Female Sprague Dawley rats were subjected to either bilateral ovariectomy or sham surgery. Tetracycline derivatives were administered to each rat on two separate occasions to label sites of bone formation. All rats were sacrificed at 5 weeks postovariectomy and their proximal tibiae were processed undecalcified for quantitative bone histomorphometry. A twofold decrease in trabecular bone volume was noted in the proximal tibial metaphysis of ovariectomized rats. This bone loss was associated with elevated histomorphometric indices of bone resorption and formation. Ovariectomy increased osteoclast surface and numbers as well as osteoblast surface and numbers. Elevations in calcification rate and fractional trabecular bone surface with double tetracycline labels also suggest that bone formation was stimulated in ovariectomized rats. In addition, ovariectomized rats exhibited a greater rate of longitudinal bone growth relative to sham-operated control rats. These histomorphometric data indicate that ovariectomy induces marked bone loss and accelerated skeletal metabolism in rats.

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Whole-animal net electrolyte fluxes (Ca2+, apparent H+, titratable acidic equivalents, ammonia, Na+, Cl−, K+, Mg2+, phosphate and sulphate) and respiratory gas exchange were monitored throughout the moulting cycle in juvenile freshwater crayfish Procambarus clarkii (Girard) at 21 °C. Intermoult crayfish were essentially in ion balance. As crayfish approached ecdysis (−3 days, where t=0 is the day when the cuticle is shed), there was a net efflux of Ca2+ (−1000μmolkg−1 h−1) correlated with a corresponding uptake of acidic equivalents (or base output) of +2000μmolkg−1 h−1. Following ecdysis, both fluxes switched vector; uptake of Ca2- (+2000μmolkg− h−) and basic equivalents (+4000μmolkg−1h−1) were completed within 6 days. The moulting cycle also affected fluxes of electrolytes other than those involved in CaCO3 resorption and deposition. Crayfish remained in Na+; and C−; balance from intermoult up to ecdysis. Following ecdysis, both were taken up actively at rates of around plus;500μanolkg−1h−1 for 3 days, presumably restoring the haemodilution that would have resulted from water loading. A premoult efflux of K+ was partially offset by postmoult uptake. Meanwhile, crayfish experienced increased efflux of phosphate following ecdysis, probably because of increased integumentary permeability. Rates of O2 uptake (MO2) and CO2 excretion (Mco2) increased to peak values (double intermoult rates) immediately prior to ecdysis. While MO2 recovered during postmoult, Mco2 dropped precipitously, significantly reducing the gas exchange ratio. Since the Mco2 deficit agreed well with the postmoult basic equivalent uptake, the latter is probably attributable to HCO3− uptake for calcification.

Gastric dilatation‐volvulus (GDV) is a dramatic and enigmatic disease of large and giant breed dogs characterised by the rapid accumulation of gas in the stomach. This causes gastric dilatation, twisting of the stomach about its long axis, compression of surrounding organs, hypovolaemic and cardiogenic shock, and if untreated, death. It has been estimated that the disease afflicts approximately 60,000 dogs in the USA each year with a mortality rate ranging from 7 to 60 per cent depending on accessibility to adequate veterinary care. The cause is unknown. While diet was at one time believed to be associated with the genesis of the disease, critical review of available data provides no evidence to support this hypothesis. A variety of predisposing or risk factors have been identified but none is suspected of being the cause, indeed, the disorder may have a multiple aetiology. Current thinking suggests that the final common pathway in the development of GDV may be an inhibition of gastric motility and emptying. This could come about through a primary disruption of normal gastric electrical patterns or through the effect of extraneous stressful events that disrupt gastric motility. After dilatation a series of potentially lethal events is unleashed which include compression of the caudal vena cava, pooling of blood in the microcirculation of the viscera and hindlimbs, metabolic acidosis, gastric necrosis, cardiac arrhythmias, disseminated intravascular coagulation, hypotensive and cardiogenic shock and death. Nevertheless, even advanced cases can survive if treated appropriately. If the cause could be identified logical prophylaxis might follow. Studies at the University of Florida have failed to demonstrate any effect of diet on gastric function in large breed dogs, suggesting that diet is probably not the cause of the disease. Researchers at Colorado State University also found no association with diet in clinical patients. Recent studies at the University of Florida have revealed distinct abnormalities in gastric electrical activity in GDV patients. In human patients these abnormalities, called dysrhythmias, have been associated with gastric distention, bloating, delayed emptying, nausea and retching. Unfortunately, dysrhythmias are also present, albeit to a lesser degree, in experimental GDV. These findings leave unanswered the question as to whether abnormalities in gastric motility play a role in the genesis of GDV.