Influence of ovine oviducal amino acid concentrations and an ovine oestrus-associated glycoprotein on development and viability of bovine embryos.

This study examined the effects of incorporating an ovine oviducal oestrus-associated glycoprotein (oEGP) and amino acids, at the concentrations present in the ovine oviduct around the time of oestrus, on in vitro production and subsequent viability of bovine embryos. The first experiment compared the influence of ovine oviducal concentrations of amino acids with MEM and BME amino acids. There was no treatment effect on cleavage rate (74.9% vs. 75.5%), but there was a higher (P < 0.05) blastocyst yield (30.4 vs. 25.2) and a shorter time (P < 0.05) to blastocyst formation (7.16 +/- 0.64 vs. 7.27 +/- 0.56 days) following use of oviducal concentrations of amino acids. Experiment 2 examined the influence of oEGP in combination with each of the amino acid treatments. oEGP had no effect on cleavage or blastocyst yield within amino acid treatments. Day of blastocyst formation significantly influenced nuclei numbers (P < 0.001) with higher numbers being obtained on day 7 than on either day 6 or day 8. There was also a significant (P < 0.01) interaction between day of blastocyst formation and amino acid treatment on blastocyst nuclei numbers. The third experiment studied the effects of the amino acid treatments on embryo viability. There was no effect of amino acid treatment of embryos on pregnancy rates (34.5 vs. 44.4%) following transfer of days 6 and 7 blastocysts to synchronized recipients. oEGP did not influence any of the parameters of bovine embryo development that were measured, suggesting that effects of this protein observed on ovine embryos are species specific. It is concluded that ovine oviducal amino acid concentrations are beneficial to blastocyst development in vitro but do not have any further beneficial effect following transfer of blastocysts to recipients.

Military operations at moderate altitude: effects on physical performance.

The purpose of this study was to examine changes in select anaerobic and aerobic dependent physical performance tasks in U.S. Marines exposured to field operations at moderate altitude. The subjects (N = 16) completed Wingate anaerobic power, submaximal aerobic cycle ergometry, hand grip strength, and push-up tests on three separate occasions. Testing sessions occurred at sea level, at altitude after a 10-day acclimatization period (immediately before field operations), and at altitude immediately after 4.5 days of field operations. Anaerobic power was significantly (p < 0.05) reduced after the field operations at altitude. In contrast, the aerobic cost of doing submaximal exercise was slightly elevated (p < 0.05) after the altitude field operations. No physiologically significant effect was noted for hand grip or push-up results. The findings of this study indicate that field operations at moderate altitude do result in slight, but significant, anaerobic-aerobic performance decrement in U.S. Marines.

Cold exposure during military operations: effects on anaerobic performance.

This study examined the effects of military field operations (MFO) under different environmental conditions on anaerobic performance. US Marines were tested in the field under the following conditions: 1) noncold environment (NC; n = 30, 10-32 degrees C) and 2) cold environment (CO; n = 32, -2 to -22 degrees C). Subjects performed 30-s Wingate tests (WIN) pre- and immediately post-MFO to assess anaerobic performance. The MFO consisted of approximately 4.5 days of combat training maneuvers while carrying field equipment (packs and weapon, approximately 25 kg). WIN measures obtained were absolute and relative mean power (MP), 5-s peak power (PP), and fatigue index (% decline). Significant main effects (P less than 0.01) were observed for time (pre-post MFO). Reductions occurred in absolute MP [651.8 +/- 30.3 to 616.4 +/- 28.5 (SE) W] and PP (897.8 +/- 41.6 to 857.0 +/- 39.1 W); however, no effect on fatigue index was seen. Significant interaction effects (P less than 0.05) were observed in relative measures. Reductions (pre-post) in MP (NC = 8.64 +/- 0.16 to 8.37 +/- 0.14 W/kg; CO = 8.91 +/- 0.26 to 8.04 +/- 0.15 W/kg) and PP (NC = 11.80 +/- 0.24 to 11.61 +/- 0.33 W/kg; CO = 12.23 +/- 0.35 to 11.20 +/- 0.19 W/kg) were greater under CO than NC conditions. These changes were found despite significant (P less than 0.05) but comparable pre-post weight reductions in both CO and NC conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Diminished metabolic responsiveness to beta-adrenergic stimulation in estradiol benzoate-treated rats.

Earlier studies have shown that chronic treatment with estradiol benzoate reduced the responsiveness of heart rate, drinking, and tail-skin temperature to administration of the beta-adrenergic agonist, isoproterenol. The objective of the present study was to assess the relationship between the isoproterenol-induced elevations in rate of oxygen consumption and tail-skin temperature in adult ovariectomized rats treated chronically with estradiol benzoate (28 micrograms/day) and untreated, ovariectomized controls. Isoproterenol (0, 10, 25, and 50 micrograms/kg, s.c.) elevated both rate of oxygen consumption and tail-skin temperature in ovariectomized and ovariectomized plus estradiol benzoate-treated rats in a dose-related fashion. However, in both cases the response of the estradiol-treated group was less than that of controls. A comparison of the regressions of rate of oxygen consumption versus dose of isoproterenol administered to each group revealed significant differences between the intercepts, but not the slopes. A similar comparison with respect to the regression of tail-skin temperature versus dose of isoproterenol administered to each group revealed significant differences between both the slopes and intercepts of the relationships. A comparison of the regressions of rate of oxygen consumption versus tail-skin temperature for control and estrogen-treated rats revealed significant differences between both slopes and intercepts of the relationships. The latter comparison suggests a reduced change in tail-skin temperature for a given change in rate of oxygen consumption in the estrogen-treated group. It is concluded from these results that the reduction in metabolic response to beta-adrenergic stimulation in estrogen-treated rats explains, in part at least, the attenuated response of tail-skin temperature. The tail of the rat is important in short-term temperature regulation. When threatened acutely with overheating, the rat uses its tail as a heat radiator, increasing its skin blood flow, temperature, and heat loss. Administration of isoproterenol to rats at doses of 50-100 micrograms/kg, subcutaneously can increase tail-skin temperature as much as 6 degrees C. This response is mediated by beta-adrenoceptors since it can be either attenuated or prevented by prior administration of propranolol. It serves as a simple and reliable test of beta-adrenergic responsiveness in rats. Chronic treatment with the oral contraceptive, Enovid (7.5 mg/kg food) attenuated this response. Chronic administration of the estrogenic component (ethinyl estradiol, 48-50 micrograms/kg/day) of Enovid also attenuated the response.(ABSTRACT TRUNCATED AT 400 WORDS)

Action of tetrodotoxin and verapamil on cardiac Purkinje fiber action potentials in a sodium-free, calcium-rich medium.

The ability of tetrodotoxin and verapamil to block Ca++-dependent action potentials (CaP) produced in superfused, canine cardiac Purkinje fibers was studied using intracellular microelectrodes. CaP were produced in fibers superfused with a Na+-free (substituted by tetraethylammonium chloride) high Ca++ (16.2 mM) Tyrode's solution (pH 7.4 or pH 6.0). In 30 fibers studied two populations of resting membrane potentials (RMP) were observed. In one, the mean RMP was -43 +/- (SE) 3 mV, in the second it was -63 +/- 2 mV. The high RMP was seen at pH 7.4, while the low RMP was observed at pH 6.0. It was possible to block low pH, CaP with verapamil alone, while high RMP, high pH, CaP could be totally blocked only with a combination of verapamil plus tetrodotoxin.

Metabolic and hormonal changes following endotoxin administration to diabetic rats.

The aim of these investigations was to study the time course and cause of the altered metabolic response of diabetic rats to endotoxin administration. Escherichia coli endotoxin was administered to streptozotocin-diabetic and control normoglycemic rats. At 1, 2, 5, 8, and 24 h following endotoxin, animals were decapitated. Plasma samples were analyzed for glucose, lactate, insulin, glucagon, and corticosteroids. In addition, tissue glycogen content of liver and skeletal muscle was determined. Endotoxin caused an elevation of plasma glucose in both diabetic and normoglycemic rats by 1 h postinjection. The elevation was prolonged in diabetic rats for 8 h but lasted only 2 h in nondiabetic rats. Both endotoxin-treated groups demonstrated hyperlactacidemia following endotoxin. Endotoxin led to liver glycogen depletion in both diabetic and normoglycemic rats, whereas muscle glycogen content was only slightly affected. Plasma glucagon and corticosteroids rose immediately and remained elevated in both endotoxin-treated groups. A significant insulin response to rising plasma glucose was observed in nondiabetic but not in diabetic rats following endotoxin. These results suggest that the exaggerated and prolonged hyperglycemia observed in diabetic endotoxin-treated rats is due to hypersecretion of glucose-mobilizing hormones and elevated gluconeogenesis, unmatched by an adequate secretion of insulin to promote glucose uptake and utilization.

Glucose and lactate kinetics in septic rats.

Glucose turnover was measured in rats subjected to experimental peritonitis. Fifteen hours following cecal ligation and puncture or sham surgery, rats were anesthetized with pentobarbital and glucose metabolism was estimated by constant infusion tracer techniques. Septic rats demonstrated significantly elevated rates of glucose appearance without any elevation of plasma glucose concentration. There was also significant hyperlactacidemia in the cecally ligated rats. The elevated plasma lactate was not accompanied by a lowering of blood pH. Arterial blood pressure were not different between groups, however the blood pressure of septic rats did fall during the infusion experiment. Septic rats demonstrated significantly elevated initial heart rates and blood hematocrit. The turnover of lactate was also elevated in the septic rats. By calculation of the relative percentage of glucose production from labeled lactate, it is obvious that septic rats had elevated rates of gluconeogenesis. Determination of plasma immunoreactive insulin indicated that septic rats were not insulin resistant.

Glucose turnover five hours following endotoxin administration to normal and diabetic rats.

Glucose turnovers were measured in fasted anesthetized diabetic and normal rats prior to and 5 hours following Escherichia coli endotoxin (ET) administration. Plasma glucose, lactate, blood pH, and hematocrit were also measured. Blood pressure, heart rate, and urine flow were monitored throughout. ET treatment led to an equivalent fall in blood pressure in both diabetic and normal rats, accompanied by a rising heart rate. ET treatment resulted in a significant elevation of plasma glucose in diabetic, but not in normal rats. Plasma lactates rose in both ET-treated groups endotoxin increased glucose turnover both in diabetic and normal rats. ET did not alter glycosuria of diabetic rats, and urine flow was not affected. A significant increased urine flow was measured in normal ET rats. The results reported here indicate that hepatic glucose output was increased by ET treatment in both normal and diabetic rats, and that this elevation was maintained for at least 5 hours. Metabolic clearance rate of glucose was not altered in the diabetic rats following ET, although it was markedly elevated in the normal animals. This, the insulin-like effect of ET as indicated by changes in metabolic clearance rate was absent in the diabetic rats.

Antidipsogenic effect of clonidine on angiotensin II-, hypertonic saline-, pilocarpine- and dehydration-induced water intakes.

The dipsogenic responses of female rats to administration of angiotensin II (150 micrograms/kg b.w., IP), pilocarpine (3 mg/kg IP), hypertonic saline (1 M NaCl solution, 1% b.w.), and a 24 hour dehydration were attenuated by acute IP administration of graded doses of the central and peripheral alpha 2-adrenergic agonist, clonidine. For all treatments except dehydration, clonidine inhibited significantly the dipsogenic response at the lowest dose used (6 micrograms/kg, IP). The first significant effect on dehydration-induced drinking required approximately a 4 fold higher dose (25 micrograms/kg, IP). Attenuation of the response to these dipsogenic stimuli by clonidine, suggests that its ability to stimulate alpha-adrenergic receptors centrally may play an important role in its dipsogenic inhibitory activity.

Glucose metabolism following endotoxin administration in diabetic rats.

The altered glucose metabolism characteristic of endotoxin-induced shock was studied in diabetic and non-diabetic rats. Endotoxin administration led to an exaggerated hyperglycemia in the diabetic rats. The exaggerated hyperglycemia appeared to be a consequence of an increased hepatic output of glucose, presumably via gluconeogenesis, as evidenced by an exaggerated glucose turnover following endotoxin. Diabetic and non-diabetic rats responded to endotoxin similarly with respect to blood pressure, heart rate, hematocrit, blood pH and plasma lactate. Endotoxin administration did not affect urine flow rate or urinary glucose excretion in either diabetic or non-diabetic rats.

Tolerance of estrogen-treated rats to acute cold exposure.

Female rats treated chronically with ethynylestradiol (36 micrograms/kg per day) alone, and in combination with the progestational agent, norethynodrel (253 micrograms/kg per day), cooled significantly faster than controls when lightly restrained and exposed to air at 5 degrees C. Rate of cooling of rats given only norethynodrel was similar to that of the control group. In other studies, rate of oxygen consumption was determined for all groups during acute exposure to cold (14 degrees C). All estrogen-treated groups achieved the same maximal rate of oxygen consumption as control and norethynodrel-treated groups during cold exposure, but cooled significantly faster. Two groups of female rats were treated chronically with ethynylestradiol at two separate doses (36 and 61 micrograms/kg per day). An untreated group served as controls. Rate of oxygen consumption of all animals were measured during restraint and exposure to cold (18 degrees C). The estrogen-treated groups again achieved the same maximal rate of oxygen consumption as the control group, but also cooled significantly faster despite the fact that the cold stress was less severe than in the previous experiment. That estrogen-treated rats cooled faster than controls in both studies despite achieving a maximal rate of heat production which did not differ from controls suggests that reduced cold tolerance of estrogen-treated rats may be related to increased heat loss.

Adrenergic activity of ortho-, meta-, and para-octopamine.

DL-o-, and p-octopamine were tested for beta- and alpha-adrenergic activity in rats. When compared to DL-isoproterenol, a beta-adrenergic agonist, all three isomers failed to show significant beta-adrenergic activity as assessed by intiation of thirst and by increase in tail skin temperature. All three isomers increased mean blood pressure in pentolinium-blocked rats. Of the three isomers, m-octopamine possessed the greatest alpha-adrenergic activity. When the responses were compared with those induced by L-norepinephrine, the order of activities was: 1:0.01 :0.0005 :0.0007 for norepinephrine, m-, p- and o-octopamine, respectively. Thus, DL-m-octopamine has about 1/100th the alpha-adrenergic activity of L-norepinephrine.