To examine the effect of alendronate (4-amino-1-hydroxybutylidene bisphosphonate) on fracture repair, the drug was given to mature beagle dogs orogastrically at 2 mg/kg/day for 9 weeks preceding fracture. 16 weeks after fracture, or both before and after fracture (25 weeks). A transverse mid-diaphyseal fracture of the right radius was surgically induced and was stabilized by external coaptation splinting. Fracture healing and bone remodeling were evaluated by radiography, gross and histological examination, and bone histomorphometry. The mechanical properties of the fracture callus were determined by a four-point bending test. Radiographs and gross and microscopic examination demonstrated normal bone healing at the fracture site in all dogs. In dogs that received alendronate during the fracture healing period, at 16 weeks the calluses were approximately 2-3 times larger than those in dogs that received a placebo during the healing period. This is consistent with slower callus bone remodeling, an expected pharmacological effect of the compound. Bone histomorphometry demonstrated that treatment with alendronate did not inhibit bone formation or mineralization. Mechanical testing showed that the ultimate load at failure and the flexural rigidity of both the fractured and contralateral intact bone were unaffected by treatment with alendronate. Therefore, in this study, treatment with alendronate before or during fracture healing, or both, resulted in no adverse effects on the union, strength, or mineralization of bone in mature beagle dogs.
Freshwater algal blooms associated with outbreaks of sudden death in ducks and swine were examined for cholinesterase (ChE)‐inhibiting toxins as the possible cause of death. In both investigations, Anabaena flos‐aquae was identified as the predominant alga in the bloom material. In both cases, assays on tissues from mice dosed intraperitoneally with algal extracts revealed inhibition of ChE in whole blood, plasma, diaphragm and lung, but not in brain. With algae from the field case involving ducks, toxicosis was experimentally reproduced by oral intubation in ducks and swine, but not in mice and a steer. However, the steer, as with other species, was susceptible to toxicosis induced by parenteral administration of an algal extract. Assays on tissues from affected animals revealed inhibition of ChE in whole blood, plasma, red blood cells, diaphragm, lung and pectoral muscle, but not in brain or retina. In vitro electric eel (EC 3.1.1.7) ChE assays with HPLC‐purified extracts of the same alga revealed direct inhibition of acetylcholinesterase. Clinical signs in all animals were compatible with muscarinic and nicotinic cholinergic stimulation. Death of exposed animals is an apparent result of peripheral ChE inhibition.
Previous efforts have been made to provide concise summaries on the hazards of toxicoses from exposures of domestic animals to blue-green algae. 14 It is clear, however, that veterinarians need improved access to information currently emerging with regard to blue-green algae toxicoses. Recent investigations are shedding light on the identity of the potent toxins responsible and the pathophysiology of the syndromes produced. Reviews from the past few years provide an idea of the reported occurrence of cyanobacterial toxicoses and the toxins detected, 12,13 but the diagnosis of blue-green algae toxicosis has remained difficult because of a lack of concise information on appropriate diagnostic procedures. One must recognize that many algal blooms are not hazardous; therefore, a diagnosis of toxicosis following ingestion of an algal bloom, even when it is dominated by organisms known to have produced toxins in the past, should be confirmed. At the present time, demonstration of toxins in the algae and documentation of appropriate responses in the animal form the basis for many diagnoses.
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