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Biomedical subjects

C T Jones

Publications and source records attributed to C T Jones.

At least 73 records · Page 4Linked to original sources
PubMed1988

The role of the adrenal medulla and peripheral sympathetic nerves in the physiological responses of the fetal sheep to hypoxia.

In studies on the role of the peripheral sympathetic system during fetal life the effects of adrenal demedullation or chemical sympathectomy on the responses of the fetal sheep to hypoxaemia have been studied. Fetal sheep of 127-138 days gestation were either adrenal demedullated by injection of acid formalin into the adrenal medulla, chemically sympathectomised by chronic treatment with guanethidine sulphate, or subjected to both manipulations. None of these treatments had any effect upon resting heart rate and blood pressure, or blood gas status. Hypoxia was induced by giving the pregnant ewe 9% O2 and 3% CO2 in N2 to breathe for 60 min. This depressed fetal PO2 by about 30% in the intact and all but the adrenal-demedullated, chemically-sympathectomised fetuses, where the fall was about 50%. Similarly in this group of fetuses there was a sharp fall in plasma pH contrasting with little change in the other fetuses. Adrenal demedullation blocked completely the hypoxia-induced rise in fetal plasma adrenaline, and reduced that of noradrenaline to 10% of normal, implying that during hypoxia most of the plasma elevation of catecholamines is of adrenal origin. In contrast, and possibly to compensate for the blunted catecholamine response, plasma AVP increases during hypoxia were substantially enhanced by adrenal demedullation. Fetal hypoxia was associated normally with a fall in heart rate and rise in blood pressure. Adrenal demedullation had no effect on the heart rate changes, thought to be a reflex response to rise in blood pressure, but abolished the rise in blood pressure during hypoxia. Chemical sympathectomy, in contrast, abolished the fall in heart rate even though blood pressure rose. This shows clearly that reflex changes in heart rate during hypoxia can be uncoupled from those in blood pressure. Turning to the endocrine effects of demullation, cortisol and ACTH responses to hypoxia were much increased, whilst those of insulin were depressed. During chemical sympathectomy these responses were much accentuated in the case of cortisol and ACTH but depressed for insulin. A feature of these effects was that the endocrine changes in the adrenal-demedullated fetuses, whilst initially high, were not sustained for the 60 min of hypoxia. The same was true of the fetal matabolic responses to hypoxia reflected in plasma glucose, lactate and non-esterified fatty acids. Most of the results in this study are consistent with the proposal that in the fetus adrenal catecholamines are important in sustaining responses to hypoxia, but not normally initiating them.

Adrenal Medulla↗
PubMed1988

Studies on the growth of the fetal sheep. Effects of surgical reduction in placental size, or experimental manipulation of uterine blood flow on plasma sulphation promoting activity and on the concentration of insulin-like growth factors I and II.

The effect of long- and short-term manipulations of uterine blood flow on fetal plasma levels of IGF-I and -II have been studied in sheep at days 125-139 of pregnancy and compared with those in near term rats and guinea pig. The primary objective is to show that both long- and short-term reduction of uterine blood flow is associated with increase in the fetal plasma concentration of IGF-II while that of IGF-I falls. In the pregnant sheep long-term depression of utero-placental blood flow was caused by surgical reduction in placental mass (carunclectomy) prior to conception. This reduced fetal weight to 2.42 +/- 0.49 kg (SD) compared with 3.41 +/- 0.46 in controls; the respective values for uterine blood flow being 1694 +/- 558 and 913 +/- 324 ml/min respectively. This was associated with a fall in fetal plasma IGF-I concentration from 22.6 +/- 3.4 ng/ml to 14.9 +/- 1.31 ng/ml and a rise in IGF-II from 1952 +/- 284 ng/ml to 3360 +/- 914 ng/ml respectively. Similar changes in the plasma concentrations of IGF peptides were observed in fetal rats and guinea pigs in response to uterine artery ligation. Short-term reduction (60 min) of the uterine blood flow was caused either by compression of the common uterine artery to depress flow from 1491 +/- 375 to 648 +/- 216 ml/min or through intraarterial infusion of adrenaline at 35 ug/min to lower flow from 1628 +/- 339 to 1195 +/- 128 ml/min. Such falls in uterine blood flow had no significant effect on fetal plasma IGF-I levels but increased IGF-II levels by 30 to 60%.

Animals↗
PubMed1987

Effects of increased energy expenditure on weight gain and adiposity in the LA-corpulent rat.

Groups of lean or pre-obese LA/N-cp rats were subjected to a program of vigorous exercise (less than 4 hr/day) or remained sedentary from 6 weeks until 12 weeks of age. Sedentary pre-obese rats gained weight twice as rapidly as sedentary lean rats. Exercise treatment resulted in greater decrements in body wt in obese than in lean rats, but did not result in absolute weight loss in either group. At 12 weeks of age, fat pad weights in principle depots were 10-15 times greater in corpulent than in lean rats and were significantly smaller in the exercised groups of both phenotypes, and corresponded with lower relative adiposity compared to corresponding sedentary groups. Heart weights were greater in corpulent than lean, while gastrocnemius muscle weights were similar in both phenotypes. Exercise was without effect on the weight of either muscle tissue in either phenotype. Interscapular brown adipose tissue weights and the IBAT:BW ratio were greater in obese than in lean rats. IBAT weights were lower in exercised than sedentary rats of either phenotype, but the IBAT:BW ratio was lower only in the obese exercised rats. In sedentary rats, L-alpha-glycerophosphate dehydrogenase and malic enzyme activity were greater in obese than lean, and exercise treatment resulted in increased L-alpha-glycerophosphate dehydrogenase and malic enzyme only in lean rats. These results are consistent with a redistribution of energy expenditure from energy storing to energy dissipating pathways following vigorous exercise, resulting in slowed rates of weight gain and body fat accretion in both lean and obese animals, with the most significant decrements among pre-obese rats.

Adipose Tissue↗
PubMed1987

Changes in energy expenditure and fat metabolism in rats infused with interleukin-1.

Metabolic alterations related to resting energy expenditure (REE) and fat metabolism have been noted during sepsis, and often depend on the causative agent and the stage and severity of the illness. We studied the effect of IL-1, the protein mediator of the 'acute phase' response during infection, on REE, respiratory quotient (RQ), and fat metabolism in male rats (210 g), who were infused over an 8-h period with (1-14C)-palmitate (PALM), (2-3H)-glycerol (GLY) and either saline or interleukin-1 (IL-1). At 7-8 h post infusion, the IL-1 group showed a significant increase in REE but no change in RQ. The IL-1 group also exhibited a significant decrease in serum free fatty acid (FFA) and an increase in FFA clearance. Free fatty acid flux, %PALM oxidation, serum (GLY), glycerol clearance, and glycerol flux (a measure of lipolytic rate) were not significantly different between the two groups. We conclude that IL-1 can mimic the increase in REE seen during infection; the increase in REE is not due to a selective increase in fat oxidation only, although the unchanged RQ and increased REE suggest that there is a proportional increase in net FFA oxidation.

Animals↗
PubMed1987

The effect of splanchnic nerve stimulation on adrenocortical activity in conscious calves.

1. Right adrenal and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously. 2. The I.V. infusion of ACTH1-24 increased mean plasma ACTH concentration by about 1200 pg/ml and mean right adrenal cortisol output by about 500 ng min-1 kg-1. Stimulation of the peripheral end of the right splanchnic nerve at 4 Hz for 10 min produced a further rise in cortisol output, amounting to about 400 ng min-1 kg-1 (P less than 0.01). These changes in output were reflected accurately by changes in peripheral plasma cortisol concentration. 3. Closely similar amounts of adrenaline were released in response to splanchnic nerve stimulation in the presence and absence of exogenous ACTH. In the presence of ACTH the average mean output of noradrenaline (58 +/- 2 ng min-1 kg-1) was significantly less than that of adrenaline (102 +/- 4 ng min-1 kg-1; P less than 0.001), whereas the corresponding values were not significantly different in the absence of ACTH. 4. These results also confirm the fact that the fall in adrenal vascular resistance which occurs during splanchnic nerve stimulation is substantially reduced by ACTH, as is the rise in met5-enkephalin output. 5. It is concluded that the splanchnic innervation is capable of enhancing the secretion of adrenal glucocorticoids in response to ACTH under physiological conditions in the conscious calf.

Adrenal Glands↗
PubMed1987

The effect of splanchnic nerve section on the sensitivity of the adrenal cortex to adrenocorticotrophin in the calf.

1. Adrenal cortical responses to adrenocorticotrophin (ACTH) in conscious 2-6-week-old calves, in which both splanchnic nerves had been cut at least 7 days previously, were compared with those of normal calves of the same age in order to discover whether splanchnic nerve section affects the sensitivity of the adrenal cortex to the trophin. 2. In one series of experiments an increase in the release of endogenous ACTH was elicited by an i.v. infusion of noradrenaline (333 ng min-1 kg-1 for 10 min) and in another the concentration of ACTH in the plasma was artificially increased by infusing synthetic ACTH1-24 intravenously at either 5 or 10 ng min-1 kg-1 for 10 min. 3. In all groups mean plasma ACTH was linearly related to mean plasma cortisol and the sensitivity of the adrenal steroidogenic response to ACTH was found to be substantially reduced 7 or more days after section of both splanchnic nerves.

Adrenal Cortex↗
PubMed1987

Adrenal cortical responses to vasoactive intestinal peptide in conscious hypophysectomized calves.

1. Right adrenal and various cardiovascular responses to an intra-aortic infusion of vasoactive intestinal polypeptide (VIP; 4 micrograms min-1 kg-1) have been investigated in the presence and absence of exogenous adrenocorticotrophin, (ACTH1-24; 5 ng min-1 kg-1, i.v.). The adrenal clamp technique was employed in conscious calves in which the pituitary stalk had been cauterized 3-4 days previously. 2. The i.v. infusion of ACTH1-24 increased mean plasma ACTH concentration by between 1000 and 1100 pg ml-1 and mean right cortisol output by about 700 ng min-1 kg-1. Under these conditions the intra-aortic infusion of VIP produced a further rise in mean adrenal cortisol output, together with a consequential rise in mean arterial plasma cortisol concentration, without affecting the concentration of ACTH in the arterial plasma significantly. In the absence of ACTH the same infusion of VIP had no detectable effect on adrenal cortisol output. 3. In each of the above respects this intra-aortic infusion of VIP closely mimicked the effect of stimulation of the peripheral end of the right splanchnic nerve in these animals, as it also did by causing a substantial fall in adrenal vascular resistance in the absence, but not in the presence, of ACTH. 4. It is concluded that release of this peptide from splanchnic nerve terminals in the adrenal gland most probably accounts, at least in part, for the powerful adrenocortical steroidogenic response to splanchnic nerve stimulation, that occurs in the presence of submaximal doses of ACTH.

Adrenal Cortex↗
PubMed1987

Studies on the growth of the fetal guinea pig. Changes in the plasma concentration of sulphation-promoting activity and of insulin-like growth factors during gestation.

Plasma sulphation-promoting activity, insulin-like growth factors (IGF)-I and -II and insulin concentrations have been measured in the developing guinea. Sulphation-promoting activity fell progressively from midgestation to term in a manner that correlated fairly closely with the decline in the fractional rate of body and liver growth. The changes in plasma concentrations of IGF-I, & -II were quite different, both being substantially higher than fetal plasma insulin concentration. IGF-I, like insulin, plasma concentration rose between 35 and 50 days, then declined as term approached. These changes correlated with phases of lipid, DNA and RNA synthesis, but not of glycogen synthesis in the fetal liver. Fetal Plasma IGF-II concentration was comparatively low until about 55 days gestation then rose sharply, at the time that large quantities of glycogen are deposited in the fetal liver and myelation is initiated in the fetal brain, to achieve very high levels by 60-63 days then declining as term approaches. Plasma IGF-I and -II, measured by radioimmunoassay and radioreceptor assay respectively, showed the same cross-reactivity or binding characteristics as peptides in human or rat plasma. On separation by hplc IGF-I consisted of two major fractions and IGF-II of one. This picture was the same if the peptides were from fetal or adult plasma. There was no evidence of a distinctly fetal class of IGF. Plasma IGF-I and -II concentrations did not correlate with changes in fetal size or fractional rate of growth.

Animals↗
PubMed1987

Studies on the growth of the fetal guinea pig. Effects of reduction in uterine blood flow on the plasma sulphation-promoting activity and on the concentration of insulin-like growth factors-I and -II.

The effects of prenatal growth restriction caused by uterine artery ligation at midgestation has been studied in pregnant guinea pigs. Ligation of a uterine artery at day 30 of pregnancy commonly caused a reduction in fetal growth of greater than 45% by days 40-65 of gestation. This was associated with substantial delays in the development of a number of fetal tissues and in particular that of the skeleton which remained cartilagenous for longer than normal. Hence normally by day 50 of pregnancy clear evidence of epiphyseal ossification in the long bones of the fore- and hindlimbs was present, but in growth retarded fetuses of less than 50% of normal size such evidence was sparce. Delayed skeletal development and the slowing of fetal growth rate correlated well with marked depression of plasma sulphation-promoting activity. Indeed plasma from fetuses that were less than 40% of normal size inhibited sulphate incorporation into pig costal cartilage. This indicated the presence of inhibitory factors in the plasma of such fetuses, an interpretation that was re-inforced by the observation that plasma IGF-II concentrations were 2-4 times above normal. In contrast plasma IGF-I concentration was depressed upto 50% by growth retardation in line with the fall in fetal plasma insulin concentration. The changes in plasma sulphation-promoting activity and of IGF-I are consistent with slowing of DNA, RNA and protein synthesis and of gene expression in tissues of the growth-retarded fetus. The elevated fetal plasma IGF-II concentration provided further evidence that in the fetal guinea pig this hormone has a potentially glyconeogenic action and maintains essential glycogen stores.

Animals↗
PubMed1987

Cardiovascular, metabolic and endocrine effects of chemical sympathectomy and of adrenal demedullation in fetal sheep.

A procedure in fetal sheep for causing peripheral sympathectomy by regular intravascular guanethidine sulphate administration and for causing adrenal demedullation by intragland injection of acid formalin is reported. Demedullation substantially removed adrenaline from the fetal circulation, but has a small effect only on noradrenaline. Plasma noradrenaline levels were depressed by 50% when demedullated fetuses were also subject to peripheral sympathectomy by guanethidine sulphate treatment. This provides some evidence that the paraganglia in the sheep fetus contributes to resting plasma catecholamines. Furthermore the ability of adrenal demedullation to increase markedly this pool of extra-adrenal chromaffin tissue indicates that in the fetus adrenal activity regulates the growth of these para-aortic bodies. In response to sympathectomy plasma vasopressin concentrations rose substantially, whilst adrenal demedullation caused a small rise. Demedullation and sympathectomy depressed fetal plasma glucose and elevated plasma cortisol. In both sympathectomised and adrenal demedullated fetuses resting heart rate and blood pressure was not depressed. However in those with a depleted peripheral nervous system periods of cardiovascular instability were apparent after 2-3 days of treatment with guanethidine sulphate. Hence there were regular episodes where fetal blood pressure and heart rate fell sharply followed 60-90s later by very large increases in blood pressure sustained for up to 10 min and associated with substantial production of plasma vasopressin and catecholamines. These results show that fine cardiovascular control in the fetus requires an intact sympathetic system as the endocrine system is too slow responding to effectively maintain reflex vascular control.

Adrenal Medulla↗
PubMed1987

Metabolism of glucose by fetus and placenta of sheep. The effects of normal fluctuations in uterine blood flow.

The metabolism by the fetus and placenta of [2-3H, U-14C]glucose infused into fetal sheep has been studied. Uptake of glucose from the fetus by the placenta and transfer to the ewe, as well as placental metabolism of glucose to fructose and lactate have been quantified. About two-thirds of the glucose removed from the fetal circulation was taken up by placenta. Less than 15% of this passed back into the maternal circulation, the remainder was converted, at roughly equivalent rates, into lactate and fructose, most of which was transferred back to the fetus. It seems likely that little of this glucose is oxidised by the placenta. This data indicates that there are substrate cycles between the placenta and fetus, one possible function of which is to limit fetal glucose loss back to the mother; lactate and fructose have limited placental permeability. At uterine blood flow rates in the middle of the normal range net glucose uptake by the placenta from the maternal circulation was about 7-fold higher than that from the fetus. About 20% of this was transported to the fetus, 50% was oxidised and much of the remainder converted to lactate and transferred back to the ewe. Labelling patterns in fructose and lactate make it unlikely that this placental pool of glucose mixes freely with that derived from uptake from the fetus. Net movement of glucose across the placenta is markedly influenced by fluctuations in uterine blood flow over the normal range of 500-3000 ml/min. At low flow rates there is net output of glucose from the fetus to the placenta, and in some instances from the placenta to the ewe, i.e. there is evidence of net utero-placental production of glucose to the ewe separate from output by the fetus. There is a close linear relationship between uterine glucose supply (maternal arterial concentration x uterine blood flow) and net balance across the placenta. As uterine supply of glucose falls there is increased uptake by the placenta of glucose from the fetal circulation and corresponding enhanced recycling of fructose and lactate to the fetus. This production of fructose and lactate by the placenta may function to reduce glucose loss from the fetus to the ewe. Hence at high rates of placental uptake of glucose from the fetus placental production of lactate and particularly fructose may approach saturation and allow significant backflow of glucose from the fetus to the ewe. Under these conditions glucose uptake may in part sustain placental oxygen consumption.

Animals↗
PubMed1986

Membrane-associated pyruvate kinase in developing guinea-pig liver.

During analysis of pyruvate kinase distribution in developing guinea-pig liver it was observed that a substantial proportion of the activity remained associated with the microsomal membrane fraction ('microsomes'). Although some of this could be removed by washing with sucrose, the majority required detergent treatment for liberation, and even then at least one-half remained attached to the microsomes. Estimates of the contribution of this fraction to total cell pyruvate kinase activity indicated that it was more than 50% of the total, and this is likely to be an underestimate because of the continued latency of the enzyme even in the presence of detergent. The susceptibility of the microsomal enzyme, whether released by detergent or sucrose washing, to inactivation by Triton X-100 suggested it to be different from the cytosolic enzyme, which was stable under such conditions. (The microsomal enzyme required the presence of additional protein, such as bovine serum albumin, to maintain stability.) This view was confirmed by DEAE-cellulose chromatography and particularly isoelectric focusing, where the microsomal enzyme was shown to consist of at least four forms, which were distinctly different from those in the cytosol. Those data and the kinetic properties of the four forms in the membrane fraction indicate that the microsomal pyruvate kinase could consist of four counterparts to the cytosolic isoenzyme forms. These results are discussed in relation to the two possible explanations for the phenomenon (not mutually exclusive): that the more hydrophobic membrane forms are precursors of the cytosolic enzyme and that they may be part of functional glycolytic pathway in the microsomes of developing liver.

Animals↗
PubMed1986

Effects of synthetic adrenocorticotrophin on adrenal medullary responses to splanchnic nerve stimulation in conscious calves.

Right medullary and various cardiovascular responses to stimulation of the peripheral end of the splanchnic nerve have been investigated in the presence and absence of exogenous adrenocorticotrophin, ACTH1-24, (5 ng min-1 kg-1). The adrenal-clamp technique was employed in conscious calves, after the pituitary stalk had been cauterized and they had recovered from anaesthesia. The intravenous infusion of ACTH1-24 increased the plasma ACTH concentration by about 1100 pg ml-1 and right adrenal venous output of cortisol by about 400 ng min-1 kg body weight-1. Stimulation of the splanchnic nerve at 4 Hz for 10 min had no effect on either arterial plasma ACTH concentration or the adrenal output of cortisol. Closely similar amounts of both adrenaline and noradrenaline were released in response to nerve stimulation in the presence and absence of exogenous ACTH. In contrast, the fall in adrenal vascular resistance of about 40%, which normally occurred in response to splanchnic nerve stimulation, was completely abolished by ACTH. The adrenal produced relatively large quantities of met-enkephalin-containing peptides. During splanchnic nerve stimulation the output of these increased 2-100-fold, at which time free met5-enkephalin accounted for only 10-20% of total. During ACTH infusion the output of free met5-enkephalin was reduced at rest and during nerve stimulation, but that of total met-enkephalin-containing peptides was unaffected. These results indicate that ACTH or an adrenal steroid may alter the processing of proenkephalin in the adrenal medulla acutely but not total opiate secretion. Alternatively, the presence of ACTH could act by influencing the population of chromaffin cells activated by splanchnic nerve stimulation.

Adrenal Medulla↗
PubMed1986

Reduced adrenal cortical sensitivity to ACTH in lambs with cut splanchnic nerves.

The possibility that the sensitivity of the adrenal cortex to endogenous ACTH may be affected by splanchnic nerve activity has been investigated in conscious, weaned, 5- to 8-month-old lambs. The animals were atropinized (0.5 mg/kg) and tested with an i.v. infusion of noradrenaline (333 ng/kg per min for 10 min), which produced a significant rise in the mean concentration of both ACTH and cortisol in the arterial plasma. In lambs tested at least 7 days after section of both splanchnic nerves, just below the diaphragm, the rise in plasma ACTH concentration was significantly greater, and that in plasma cortisol significantly less, than in control lambs. The mean plasma ACTH and cortisol concentrations were linearly related to one another in both groups (r = 0.93 and 0.92) but the sensitivity of the adrenal cortex to the steroidogenic action of ACTH appeared to have been roughly halved 1 week after bilateral splanchnic nerve section.

Adrenal Cortex↗
PubMed1986

The biological activity in vivo of recombinant murine interleukin 1 in the rat.

The present study summarizes the biological response of rats to infusion with recombinant murine IL-1 (rIL-1) cloned in Escherichia coli. Thirty-seven male rats (135-180 g) were infused over a 6-hr period with either 0.008 M guanidine hydrochloride (the vehicle) or E. coli product (both groups are controls) or 1000, 3750, 7500, 15,000, or 37,500 LAF units/hr of rIL-1. The controls and the group receiving 1000 LAF units/hr of rIL-1 did not exhibit a change in body temperature during the experiment. A mild fever was noted with 3750 LAF units/hr which became significantly elevated with 7500 and 15,000 LAF units/hr. At a dose of 37,500 LAF units/hr of rIL-1 (in 0.08 M guanidine hydrochloride) the rats became hypothermic and died. An equivalent dose of guanidine hydrochloride alone (0.08 M) was not fatally toxic although the rats did become hypothermic. Plasma zinc levels were significantly depressed and white blood cell count elevated at 6 hr postinfusion onset. Resting energy expenditure (REE) was significantly depressed during an infusion of 7500 and 15,000 LAF units/hr of rIL-1 despite a concurrent elevation in body temperature. Whole-body leucine kinetics were unchanged by infusion with rIL-1. Plasma fibrinogen and serum haptoglobin and copper levels were not altered by rIL-1. In conclusion, murine rIL-1 is similar to monocytic-derived IL-1 in that it produces a fever, hypozincemia, and leukocytosis; however, rIL-1 does not induce changes in protein metabolism.

Animals↗
PubMed1986

The effect of elevation of maternal plasma catecholamines on the fetus and placenta of the pregnant sheep.

To study the effects of reduced uterine blood flow on fetal and placental metabolism, adrenaline has been infused at physiological doses (0.5 microgram/min per kg) into the circulation of the pregnant sheep. This gives a reduction of about one third of uterine blood flow at days 120-143 of pregnancy, but causes no significant change in umbilical blood flow. In contrast to the effects of constricting the uterine artery to reduce blood flow to a similar degree, placental oxygen consumption was reduced and that, together with a large increase in lactate production, indicated the placenta became hypoxic. The fetal blood gas status and hence oxygen consumption was not affected significantly. A consistent arterio-venous difference for glucose across the umbilical or uterine circulations was not detected unless the uterine blood flow was comparatively high. Glucose balance across the uterus showed a close linear relationship with uterine blood flow and more particularly with the supply of glucose to the uterus. There was clear evidence for glucose uptake by the placenta and fetus and also glucose output by both. The latter was more common when uterine blood flow was comparatively low or reduced by adrenaline infusion. The results are consistent with the concept that glucose supply has to be maintained to the placenta even at the expense of fetal stores, although lactate can substitute if there is enhanced output because of fetal hypoxia. They indicate that placental mobilisation of glycogen can lead to a net output of glucose to the mother. The manner of communicating to the fetus changes in placental state that occur during maternal adrenaline infusion is not clear. However towards the end of the 60 min infusion, elevation of fetal plasma adrenaline, probably resulting from a breakdown of the placental permeability barrier, may be an important signal.

Animals↗
PubMed1986

Influence of the Walker 256 carcinosarcoma on muscle, tumor, and whole-body protein synthesis and growth rate in the cancer-bearing rat.

The in vivo rates of protein synthesis were assessed in tumor tissue, skeletal muscle, and whole body of rats bearing the Walker 256 carcinosarcoma. Estimates of protein synthesis in the nontumorous tissues were compared to tumor-free controls. Changes in size of the whole animal and tumor (i.e., growth) were measured, and fractional rates of growth, synthesis, and breakdown were estimated. Muscle protein synthesis and whole-body growth were significantly reduced in rats bearing larger tumors, and both were negatively correlated with tumor size (r = -0.723 and -0.825, respectively; P less than 0.01). Furthermore, whole-body and muscle protein synthesis were positively correlated with body growth (r = 0.380 and 0.563, respectively; P less than 0.05). Tumor growth followed first-order kinetics between days 7 and 13 following implantation, with a mean rate constant of 34.3%/day for the larger tumors and 27.7%/day for the small tumors. The difference in tumor growth became statistically significant over the final 3 days of tumor volume measurements. Fractional protein synthesis was significantly lower in the larger compared to the smaller tumors (48.6 versus 84.8%/day; P less than 0.05) as measured on day 14. This finding indicates a lower protein breakdown rate for the larger tumors (14.3 versus 59.0%/day; P less than 0.01) and suggests that the process of protein breakdown could play a significant role in determining tumor size, leading support to the theory of tumors acting as nitrogen traps.

Animals↗