Quarterly journal of experimental physiology (Cambridge, England)最新文献

Application of ACh (10(-6) M) to the isolated rat pancreas elicited large increases in amylase secretion, radiolabelled 45Ca influx and cytosolic free Ca2+ levels in zero and normal (1.1 mM) extracellular magnesium (Mg2+). Elevated (10 mM) Mg2+ significantly (P less than 0.001) reduced the ACh-induced amylase output and Ca2+ mobilization. Similarly, ACh (10(-5) M) caused a transient increase in 45Ca efflux from pre-loaded pancreatic segments in normal Mg2+ compared with the much reduced effect in elevated Mg2+. The results suggest that a modification in Mg2+ influences ACh-evoked amylase secretion by regulating Ca2+ mobilization.

Rats were pair-fed for 28-32 days a nutritionally adequate liquid control diet or an isocaloric diet containing ethanol (5% v/v). Brush-border membrane vesicles were prepared from jejunal mucosa and Na+-dependent D-glucose accumulation was measured using sugar concentrations of 0.2-1.0 mmol l-1. In separate experiments the effects of acute ethanol exposure on glucose uptake by vesicles prepared from chow-fed rats were determined. Chronic ethanol ingestion enhanced Na+-gradient-dependent glucose uptake. In contrast, incubation of vesicles with alcohol (4% v/v), reduced active uptake of the sugar.

Fluid balance and thermoregulation were studied during an acute heat load (maximal daily temperature, 38 +/- 1 degrees C; night temperature 27 +/- 1 degrees C) in six goats during lactation and non-lactation. The goats had free access to water for 1 day, followed by 29.5 h of water deprivation and then water was returned. With water available the goats increased water intake and urinary and milk water losses, while plasma and milk osmolality decreased. Water deprivation caused plasma osmolality and vasopressin concentration to increase most in lactating goats. Milk osmolality rose to values similar to plasma osmolality. Plasma cortisol increased in lactating goats at the end of dehydration. Renal Na+ excretion increased during dehydration in lactating goats. Evaporative heat loss was larger in lactating goats when hydrated, but became less than in non-lactating goats during dehydration. Lactating goats exhibited higher respiratory frequency and rectal temperature than non-lactating goats. In conclusion, our results show that goats increase the water turnover during heat stress if allowed to drink ad libitum, but when they are deprived of water lactating goats reduce water loss in urine, milk and by evaporation, and rectal temperature reaches higher levels than in non-lactating animals. This saving of water could allow milk production to be maintained for a longer time during heat stress.

The effects of insulin on fetal growth rates were investigated by measuring crown-rump length (CRL) chronically in sheep fetuses before and after pancreatectomy, sham operation or pancreatectomy accompanied by insulin-replacement treatment. Pancreatectomy of the fetus produced hypoinsulinaemia and reduced the daily and total increments in CRL by 40-50% over the last 20-30 days of gestation. The growth rate fell immediately after pancreatectomy and remained low throughout the rest of gestation. In contrast to the sham-operated fetus no pre-partum decline in the growth rate was observed in the pancreatectomized animal. The body weight, limb lengths and actual CRL at delivery were also significantly less after pancreatectomy than in the sham-operated animals. When fetal insulin levels were maintained after pancreatectomy by exogenous insulin infusion, the daily and total increments in CRL and the body size at delivery were restored to their normal values. Raising insulin levels above normal in the pancreatectomized fetus did not lead to additional fetal growth. When the data from all the fetuses were combined irrespective of treatment, there were significant positive correlations between the plasma insulin concentration in utero and the mean daily increment in CRL after treatment and between the former value and the body weight at delivery. These observations demonstrate that insulin is a major determinant of the growth rate in utero and that it is required throughout late gestation for the normal growth and development of the sheep fetus. They also indicate that insulin deficiency is probably the primary cause of the growth retardation observed after fetal pancreatectomy.

Our purpose was to determine the amount of injury to extensor digitorum longus (EDL) and anterior tibial (ATB) muscles of mice from 1 h to 30 days following passive shortening and lengthening, shortening contractions and lengthening contractions. The shortening-lengthening cycle was of 600 ms duration and was repeated every 5 s for 30 min. Contractions were produced during either the shortening or lengthening phase with stimulation at 100 Hz for 300 ms. The amount of injury was evaluated by the decrease in the number of fibres in a cross-section of the muscle and in the maximum isometric tetanic force (Po). Passively shortened and lengthened and actively shortened EDL and ATB muscles showed no evidence of injury. At 3-5 days after lengthening contractions, EDL and ATB muscles showed an inflammatory response. At 3-5 days, the number of fibres in the cross-section of the injured EDL muscles was 65% of that of the contralateral control EDL muscle, whereas no change was observed in the number of fibres in the injured ATB muscles. By 3 days, the presence of myoblasts, myotubes and central nuclei indicated regeneration of fibres. One hour after shortening contractions, the Po of EDL and ATB muscles decreased to about 75% of the contralateral control value, but recovered completely by 3 days. In contrast, 1 h after lengthening contractions the Po of EDL and ATB muscles decreased to 52 and 40% respectively of the contralateral control value and then both recovered to about 65% within 3 h. For the ATB muscle, the Po showed a secondary decrease to 49% of the contralateral control value at 1 day and for the EDL muscle, to 47% at 3 days. Each muscle recovered gradually and by 30 days the number of fibres and the Po of the injured muscles were not significantly different from values for contralateral control muscles.

Force-velocity, power-velocity and unloaded shortening data were obtained from in situ medial gastrocnemius muscle-tendon complexes (stimulated at 60 Hz) with intact circulation of mature male rats (approximately 125 days old). Measurements were carried out at the end of a long (15 s) contraction (fatigued muscles) or with a short (1 s) contraction either in the fresh state (fresh muscles) or in muscles which had recovered for 15 min after a long contraction. Compared to the fresh state fatigue reduced isometric force by 57%, maximal shortening velocity by approximately 40% and maximal power output by 81%. These reductions were similar to data previously obtained with younger rats (40 days old). However, the velocity data of the muscles which had recovered for 15 min after a long contraction showed a greater reduction in the mature rats. This difference between the two age groups together with a difference in the changes in the initial parts of the isometric force time curves suggest an age-dependent response of the fast-fatigable fibre population of these mixed muscles. In a separate series of experiments the underlying mechanism of the recovery from fatigue was studied in a group of young rats. Fatigue was induced with five long (15 s) contractions (each at 5 min intervals). The recovery of isometric force and power output was monitored with short contractions which indicated a plateau of recovery but the absolute values were still reduced after 60 min (85 and 71% of prefatigue values, respectively). Phosphocreatine concentration recovered rapidly, whereas the ATP concentration was still markedly reduced after 1 h of recovery. The time courses of recovery of inosine-5'-monophosphate (IMP) and lactate concentrations resembled those of force and power output. Thus it is possible that age-dependent differences in IMP and/or lactate production may play a role in fatigue and recovery from fatigue.

Fetal uptakes of amino acids and ammonia via the umbilical circulation were measured in single pregnant ewes at mid-gestation (range 66-81 days). There were significant net fluxes from placenta to fetus of ammonia and twelve amino acids (in decreasing order: glutamine, glycine, alanine, proline, lysine, arginine, threonine, valine, leucine, tyrosine, asparagine, isoleucine) and net fluxes from fetus to placenta of glutamate and serine. The estimated serine flux was 139 mumol day-1 (g fetal dry wt)-1. Comparison with late gestation data indicated a similar pattern of amino acid exchange. However, the relatively large placental uptake of fetal serine was a distinctive feature of mid-gestation. The net fetal uptake of amino acid nitrogen was 2.83 +/- 0.66 micrograms N (mumol O2 uptake)-1, or 18 mg N day-1 (g dry wt)-1. This uptake was similar in magnitude to the combined fetal requirements for nitrogen accretion and urea synthesis and represented approximately 32 and 43% of fetal carbon and energy requirements, respectively.