Effects of lithium salts on experimental neurogenic lesions of the stomach and heart

It has been demonstrated in experiments on noninbred rats that lithium chloride and lithium hydroxybutyrate exert a prophylactic therapeutic effect in respect to neurogenic gastric lesions and reduction in the content of creatine phosphate in gastric and cardiac tissues, induced by stressful exposures (3-hour immobilization and electric stimulation of hungry animals). The effects of lithium hydroxybutyrate were more demonstrable than those of lithium chloride.     

The effect of hyperglycemia on the development of experimental myocardial infarct

Experiment on 72 dogs has shown that myocardial infarction (M1) against a background of hyperglycemia proceeds as shifts healing hyperactive MI. Shifts in carbohydrate metabolism results in disturbances of dynamics of the necrotic infarction zone processes that induces complications of healing changes in the content of myoglobin, creatine kinase, aspartateaminotransferase with MI against a background of hyperglycemia greatly differ from those typical of noncomplicated and complicated hyperactive MI.     

Myocardial lesions in experimental acute heart failure

The present study concerns the morphological and biochemical lesional picture of the myocardium in cases of acute heart failure induced by various experimental models: ligature of the coronary artery, direct electric stimulation of the heart by catheterism, lethal hemorrhage, pneumothorax, beta-adrenergic shock. Worthy of note was the similitude of the lesional myocardium pictures characterized electron microscopically by a wide range of lesions, from reversible to focal cytolysis, and biochemically by decrease of mitochondrial enzymes, ATP, Mg2-1 X K+ and increase of Na+ X H2O, Ca2+. Problems linked to the pathogenesis, reversibility of the lesions and efficiency of certain therapeutical means are discussed.     

The endocrine pancreas during pregnancy and lactation in the rat

The percentage of endocrine tissue in the whole pancreas, the volume density of the insulin producing beta-cells, the non-fasting plasma glucose level and the plasma insulin level were studied in pregnant rats and in puerperal lactating and non-lactating rats. During pregnancy there was a progressive rise in the percentage of endocrine tissue, in the volume density of the beta-cells and in the insulin level in peripheral blood. Plasma glucose levels declined during pregnancy. A lower plasma glucose level, a lower plasma insulin level, a lower percentage of endocrine tissue and a lower volume density of the beta-cells was found in lactating compared to non-lactating rats.     

The effect of exogenous prolactin on lactation performance of first-litter sows given protein-deficient diets during the first pregnancy

Twenty-four sows were used to study the effects of dietary protein restriction during pregnancy and exogenous porcine prolactin (pPRL) during late pregnancy and throughout lactation on lactation performance. Eight sows were given a protein-adequate diet containing 179 g crude protein (CP)kg⁻¹ during their first pregnancy while the remaining 16 sows received the same amount of a diet containing 80 g CP kg⁻¹. Eight of the sows given 80 g CP kg⁻¹ during pregnancy were injected with 15 mg pPRL i.m. twice daily at 08:00 and 20:00 between day (d) 102.1 (±0.3) of pregnancy and weaning after their first lactation. Pregnant sows offered the low protein diet gained significantly less body weight during gestation and tended to eat less in the subsequent lactation than sows given the protein-adequate diet. Dietary protein had no significant effect on birth weight, milk yield, milk composition or growth rate of the litter during lactation. Neither dietary protein intake during pregnancy nor exogenous prolactin affected the concentrations of plasma glucose, serum insulin, urea or non-esterified fatty acid (NEFA) during lactation. The concentration of lactose in plasma during lactation was unaffected by treatment, but at d 105 of pregnancy, plasma lactose levels were greater in sows which had received exogenous prolactin (32.4 vs. 6.2 mg l⁻¹, P < 0.05). The concentrations of RNA and DNA in mammary tissue biopsies were unaffected by either dietary protein or pPRL. The concentration of RNA and DNA increased between d 70 and 90 from 0.66 to 2.77 mg g⁻¹ and from 0.54 to 1.19 mg g⁻¹, respectively. Thereafter, RNA increased to 4.40 mg g⁻¹ at d 14 of lactation whilst DNA concentration remained at a similar level of 0.90 mg g⁻¹.Milk yield of sows between d 5 and 8 and between d 19 and 22 of lactation was reduced from 8.36 to 7.00 kg day⁻¹ and from 10.74 to 8.22 kg day⁻¹, respectively, in sows given pPRL. The protein content of colostrum from sows treated with pPRL was reduced from 164 to 104 g kg⁻¹ whereas the fat content increased from 47 to 127 g kg⁻¹. These results indicate that the administration of exogenous pPRL during late pregnancy and throughout lactation initiated lactogenesis prematurely and reduced subsequent milk yield during established lactation.     

The food intake of rats during pregnancy and lactation

Quantities of food required by Sprague-Dawley rats during gestation and lactation and in the post-lactation period were examined. Rats allowed to eat ad libitum during pregnancy consumed quantities of food only slightly greater than the amount reported to be the average intake of pregnant Sprague-Dawley rats (20 g/day). Rats delivered their pups on day 22 or day 23 of the gestation period, but regardless of the day of delivery, the food intake of each rat decreased on day 21 of pregnancy and then decreased a second time on the day of parturition. During lactation, food consumption of the rats soon exceeded the amount reported as the average intake of lactating rats (30-35 g/day). Food intake was found to escalate from 12.2 +/- 3.1 g/rat on day 0 of lactation, the lowest intake in the study, to 94.4 +/- 23.7 g on day 21 of lactation. However, in the latter part of the lactation period, the intake represented the combined food intake of dams and pups. Eight days in the post-lactation period were required for food intake of dams to return to a level near that recorded at the beginning of pregnancy.     

Thermogenesis and the energetics of pregnancy and lactation

Energy balance studies suggest that the overall efficiency of energy utilization does not increase during pregnancy in rodents, other than as a consequence of "hyperphagia". Diet-induced thermogenesis is not stimulated in response to the increased energy intake of the pregnant animal, the extra intake being retained at the maximum efficiency. Biochemical studies on brown adipose tissue, the main site of adaptive thermogenesis in rodents, are consistent with the energy balance data, at least in rats and mice. However, in hamsters (golden and Djungarian) some atrophy of the tissue is evident during pregnancy. In contrast to pregnancy, the thermogenic activity (mitochondrial GDP binding) and capacity (uncoupling protein content) of brown adipose tissue are substantially reduced during lactation in rats and mice. These changes result from a fall in sympathetic activity in the tissue in lactation. Sympathetic activity and thermogenic capacity are, however, fully restored following weaning of the pups. The functional atrophy of brown adipose tissue during lactation is linked to a substantial saving in maternal energy expenditure, reducing the energy requirements for milk production. The lactating-post-lactating animal provides an excellent example of a physiologically programmed reversible atrophy of brown adipose tissue.     

Quantitative evaluation of the development of isoprenaline-induced heart lesions

The development of heart lesions induced by isoprenaline (ISO) was quantitatively evaluated by 203Hg-Mercurascan (MSC) which was taken up and retained in the damaged cells. After the administration of ISO, the MSC uptake increased immediately at a constant rate, which was independent of the dose of ISO. A higher cardiotoxic effect of increased doses of ISO was caused by prolongation of the time during which the development of heart lesions proceeded. Later, when the damaged cells were subjected to cytolysis, MSC uptake decreased. The blockade of the effect of ISO by methypranol immediately stopped any further increase of MSC uptake. The accumulation of other labelled substances (Neohydrin, HgCl2, CaCl2) in the damaged myocardium was compared with the uptake of MSC. MSC and HgCl2 in particular are suitable for the observation of early changes; relatively less CaCl2 accumulated in the damaged hearts, but it can be used for the detection of more advanced lesions.