cartilage necrosis, and accumulations of inflammatory cells and exudates. More peripheral lung damage was manifested by lung gravimetric increases and histopathologic changes primarily in the larger conducting airways. The results of this study demonstrate that the injurious response profiles to HF, HBr, and HCl markedly differ as a function of the route by which they are inhaled. Furthermore, examinations of the magnitudes of injury caused by exposure to the halides during nose or mouth breathing in conjunction with animal ventilatory data obtained during exposure to the halides suggest that HF, HBr, and HCl are quantitatively similar in their toxic effects in the respiratory tract.

The biodistribution of radiocopper-labeled compounds.

Porphyrins form extremely stable chelates with Cu2+. Two copper radionuclides, 67Cu and 64Cu, have attractive nuclear decay properties for use in nuclear medicine applications. We have investigated the use of radiocopper-labeled porphyrins for localization in inflamed tissue and for attachment to antibodies for tumor imaging and therapy. We have examined the biodistribution of a 67Cu labeled porphyrin, [5, 10, 15, 20-tetrakis(4-carboxyphenyl) porphinato [67Cu] copper (II)], 67 CuTCPP. The 67CuTCPP was intravenously injected into the tail vein of Fischer F344 male rats. The kidneys, liver, and spleen localize the greatest amounts of 67CuTCPP. The elimination of 67CuTCPP from the body is described by a normal exponential decay curve with a biological half-life of 108 hours and an effective half-life of 32 hours. We have also examined the biodistribution of 5-(4-carboxyphenyl)-10, 15,20-tris(4-sulfophenyl) porphinato [67Cu] copper (II) anti-Thy 1.2 antibody conjugates in normal and tumor-bearing male AKR/J mice. The liver, kidney, and tumor have the highest uptake of the 67Cu labeled antibody conjugate. In all 67Cu labeled compounds studied, the blood clearance was rapid and the bone concentration of the radiolabeled species was low.

Flexible intramedullary nails for ipsilateral femoral and tibial fractures.

Between June 1981 and August 1983, six patients were treated with flexible intramedullary nails for both femoral and tibial fractures in six floating knees. All six patients were males averaging 26 years of age and all six were involved in motor vehicle accidents. Concomitant associated injuries were common. Two femoral and five tibial fractures were open. All fractures were stabilized within 24 hours of injury by closed intramedullary nailing with Ender nails. At final followup, there was one femoral and one tibial nonunion in the same patient. For the remaining patients, femoral union averaged 10.3 weeks and tibial union averaged 18 weeks. Five patients regained full motion at the hip, and four regained full motion at the knee and ankle. Four patients returned to their preinjury level of function; two were less active, one ambulating without the use of external assistive devices, and one using a cane.

Placental prostacyclin production in normal and toxemic pregnancies.

Prostacyclin is a potent vasodilator and inhibitor of platelet aggregation. Because toxemia is characterized by increased vasoconstriction frequently associated with increased platelet aggregation and reduced uteroplacental blood flow, a deficiency in prostacyclin production during pregnancy could contribute to the development of toxemia. Placentally produced prostacyclin could have both local effects on the uteroplacental vasculature and systemic effects because prostacyclin, unlike the other prostaglandins, is not extensively metabolized by the lungs. Fresh human term placentas were obtained immediately after delivery from 12 normal and 12 toxemic (blood pressure greater than or equal to 140/90 mm Hg, urinary protein greater than 0.3 gm/24 hours) pregnancies. Tissues (300 mg) were incubated in a sterile manner in 5 ml of Dulbecco's Modified Eagle's Medium for 48 hours at 37 degrees C with 95% oxygen and 5% carbon dioxide in a metabolic shaker. Samples were collected at 8, 20, 32, and 48 hours and analyzed for prostacyclin by radioimmunoassay of its stable metabolite, 6-keto-prostaglandin F1 alpha. Prostacyclin production was significantly decreased in toxemic placental tissue compared with normal placental tissue (2.72 +/- 0.49 versus 7.22 +/- 0.44 pg/mg/hr, mean +/- SE, p less than 0.01). In both normal and toxemic placentas, prostacyclin production was inhibited by indomethacin (5 or 50 mumol/L) and not affected (p greater than 0.10) by arachidonic acid (5 or 100 mumol/L). Lowering the oxygen concentration from 95% to 20% significantly (p less than 0.01) decreased prostacyclin production in normal but not toxemic placentas. Prostacyclin production rates in the amnion and chorion were not affected (p greater than 0.10) by toxemia. The amniotic and chorionic prostacyclin production rates were not different from each other (p greater than 0.10) and were only one seventh of the normal placental production rate. These data indicate that placental prostacyclin production is decreased in toxemia; therefore, this vasoactive prostaglandin may be involved in the causation and the associated hypertension and coagulation abnormalities of this disorder.

Metabolic abnormalities associated with rupture of the urinary bladder in neonatal foals.

Rupture of the urinary bladder was diagnosed in 4 neonatal male foals. Marked hyponatremia, hypochloremia, and hyperkalemia developed in all 4 cases, and the electrolyte abnormalities were considered to be of potential diagnostic value. Blood urea nitrogen concentration was normal or only slightly higher than normal in 3 of 4 cases and therefore was not a reliable diagnostic test.

Acute effects of cigarette smoking on left ventricular function at rest and exercise.

In this study we investigated the acute effects of cigarette smoking on cardiac function during exercise in 12 normal young males. Radionuclide angiocardiography was used to assess cardiac performance at rest and during upright-bicycle exercise on two consecutive days. On the second day each subject smoked three cigarettes. Exercise studies were continued until 85% of age-predicted heart rate for an individual was achieved. At rest cigarette smoking induced significant increases in resting heart rate, blood pressure, and contractility and significant decreases in end-systolic volume and pulmonary transit time. Comparison of hemodynamic data during exercise before and after smoking showed the only significant change to be a decrease in pulmonary transit time. These results suggest that cigarette smoking in healthy young males does not significantly alter cardiac function during submaximal exercise.