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Biomedical subjects

R R Rodríguez

Publications and source records attributed to R R Rodríguez.

At least 19 recordsLinked to original sources

Growth of skeletal components in the young squirrel monkey (Saimiri sciureus boliviensis): a longitudinal experiment.

A functional skeletal criterion, as an extension of the van der Klaauw's cranial theory, was adopted in the present study. The null hypothesis tested was: "The major skeletal components of the platyrrhine body grow linearly, regardless of their functional dependence to different demands." The acceptance of the hypothesis will imply that all Saimiri skeletal growth may be satisfactorily explained by independent variables in a single equation. The rejection will suggest that such skeletal growth patterns have to be explained by variables in several different equations, and perhaps these equations may vary with the effect of sex and undernutrition. Control and undernourished squirrel monkeys were radiographed monthly for 2 years; they were also measured; and their volumetric and morphometric neurocranial, facial, and pelvic indices were calculated. The curves that best described each of the 24-point sequences were obtained. Three main growth patterns were observed: 1) Simple linear (femur length for all groups, and pelvic index for control and undernourished females), for which the simple regression equation explained more than 95% of the variation; 2) Complex linear (pelvic index for control and undernourished males, and neurocranial and facial indices for all of the groups), for which more than 95% of the variation was explained by one of the four four-function type equations; and 3) Noncorrelated with age (neurofacial index for undernourished males, and pelviofemoral index for control females and undernourished males and females), which showed nonsignificant correlations with respect to age. The food intake and the oscillations of the environmental temperature might help to explain the undulating growth trajectory observed in the complex linear components.

Animals↗

Offspring of streptozotocin diabetic rats: size changes in Langerhans islets with time after birth.

It has been demonstrated that, in the diabetic rat, pregnancy and lactation are severely altered: in this study, we have measured the size of Langerhans islets of rat pups, the offspring of experimental diabetic mothers and nondiabetic controls. Diabetes was induced through streptozotocin administration (dose, 60 mg/kg body wt.). This drug was injected in every animal; their blood sugar was measured 1 week later (Haemo-Glukotest, Boehringer Mannheim), and they were then separated into three groups according to their fasting blood sugar levels: (a) severe diabetics (above 16.5 mM/l); (b) mild diabetics (6.5-16.5 mM/l); and (c) nondiabetic normals. They received insulin therapy (2-4 I.U./day) as the mild diabetics exhibited a slightly higher than normal fasting blood sugar, and the diabetic ones, above 15 mM/l. The areas of Langerhans islets of pups were measured 1 and 5 days after parturition; pancreas sections were dyed (haematoxylin-eosin) and morphometry was then performed using a digitalized magnetic tabloid connected to a Zeiss Morphomat 30 (Kontron). On the first day after parturition, the pancreas section areas in pups from mildly and severely diabetic mothers were smaller than those in neonates from nondiabetic controls (P < 0.001). The areas in neonates from severely diabetic mothers showed a more intense decrease than those from mildly diabetic animals (P < 0.01). On day 5 after delivery, the areas of Langerhans islets in offspring from normal mothers decreased and those in pups from diabetic mothers tended to normalize (P < 0.01), particularly those from the severely sick group (P < 0.01). We conclude that after parturition the offspring is no longer exposed to the high blood sugar levels found in both diabetic groups of mothers, thereby no hyperinsulinemia is needed; as time elapses, then, the area of their Langerhans islets tends to normalization.

Aging↗

[Effect of gonadal hormones on sexual dimorphism in malnutrition substrates].

The environmental effect on growth and sexual dimorphism is mediated by endocrinological dysfunctions. It was shown that malnutrition acts on the hypotalamus-pituitary-glandular axis. An experiment was made in Wistar rats to determine the effect of some gonadic hormones on the functional components of the skull to which sex dimorphism was alterated by a postnatal undernutrition. The effects of these hormones in restoring sexual cranial dimorphism was tested. Four treatments were applied: control, with food intake ad-libitum; undernutrition (50% of the control food intake); undernutrition plus periodic injections of testosterone and estradiol to males and females, respectively and sham-operated animals, which were injected with oil vehicle only. A radiological longitudinal study was performed between 20 and 80 days of postnatal age. The length width and height of the neural and facial components were measured on each radiograph. Data were processed by ANOVA and Mann-Whitney statistical tests were performed by means of the SYSTAT 7.0 statistical package. Results showed that gonadic hormones restored the sexual cranial dimorphism by stimulating (testosterone) or suppressing (estradiol) the growth of the cranial components.

Analysis of Variance↗

Favourable, significant effect of the dose-dependent treatment with RU 38486 (RU) on the alterations of the hepatic mitochondrial function of diabetic rats.

In the present work, the effect "in vivo' of increasing doses of RU 38486 upon the hepatic mitochondrial function of diabetic rats has been studied. At the same time, the action of adrenalectomy and corticosterone restitution on this function were comparatively demonstrated. The parameters measured were oxygen consumption with the substrates: 3-hydroxybutyrate (HB), succinate (Suc) and malate-glutamate (Mal-glut) in intact liver mitochondria and the activities of 3-hydroxybutyrate dehydrogenase (HBD) and cytochrome c oxidase (Cyt.c oxid.) enzymes in broken liver mitochondria. The groups of animals studied were normal controls (N) and the following groups of diabetic rats: rats without any treatment (D), adrenalectomized rats (D+ADX), rats that were adrenalectomized and treated with corticosterone (D+ADX+C) and four groups treated with increasing oral doses of RU (in mg/kg body wt.), that is, 12.5 (D+RU1), 25.0 (D+RU2), 37.5 (D+RU3) and 50.0 (D+RU4). The results showed a tendency of increasing values of mitochondrial oxygen consumption in diabetic animals treated with RU. The favourable effect of increasing doses of RU on O2 consumption of diabetic rat liver mitochondria with each of the substrates showed a significant association as indicated by the values obtained for the correlation coefficients r (0.95, 0.97 and 0.99 according to the substrate HB, Succ or Mal-glut, respectively). Likewise, the correlation between the treatment with increasing doses of RU and the recovery of enzyme activities showed a significant dose-effect association with r 0.94 for HBD and r = 0.95 for Cyt.c oxid. Adrenalectomy showed a similar effect to treatment with the maximum dose of RU while corticosterone restitution gave measured values similar to those of the D group. In conclusion, the favourable, significant variation of the hepatic mitochondrial function of diabetic rats was demonstrated by the dose-dependent treatment with RU as seen by the correlation statistical study performed. At the same time, the pernicious effect that glucocorticoids exert upon such function in experimental diabetes was confirmed.

3-Hydroxybutyric Acid↗

Skeletal stability after mandibular setback surgery.

Postsurgical stability of mandibular setback to correct class III malocclusion was studied in 14 patients who underwent sagittal split osteotomy with circummandibular wiring and elastic IMF. Lateral cephalograms were analyzed before surgery, immediately after surgery, and at least 6 months after surgery, using three linear measurements. A simple regression analysis was used to determine the relationship between skeletal relapse and the magnitude of mandibular setback. Methods for preventing relapse are discussed.

Adolescent↗

Blood sugar concentrations during ketamine or pentobarbitone anesthesia in rats with or without alpha and beta adrenergic blockade.

Plasma glucose concentrations were measured in: 1) conscious and anesthetized rats during an iv glucose tolerance test (IVGTT) and 2) conscious and anaesthetized phentolamine/propranolol blocked rats during an IVGTT. Anesthesia was induced with ketamine (120 mg.kg-1) or pentobarbitone (60 mg.kg-1) ip at -30 min of the beginning of the IVGTT, which was followed by 2 injections of the anesthetic agents at intervals of 30 min. Propranolol (2 mg.kg-1) was given ip at -25 and -5 min. An iv infusion of phentolamine (0.015 mg.min-1) was started at -20 min and continued up to the end of the experiment. During the IVGTT, the anesthetized rats showed a moderate hyperglycemic response to glucose load compared to conscious animals (ketamine: p < 0.01 at 5 min; and p < 0.05 at 10-20 min; pentobarbitone: p < 0.05 at 5-20 min). The hyperglycemic response to glucose administration in the conscious rats was not affected by adrenergic blockade (p > 0.05). While in ketamine anesthetized rats the increased glucose response was abolished by adrenergic blockade (p < 0.05 at 5-10 min), this effect was not seen in pentobarbitone anesthetized animals. These results suggest the existence of an inhibitory tone on insulin secretion and a glycogenolytic response in ketamine anesthetized rats, probably mediated by adrenergic inervation of the pancreas and liver and by circulating catecholamines secreted from the adrenal medulla.

Adrenergic alpha-Antagonists↗

Blood sugar, serum insulin and serum non-esterified fatty acid levels during thiopentone anaesthesia in dogs.

The purpose of this study was to determine the effect of thiopentone anaesthesia on glucose metabolism. Blood sugar (BS), serum immunoreactive insulin (IRI) and serum non-esterified fatty acid (NEFA) concentrations were measured during the course of (1) an intravenous glucose tolerance test (IVGTT), and (2) an intravenous insulin test (ITT), in conscious and anaesthetized fasted dogs. The IVGTTs were repeated in dogs under alpha- or beta-adrenergic blockade, induced by phentolamine or propranolol. During the IVGTT, the anaesthetized dogs showed glucose intolerance (blood sugar levels were higher than in the control group) and little serum IRI response to hyperglycaemia was detected. An attenuated initial decrease and a slower rebound of NEFA concentration was observed in anaesthetized animals than in controls. Phentolamine administration (5 mg.kg-1 iv) partly restored the IRI response without affecting the BS levels; propanolol (1 mg.kg-1 iv) had no effect. Anaesthetized dogs showed a moderate resistance to insulin induced hypoglycaemic action and a lack of serum NEFA response during counter-regulation of hypoglycaemia, while in conscious controls an intense rebound was observed. Hyperinsulinaemia after iv insulin administration was longer in anaesthetized dogs than in controls. The insulin distribution space was 78% of body weight and insulin t1/2 in blood group compared with 54% and 16 min, in controls. We conclude that thiopentone provokes disturbances in glucose and serum NEFA metabolisms and abolishes the serum IRI response to hyperglycaemia. These effects are influenced by extrapancreatic factors regulating serum IRI levels and by an alpha-adrenergic mechanism, via the inhibition of insulin secretion.

Anesthesia, Intravenous↗

Adrenocorticotrophic hormone, cortisol and catecholamine concentrations during insulin hypoglycaemia in dogs anaesthetized with thiopentone.

Glucose homeostasis is maintained by complex neuroendocrine control mechanisms. Increases in plasma concentrations of various glucose-raising hormones such as glucagon, catecholamines, adrenocorticotrophic hormone (ACTH), and cortisol are observed under certain conditions associated with stress (haemorrhage and hypoglycaemia). The purpose of this study was to determine the effect of thiopentone anaesthesia on the catecholamine, ACTH and cortisol response to insulin hypoglycaemia in dogs. Blood sugar (BS), plasma catecholamine, and ACTH, and serum cortisol concentrations were measured during the course of (1) an intravenous insulin test (ITT) and (2) an ACTH test in conscious and in anaesthetized fasted dogs. During the ITT, the anaesthetized dogs showed a moderate resistance, compared with conscious dogs, to the hypoglycaemic action induced by insulin (blood sugar concentration 30 min after insulin injection: 2.91 +/- 0.25 vs 1.93 +/- 0.12 mM.L-1; P < 0.01). In addition, decreased epinephrine (220 +/- 27 vs 332 +/- 32 pg.ml-1), ACTH (65 +/- 6 vs 90 +/- 5 pg.ml-1) and cortisol (4.48 +/- 0.3 vs 6.25 +/- 0.5 micrograms.ml-1) concentrations were detected 60 min after insulin injection (P < 0.01). The norepinephrine response to hypoglycaemia was not altered by anaesthesia (273 +/- 33 vs 325 +/- 25 pg.ml-1). Anaesthetized dogs showed a decreased cortisol response to ACTH at 45 min (5.68 +/- 0.54 vs 8.87 +/- 0.47 micrograms.ml-1) when compared with control dogs (P < 0.001). Haemodynamic variables during anaesthesia showed little changes (P < NS); while respiratory rate was altered (P < 0.01 between 60 and 105 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

[Cardiovascular effects of ketamine anesthesia in rats treated with enalapril and propranolol].

It is well-known that ketamine (Kt) anaesthesia produces a rise in blood pressure and heart rate in man. These cardiostimulatory effects were adscribed to several factors such as: a) increased sympathetic nervous system activity by direct stimulation of central nervous structures, b) increased catecholamine release from the peripheral sympathetic system, c) high plasmatic renin levels. However, the quantitative participation of these mechanisms in the cardiovascular effects of this anaesthetic agent is unknown. While some authors have shown a major rise in serum renin activity in experimental anaesthesia, others have been unable to confirm these results. The present study was undertaken to assess if the cardiostimulatory effects of Kt anaesthesia were due to an activation of renin-angiotensin system or to increased sympathetic activity. In consequence we used rats treated with enalapril (an angiotensin-converting enzyme inhibitor) or propranolol prior to anaesthetic procedures. Thirty male Wistar and six spontaneously hypertensive rats (SHR) weighing 240-300 g were used in all the experiments. The rats were randomly grouped into six groups. I- Non-anaesthetized rats, II- Anaesthetized rats (trained in the experimental procedures), III- Anaesthetized rats (without training), IV- Anaesthetized rats previously treated with enalapril, V- Anaesthetized rats pretreated with propranolol, VI- SHR treated with enalapril. The rats of groups IV and VI received enalapril p.o. for three weeks (25 mg/Kg body wt). The animals of group V were submitted to acute beta-adrenergic blockade. Propranolol dose: 10 mg/Kg body wt, was given i.p. 15 min before Kt anaesthesia. Blood pressure and heart rate were measured with a sphygmomanometer and photoelectric sensors and recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

Improving effects obtained by the ovariectomy or treatment with tamoxifen of female diabetic rats over the function and enzyme activities of liver mitochondria.

In the present work we studied, in female chronic diabetic rats the effect of either the parenteral administration of tamoxifen (TAM) (500 micrograms.kg-1.day-1) for 15 days or the ovariectomy upon the respiration and oscillatory behaviour of intact mitochondria and the activities of 3-hydroxybutyrate dehydrogenase (HBD) and cytochrome c oxidase (Cox) of disrupted liver mitochondria. The treatment with TAM as well as the ovariectomy of diabetic animals significantly increased the respiratory control (RC) and the state 3 (S3) of respiration of intact liver mitochondria with the three substrates assayed (3-hydroxybutyrate, malate-glutamate and succinate). Both treatments also lowered significantly the damped factors of the oscillatory variation of liver intact mitochondria of diabetic rats. Moreover, the two above-mentioned treatments restored the activities of HBD and Cox of liver disrupted mitochondria to normal values. The effect of estrogens at level of its receptors in the modulation of liver mitochondrial function and liver HBD and Cox activities in chronic diabetes is discussed.

Analysis of Variance↗

Effects of withdrawal of glucocorticoids on improving the function and enzymatic activities of liver mitochondria in female diabetic rats.

In the present work the effects of corticosterone restitution were examined in female rats with chronic streptozotocin (SZ)-induced diabetes upon intact liver mitochondrial function and the activities of 3-hydroxybutyrate dehydrogenase (HBD), succinate dehydrogenase (SD) and cytochrome c oxidase (Cox) of the ruptured organelle. The liver mitochondrial function was analyzed by the respiration and the osmotic oscillatory behaviour. Respiration was measured by polarographic method and both the state 3 of active respiration (S3) and the respiratory control (RC) were determined using the following substrates: 3-hydroxybutyrate, succinate and malate-glutamate. The oscillatory behaviour was measured using as parameters the damping factors (DF) which are the ratios of amplitudes of two consecutive peaks or troughs of the spectrophotometrical tracings of this phenomenon. A group of control normal rats (N) and the following three groups of diabetic rats were studied: controls (D), adrenalectomized (D + ADX) and adrenalectomized with corticosterone restitution (D + ADX + C). The results of mitochondrial respiration showed that the mean values of S3 and RC decreased with the three substrates in the group D + ADX + C compared with D + ADX group (p < 0.001). This group demonstrated a significant increase of S3 and RC values of the respiration compared with the D group. The oscillatory behaviour of liver mitochondria of D + ADX + C group demonstrated a significant increase in the DF of peaks and troughs compared with D + ADX group. The values of DF of the latter group were not significantly different from the N group. The behaviour of the enzymes activities of ruptured liver mitochondria were different for each enzyme in the different groups of treated rats. Thus, in the D + ADX + C group the mean value of the activity of HBD significantly decreased, that of the Cox increased (p < 0.02) and that of SD did not show any variation compared with the corresponding values of the D + ADX group. Likewise, the mean value of HBD activity in this latter group was similar to that of the N group and that of Cox activity was lesser (p < 0.01) than that of the D group. The conclusion is drawn that corticosterone has significant additional diabetogenic effects upon biochemical functions of liver mitochondria in the SZ-induced diabetic state which could occur through the hormone cellular receptors.

Adrenalectomy↗

[Effects of beta-adrenergic blocking with propranolol on the mechanisms of glucose regulation in the dog].

Propranolol (P) administration is known to cause hypoglycemia in insulin-dependent diabetic patients. The mechanisms whereby this response is produced remain controversial. Some authors postulate an inhibition in the beta-adrenergic action of catecholamines, responsible for hepatic glycogenolysis, while others indicate that these hormones are not so important in the regulation of blood sugar (BS) level. The present studies were undertaken to assess the mechanism whereby hypoglycemia is developed in the dog, with or without beta-adrenergic blockade. Unanesthetized male mongrel dogs were used, weighing 10-20 kg body wt., fed on dog chow pellets and water ad libitum up to 18-22 hours before the test performances. The dogs were randomly grouped into two groups, A and B in which the effect of P on several hormonal and metabolic responses basally and during insulin (I) test, were respectively studied. Group A was constituted by two subgroups of 6 animals each; the animals of one subgroup were beta-blocked, receiving P p.o. for 10 days (80 mg every 8 hours); the dogs of the remaining subgroup received only P excipient in the same way as the treated ones, for the same period. As P treatment was completed, blood samples were taken by venipuncture, in a peripheral vein, at 0 and 60 min. Some biological controls of beta-blockade, assessed at 0, 30 and 60 min, indicated that mean pulse rate (+/- SE) in the control dogs was 123 +/- 2, 128 +/- 2 and 128 +/- 3 beats/min while in the P treated ones was 106 +/- 2, 103 +/- 1 and 103 +/- 3 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Effect in vivo of endogenous sexual hormones upon the liver mitochondrial function compared in male and female diabetic rats.

Chronic diabetes induced by the injection of streptozotocin in male and female albino adult rats provoked significant alteration of liver mitochondrial function 30 or 35 days after administration of the drug. Thus, we obtained mean values of respiratory control (RC) and state 3 (S3) with 3-hydroxybutyrate as substrate 40 or 50% lower than those of non-diabetic animals. With other substrates (malate-glutamate, succinate) the decrease of RC and S3 in the diabetic animals was 20% or 30% of the normal mean values. The osmotic damped oscillations of mitochondria were measured as another parameter of the organella function. It was assayed with valinomycin as K+ ionophore and succinate as substrate. In diabetic rats of both sexes we found a significant increase of the mean damping factor of these oscillatory variations compared with normal values. The above-mentioned results indicate a lesser elasticity and an impaired K+ transport of mitochondria across the inner membrane in diabetic animals. Both reported parameters, respiration and oscillatory variations of liver mitochondria, were measured in normal non-diabetic rats and in the groups of diabetic rats referred to as follows: 1) intact (male and female), 2) gonadectomized (male and female), 3) oophorectomized with restitution of 17 beta-estradiol. Ovariectomized diabetic rats showed a significant increase in the values of the RC and S3 of liver mitochondria compared with intact female diabetic animals. The withdrawal of the ovarian hormone in female diabetic rats significantly decreased the values of the damping factors of the oscillatory mechanism and they were similar to the normal. The restitution of 17 beta-estradiol to oophorectomized diabetic rats resulted in a decrease of liver mitochondrial respiration. The damping factor of liver mitochondria of the oophorectomized diabetic rats treated with the estrogen showed values significantly higher than those of female diabetic animals without the hormone and similar to the values of the intact diabetic female rats. Castration of male rats did not produce any effect upon the liver mitochondrial RC and S3 or upon the mean damping factor of the oscillatory variation either. Then the castration of male diabetic rats did not modify the mitochondrial function. In contrast, the oophorectomy of diabetic animals produced amelioration of mitochondrial respiration and oscillatory behavior. The conclusion is drawn that in female rats the circulating 17 beta-estradiol produced a pernicious effect upon liver mitochondrial function in the experimental diabetic state.

Animals↗

Effect of ovarian hormones upon liver mitochondrial function in diabetic rats.

In the present study it is shown that streptozotocin (SZ)-induced chronic diabetes of female albino rats produced significant alterations in liver mitochondrial function after 30-35 days of diabetes. The disturbances were as follows: (1) a significant fall of the mean values of the respiratory control ratio and of state 3 of respiration using three substrates, 3-hydroxybutyrate, malate-glutamate and succinate, and (2) a significant increase of the mean damping factor of the oscillatory osmotic variations (with valinomycin as K+ ionophore and succinate as substrate). The same mitochondrial function parameters were analyzed for comparison in control non-diabetic rats (group N) and in the following groups of female rats with chronic diabetes: intact (group I), oophorectomized (6 days after the injection of SZ) (group O), and oophorectomized with restitution therapy of 17 beta-estradiol (from the operation until the day before killing) (group O + Eol). The O group showed significantly higher values of the respiratory control ratio and of state 3 of respiration and significantly lower damping factors than group I. The restitution treatment in the O + Eol group restored the mitochondrial functions assayed to values similar to those of group I. These data provide strong evidence that estrogens exert a negative effect at the molecular level upon impaired liver mitochondrial functions in SZ-induced diabetes.

Animals↗

On changes in pancreas cytomorphometry, serum insulin and metabolic adjustments induced by long term orchidectomy and substitutive therapy with testosterone in dogs.

Mongrel, male, fasted, unanesthetized dogs under the following alternative treatments: 1) nil, 2) orchidectomy 4 months before the study, 3) orchidectomy 10 months in advance, 4) orchidectomy like in (3) followed by i.m. propylenglycol treatment, 0.05 ml/kg body wt./day, 15 days (vehicle controls, and 5) testosterone hemisuccinate in propylenglycol, 0.75 mg in 0.05 ml/kg body wt./day, for 15 days, were used in this study. Pancreas slices of animals of every group were stained with immunoperoxidase. The animals were fasted, anesthetized for pancreas removal. Pancreatic section mean absorbance was estimated in a Zeiss cytospectrophotometer with a coupled computer. Blood sugar (BS) and both serum, immunoreactive insulin (IRI) and free fatty acids (FFA) were assayed in these.

Animals↗

Metabolic and histological pancreatic changes induced by ovariectomy in the female dog.

The actions of ovariectomy performed 4 months in advance on pancreas cytology and also upon the blood sugar, serum immunoreactive insulin and circulating free fatty acid changes over glucose and insulin tests, were studied in female dogs. We concluded that ovariectomy does not affect blood sugar -basally or during the tests-, glucose space and clearance rate of glucose from circulation. Conversely, the integrated insulinemic response over glucose test was highly risen (956%) by ovariectomy in such animals; the rise occurs despite they show a broadened (59%) insulin space, is slightly mediated by a reduction (132%) in insulin clearance from circulation, and appears to be chiefly mediated by a major enhancement in insulin secretion. The immunocytolocalization of insulin in the pancreatic tissue of ovariectomized female dogs showed hypertrophy of Langerhans islets, beta-degranulation but no vacuolation. However, the piling up of the beta-granules by the vascularly pole of the B-cells as well as the appearance of a pretty number of small islets and microislets widespread over the acini, absent in the pancreatic tissue of the untreated controls in anestrous, indicate for the insulin secretory potency of the pancreas of the ovariectomized female dog to be apparently high. In the female dog, ovariectomy affects serum free fatty acid levels via at least two mechanisms, viz., a) stimulation of lipid storage over the glucose test, and b) reduction in lipomobilization as insulin antagonism predominates.

Animals↗

Metabolic and pancreatic changes caused in male dogs by testosterone chronic administration.

The pancreatic cytology and the glycemic, insulinemic and serum free fatty acid responses in dogs during hyperglycemia induced by glucose and over hypoglycemia evoked by insulin have been studied. The dogs were in the alternative following conditions: untreated, under propylenglycol treatment (vehicle controls) and under testosterone propionate plus its vehicle. Testosterone dose: 0.75 mg/kg body wt./day, once daily. Both intramuscular treatments lasted 2 weeks. In the pancreas of the untreated dogs, the islets presented irregular edges with acute prominences, and B-cells could be clearly appreciated, with a high content of dark brown beta-granules of insulin. B-cells presented negative images of nuclei located in the central areas of such cells. In the pancreas of the testosterone treated dogs, the yellowish cytoplasms of the B-cells looked empty, bearing just a few beta-granules (small amount of stored insulin). The B-cells appear to present a great number of vacuoles in testosterone treated dogs. The curve of glycemia in the glucose and insulin tests, the glucose space and the half-life time of insulin in circulation in dogs under testosterone plus vehicle treatment were similar to those observed in dogs treated with propylenglycol pursuant to the same experimental design used in the other two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of diet composition on the metabolic and heart rate responses to cold water exposure in men.

The reaction to immersion in cold water (22 degrees C) was studied in ten healthy male volunteers successively receiving balanced (C), hypercarbohydrate (HC), hyperprotein (HP), and hyperlipid (HL) normocaloric diets with a three week equilibration period on each diet. Oxygen consumption (ml min-1 m-2) increased from 149 to 224 during C, from 160 to 196 during HL, from 154 to 178 during HP, and from 166 to 187 during HL. Only the first two differences were significant. Pulmonary ventilation (ml min-1 m-2) increased from 4.08 to 6.24 during C, from 4.01 to 5.48 during HC, from 3.41 to 3.83 during HP, and from 3.77 to 5.48 during HL. The difference was statistically significant only for C. Heart rate (beats/min) decreased from 73 to 64 during C, from 74 to 61 during HC, from 73 to 60 during HP and from 72 to 64 during HL. The differences were statistically significant for all diets except HL. Oral temperature decreased in all groups (range 0.4 to 1.6 degrees C). Respiratory rate changes were not statistically significant. The calorigenic reaction to cold water immersion was demonstrable for all groups but more efficient in subjects receiving either balanced or HC diets, suggesting that HP and HL diets reduce cold adaptation.

Adult↗