L. Jönsson

Histopathological changes in relation to cadmium concentration in horse kidneys

Abstract Histopathological changes in kidney cortex, as observed by light microscopy, are related to cadmium concentration in kidney cortex from 69 normal Swedish horses. Cadmium concentrations in kidney ranged from 11 to 186 μg Cd/g wet wt with an average of 60 μg Cd/g, which is considerably higher than those normally found in humans. The microscopical changes were rated and related to cadmium concentrations in kidneys by dose—response curves. A relationship existed between frequency of morphological changes and cadmium concentration in the renal cortex. There was no obvious relationship between age and frequency of histopathological changes. This indicates that in horse kidneys morphological changes occur at cadmium concentrations which are lower than the tentative critical level for humans of 200 μg Cd/g. It is concluded that horses constitute a population at risk for environmental cadmium contamination.

The role of sympathetic activity in initiating malignant hyperthermia

The role of sympathetic activity in triggering malignant hyperthermia (MH) is controversial. Increased sympathetic activity has been considered by some to be the causal factor, whilst others believe this activity to be secondary to metabolic events in the MH syndrome. In this study, a number of parameters, including the blood levels of noradrenaline and adrenaline, were followed in pigs susceptible to MH during exposure to halothane. Seven pigs, crossbreeds of Swedish Landrace and Yorkshire, females and castrated males, aged about 9 months were used. Results are presented for individual pigs. One of the pigs was a nonresponder. The time of onset for different signs of MH varied greatly, as judged by ten independent observers. Onset of changes in heart rate, muscle temperature, blood Pco2 and pH, plasma adrenaline and noradrenaline could be scored. The metabolic events (increased Pco2 and decreased pH in blood) significantly preceded the signs of increased sympathetic activity (increased heart rate and elevated levels of catecholamines in blood). Our results support the view that increased sympathetic activity does not initiate MH. The sympathetic activity, however, strongly contributes to the fulminant MH syndrome.

Associations between cardiac pathology and clinical, echocardiographic and electrocardiographic findings in dogs with chronic congestive heart failure

The objective of this study was to correlate defined pathological features with clinical findings in dogs with naturally occurring congestive heart failure (CHF). Fifty-eight dogs with CHF were examined clinically and using echocardiography and electrocardiography. Detailed cardiac post-mortem examination was used to assess intra-myocardial arterial narrowing, myocardial fibrosis and atrophy and myxomatous mitral valve degeneration (MMVD). Arterial narrowing significantly correlated with fibrosis (P<0.0001) and with fractional shortening, an indicator of systolic function (P=0.002). The grade of fibrosis was associated with shorter survival time (P=0.002), and the papillary muscle fibrosis score tended to correlate with proximal isovelocity surface area radius (P=0.03). Data from this study lend support to the hypothesis that naturally occurring canine CHF is affected by several factors such as MMVD, myocardial atrophy and fibrosis, and by arteriosclerosis. Further, more extensive research will be required to establish cause-effect relationships between these cardiac lesions and the pathophysiology of CHF in dogs.

Cadmium, zinc, and copper in rabbit kidney metallothionein--relation to kidney toxicity.

Exposure to cadmium results in the production of renal metallothionein (MT) (1–5). In the kidney, MT will bind zinc as well as cadmium (1,2). Studies of renal MT obtained from normal horses, with a comparably high concentration of cadmium in their kidneys, have shown that the relative content of zinc in MT decreases with increasing cadmium concentration in the kidney (4). In rats it has been demonstrated that renal MT may also bind copper (6). It is believed that toxic effects caused by cadmium in the kidney will emerge when the tubular cells are unable to produce enough MT to sequester all cadmium ions (2,7).