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Biomedical subjects

R Francesconi

Publications and source records attributed to R Francesconi.

At least 37 records · Page 2Linked to original sources
PubMed1989

2,3-diphosphoglycerate in normal and pathologic pregnancy: relationship to neonatal weight.

2,3-Diphosphoglycerate levels were assayed in 154 pregnant women in third trimester (61 normal, 52 diabetic, 19 with gestational hypertension, 7 with fetal macrosomia, and 15 with idiopathic fetal underdevelopment). A correlation was found between 2,3-diphosphoglycerate levels and birth weight (absolute and relative birth weight or birth weight expressed as percentile), which was negative in normal patients evaluated in the last 7 days before delivery (r = 0.38; p = 0.04) and positive in diabetic patients (evaluated in the third trimester and in the last 7 days before delivery) and in patients with gestational hypertension (evaluated in the third trimester) (r and p values differ according to whether birth weight is expressed as absolute, relative, or a percentile). No correlation was found between 2,3-diphosphoglycerate levels and birth weight in patients with neonatal underdevelopment or macrosomia of unknown origin. On the basis of these results we hypothesize that in some conditions the fetus can influence maternal 2,3-diphosphoglycerate levels and hence its own oxygen supply and growth in utero.

2,3-Diphosphoglycerate↗
PubMed1986

Oral pyridostigmine administration in rats: effects on thermoregulation, clinical chemistry, and performance in the heat.

We have recently reported that acute intraperitoneal administration of pyridostigmine bromide to rats resulted in significant decrements in physical performance in the heat, adverse thermoregulatory effects, and exacerbated elevations in several indices of heat/exercise injury. Since it will be consumed orally as a prophylaxis for organophosphate poisoning, pyridostigmine was dissolved in the drinking water of rats. Consumption of pyridostigmine for 7 days (n = 34, 6.6 mg/day) resulted in a 23% (p less than 0.001) reduction of circulating cholinesterase when compared with a control group (n = 31) while ingestion for 14 days (n = 35, 8.9 mg/day) elicited a 39% (p less than 0.001) inhibition of circulating cholinesterase when compared to a second control group (n = 33). Water and food consumption, rate of weight gain, and overt behavior were unaffected by pyridostigmine consumption. When approximately half the animals in each group were exercised (9.14 m/min) in the heat (35 degrees C) to hyperthermic exhaustion (Tre = 42.5-43 degrees C, rats unable to right themselves), pyridostigmine consumption for 14 days effected a significantly (p less than 0.05) increased rate of weight loss, but no further effects on thermoregulation or performance were noted. Several minor increments were observed in clinical indices of heat/exercise injury in rats consuming pyridostigmine for 14 days. These data indicate that oral dosages of pyridostigmine can probably be titrated to levels of cholinesterase inhibition which are efficacious in prophylaxis against organophosphate toxicity without significant effects on selected physiologic and metabolic processes.

Administration, Oral↗
PubMed1986

Simultaneous determination of fluid shifts during thermal stress in a small-animal model.

We have developed methodology to simultaneously measure fluid redistribution among the major compartments during moderate and severe hypohydration. Total body water (TBW) was determined using tritiated water, extracellular fluid volume (ECF) was measured using a single-injection [14C]inulin technique, and plasma volume (PV) was determined by indocyanine green dye dilution. Moderate (10% decrease in body wt) and severe (15%) hypohydration resulted in significant losses in TBW, ECF, and PV. Plasma volume was decreased by approximately 25% in both groups, and other fluid compartments were differentially affected. For example, the moderately dehydrated group maintained PV by shifting fluid from the interstitial fluid volume (ISF) compartment while preserving the intracellular fluid volume (ICF); conversely, the severely dehydrated group maintained PV by redistributing fluid from both the ISF and ICF compartments. The data indicated that the initial response to fluid loss was the movement of fluid from the ISF pool to sustain both PV and ICF. In severely hypohydrated rats, PV was maintained at the expense of ICF. These experiments indicated that PV and ICF were maximally protected, probably to preserve the integrity of the cardiovascular system and to minimize organ injury.

Animals↗
PubMed1986

An atropinized heat-stressed rat model: dose response effects and pharmacokinetics.

Atropine and other anticholinergic drugs are widely used in common medications and in the treatment of organophosphate poisoning. Man dissipates heat by the evaporation of sweat. Analogously, rats spread saliva over their bodies for evaporative cooling. Atropine inhibits both sweating and salivation. Therefore, we sought to quantitate the effects of atropine in our rat heatstroke model. While heat-stressing adult male rats of 500 or 250 g at 41.5 degrees C, we measured the effects of i.v. atropine (10-4000 micrograms X kg-1) on the following: heating rate (HR), % wt loss (saliva production), and fecal loss (intestinal motility). HR (degree C X min-1) was the most sensitive index of drug activity with a 200 micrograms X kg-1 dose (equivalent to 2 mg in man for organophosphate poisoning) eliciting an increased HR from 0.022 degrees C (saline) to 0.087 degrees C X min-1 (atropine). Atropine (200 micrograms X kg-1) increased HR even if administered 3 h prior to heat exposure. Large (500 g) rats showed an increase in HR with 25 micrograms X kg-1 of atropine, but 250 g rats required 50 micrograms X kg-1. This model could be used to assess the relative effects of other anticholinergic drugs and as a non-dehydrated heatstroke model.

Animals↗
PubMed1984

Effects of pyridostigmine on ability of rats to work in the heat.

Adult, male rats (300-325 g) were treated with pyridostigmine bromide (n = 22) or saline (n = 22) to quantitate the effects of cholinesterase inhibition (64%) on the ability to work (9.14 m/min, level treadmill) in the heat (35 degrees C). Pyridostigmine-treated rats had a mean endurance of 23 min, whereas saline-treated animals ran for nearly 35 min (P less than 0.001). Rates of rectal and skin temperature increments were significantly higher (P less than 0.001) in pyridostigmine-treated rats as were water losses (P less than 0.001). Exercise in the heat to hyperthermic exhaustion effected anticipated increments in circulating urea nitrogen, creatinine, lactate dehydrogenase, and potassium levels, whereas pyridostigmine pretreatment had additive effects on lactate and creatine kinase concentrations. Additionally, pyridostigmine elicited a significant (P less than 0.01) hyperglycemia before exercise, an effect noted also with other organophosphate simulants. We concluded that pyridostigmine-induced cholinesterase inhibition had a variety of debilitating effects during work in the heat.

Animals↗
PubMed1984

Albumin-induced plasma volume expansion: diurnal and temperature effects.

To develop a reliable procedure for the acute expansion of plasma volume (PV), 26 male volunteers were randomly assigned to either a thermoneutral (25 degrees C and 40% relative humidity) or hot-dry (37 degrees C and 25% relative humidity) environment; subsequently each subject was seated for at least 1 h and then infused intravenously with either 100 or 200 ml of a 25% albumin solution or 0.9% saline. On the day before each infusion, PV was estimated by dye dilution using indocyanine green. Net percent change in PV (using hematocrit and hemoglobin values) was calculated at 1, 3, 6, 9, 12, and 24 h postinfusion. The PV of subjects residing in the heat after a 100-ml saline infusion increased significantly over 1-h values at 6, 9, and 12 h postinfusion but not at 24 h. The same trend, although not significant, was apparent at room temperature. The data suggest a slow isooncotic circadian pattern of PV expansion and contraction. The infusion of hyperoncotic albumin produced rapid expansion of plasma volume. With the low dose (25 g) at 1 h postinfusion, the expansion was 379 +/- 102 ml in the heat and 301 +/- 160 ml at room temperature. With the high dose (50 g) at 1 h postinfusion, the expansion was 479 +/- 84 ml in the heat and 427 +/- 147 ml at room temperature. The high dose produced an expansion that persisted for at least 9 h in subjects in either environment. The data suggest a mechanism for the retention of fluid during heat acclimatization and a useful procedure for plasma volume expansion in humans.

Acclimatization↗
PubMed1984

Exercise in the heat: effects of saline or bicarbonate infusion.

Adult male rats (n = 17/group, 300-320 g, physically untrained) were exercised (9.14 m/min) in the heat (35 degrees C) to hyperthermic exhaustion (rectal temperature 43 degrees C) after infusion of 2 ml of 7.5% sodium bicarbonate (BIC) or 2 ml of 0.9% sodium chloride (SAL). Rats receiving BIC or SAL had no effects on endurance when compared with rats receiving no exogenous fluid [control (CON]), whereas the rate of heat gain, was significantly increased in the BIC-treated group. After exercise, the BIC group manifested significantly decreased hematocrit and plasma protein levels but exaggerated increments in plasma osmolality. Lactate levels were significantly increased in all three groups with no notable intergroup differences. Although venous blood pH and bicarbonate levels were decreased after exercise in the SAL and CON groups, they were unchanged in the BIC group. Although venous PCO2 was unaffected by fluid administration in all three groups, venous PO2 was significantly increased after exercise in the heat in all groups. We concluded from these experiments that even though BIC infusion prevented the acidosis and hypobicarbonatemia induced by exercise in the heat to hyperthermic exhaustion, the hypertonicity and Na+ content of the bicarbonate solution may have increased the rate of heat gain and precluded beneficial effects on physical performance.

Acidosis↗
PubMed1983

Acute heat/exercise stress in rats: effects on fluid and electrolyte regulatory hormones.

Adult, male rats were exercised in the heat until hyperthermic exhaustion ensued. Plasma aldosterone levels were significantly (p less than 0.001) elevated after 8 min of exercise and remained increased throughout the exercise and recovery periods. Alternatively, plasma angiotensin I levels were unaffected during exercise, but increased significantly (p less than 0.001) during the recovery period. These rapid elevations in hormonal levels may be part of a sympathicoadrenal response to heat/exercise stress as well as an adaptational response to maintain plasma volume during and following exercise in the heat.

Aldosterone↗
PubMed1983

Malathion administration: effects on physiological and physical performance in the heat.

To determine the effects of low-dosage organophosphate administration on exercise in a hot environment, malathion (7.5 mg/day, 4 days) was administered IP to rats, and effected a 35% (p less than 0.01) reduction in plasma cholinesterase levels. Treadmill endurance (9.14 m/min, no incline, 35 degrees C ambient) was unaffected when the animals were exercised to hyperthermic exhaustion (Tre approximately 43 degrees C). While rates of heat gain were similar between groups, malathion-treated rats displayed higher Tsk (p less than 0.05) at a number of sampling times during the treadmill run. While creatine phosphokinase levels were unaffected by either cholinesterase inhibition or exercise in the heat, lactate dehydrogenase activities were increased (p less than 0.01) in both groups following hyperthermic exhaustion. Although plasma levels of lactate, potassium, urea nitrogen, and creatinine were all significantly (p less than 0.01) increased as a result of exercise in the heat, these increments were not exacerbated by cholinesterase inhibition. Results generally indicated that at this moderate level cholinesterase inhibition, malathion administration did not adversely affect physiological, physical, or thermoregulatory efficacy.

Animals↗
PubMed1983

Hypo- and hyperglycemia in rats: effects on endurance and heat/exercise injury.

To investigate the hypothesis that circulating glucose levels may affect exercise performance and the severity of hyperthermic injury, rats were made hypoglycemic (n = 12, IV insulin, 4 U) or hyperglycemic (n = 12, IP glucose, 750mg) before exercise in the heat to hyperthermic exhaustion (Tco = 42.5-43 degrees C). The endurance of rats administered glucose was significantly greater than insulin-treated controls (n = 12). Hematocrit levels were unaffected by exercise in control and insulin-treated rats, but were significantly (p less than 0.01) increased in those glucose-treated. Lactate levels were increased (p less than 0.001) post-run in all groups, and these increments were exacerebated in glucose-treated rats. Glucose levels pre-run were decreased by insulin and increased by glucose, and remained depressed (p less than 0.01) post-run in the insulin-treated group. Potassium concentrations were reduced (p less than 0.05) by insulin administration. Urea nitrogen and creatinine were increased (p less than 0.001) post-run in all groups. We concluded that, while hyperglycemic rats had increased endurance compared to hypoglycemic animals, mortality of at least 50% in all groups was unaffected by circulating glucose levels.

Animals↗
PubMed1982

Thermoregulatory responses in the rat to exercise in the heat following prolonged heat exposure.

To determine the effects of prolonged exposure to severe thermal stress on the subsequent ability to exercise in the heat, rats were exposed to a hot (35 degrees C) environment for 1, 2, 3, or 4 wk. At each of these weekly intervals the rats ran on a treadmill to hyperthermic exhaustion (41.5--43.0 degrees C), and tail-skin (Tt-sk) and rectal (Tre) temperatures were monitored. The results indicated that prolonged heat exposure did not enhance the rats' endurance capacity. Further, as the period of heat stress increased, there was a concomitant significant decrement in tail-skin vasodilation; indeed, after 3 and 4 wk at 35 degrees C Tt-sk reflects a complete shutdown of blood flow to the tail during exercise. Additionally, slight evaporative cooling from exogenous fluid (saliva or urine from the treadmill surface) might account for the low Tt-sk in relation to Tre and Ta. Hematocrit ratios ordinarily decreased from week to week during heat exposure, whereas body weights remained very consistent throughout the 4-wk interval. The mechanism of this decrement in vasodilation is undergoing further study.

Adaptation, Physiological↗
PubMed1982

Heat-stressed rat: effects of atropine, desalivation, or restraint.

Heat-stressed rats thermoregulate behaviorally by spreading saliva onto body surfaces and thus lose body water through evaporative cooling. Prior to exploring the role of dehydration in our rat heatstroke model, we sought to compare the abilities of physical restraint, surgical desalivation, and/or atropine to increase the rate of body heat storage by inhibiting body water loss and evaporative cooling during heat exposure. In these experiments, male Sprague-Dawley rats were stressed at an ambient temperature of 41.5 degrees C either in their own cages or in a restraining device until a rectal temperature of 42.6 degrees C was attained. Unrestrained control rats heat-stressed at this temperature lost approximately 8% of body weight (water) during a 258-min exposure. Physical restraint or desalivation reduced both the exposure time and body weight loss by about 72%. Surgically desalivated, heat-stressed rats were observed to engage in voluntary urine-spreading behavior. Maximal heat storage and therefore maximal reduction in exposure time and inhibition of body weight loss to less than 10% of control values were achieved by either physical restraint plus desalivation or by a 500-micrograms dose of atropine.

Animals↗
PubMed1981

Thermoregulatory effects of centrally administered bombesin, bradykinin, and methionine-enkephalin.

Bombesin (BO, 100 ng), bradykinin (BR, 10 microgram), or methionine-enkephalin (EN, 10 microgram) was administered intracerebroventricularly to adult male rats at an environmental temperature of 4 degrees C, 22 degrees C, or 35 degrees C, and rectal (Tre) and tail-skin (Tsk) temperatures were monitored for 5 hours. At 4 degrees C and 22 degrees C BO-treated animals developed acute hypothermia (max delta Tre=-3.25 degrees C and -2.71 degrees C, respectively) which persisted for 2 hours (p less than 0.05). At 22 degrees C and at 300 min post-injection, BO-treated animals became significantly (p less than 0.05) hyperthermic (deltaTre = +1.28 degrees C) when compared to controls. While BR had no effects at 22 degrees C, en-injected rats demonstrated significant (p less than 0.05) hyperthermia from 180 min through 300 min (delta Tre=+1.40 degrees C). At 22 degrees C both BO and, surprisingly, EN increased Tsk (e.g. delta Tsk =+ 3.49 degrees C and + 2.01 degrees C at 60 min). At 35 degrees C EN elicited hyperthermia which was significantly (p less than 0.05) increased from time 0 at all sampling time (mean delta Tre =+ 1.85 degrees C) and from control levels at 300 min (delta Tre =+1.07 degrees C, p less than 0.05). BO again caused a significant (p less than 0.05, BO vs control, 30 min) decrement (delta Tre =-1.22 degrees C) followed by increments (p less than 0.05) from 12-0-300 min. We conclude that the hypothermic effect of BO is dependent upon environmental temperature, partially caused by vasodilation, and possible biphasic in nature; EN treatment generally elicits hyperthermia under these conditions while BR produced no effects on thermoregulation.

Animals↗
PubMed1981

Chronic chlorpromazine administration in rats: effects on ability to work in the heat.

To identify and quantitate the effects of chronic chlorpromazine (CPZ) administration on the ability to work in the heat, 2 mg CPZ were administered by intraperitoneal injection daily for 14 days to rats weighing between 250 and 350 g at the time of experimentation. When these animals exercised in the heat (35 degrees C) to hyperthermic exhaustion (Tre = 42.5-43 degrees C), it was demonstrated that their endurance capacity was significantly reduced (P less than 0.001) when compared with saline-treated controls. Increments in rectal temperature while on the treadmill were significantly (P less than 0.02) elevated among th CPZ-treated rats. Exercise on the treadmill to hyperthermic exhaustion resulted in significantly (P less than 0.001) increased circulating levels of lactate and potassium when these were compared in blood samples taken immediately before and after exercise in the heat for both groups, but creatine phosphokinase levels were unaffected. Additionally, lactate levels were significantly (P less than 0.05) increased in the postrun blood samples of CPZ-treated rats when compared with the appropriate saline-treated controls. We concluded from these studies that chronic administration of CPZ in rats reduces their ability to work in the heat. Further, their rate of heat gain while exercising in the heat is increased, and the combined effects of exercise in the heat and CPZ administration exacerbated the effects on the clinical chemical indices of heat-exercise injury.

Animals↗
PubMed1981

Alcohol consumption in rats: effects on work capacity in the heat.

To quantitate the effects of ingestion of ethanol (EtOH)-water mixtures on the ability to work in the heat (35 degrees C), adult male rats (250-350 g) were given 0, 4, 8, 12, or 16% EtOH as the sole source of drinking water for 14 days. The endurance capacity (treadmill time) of rats drinking 4% EtOH was similar to that of rats consuming water (32 vs. 32.9 min, respectively). However, the treadmill time of rats drinking of 16% EtOH was significantly (P less than 0.05) reduced when compared with that of animals drinking 4 or 8% EtOH. Maximal rectal and skin temperatures were likewise lower in the group consuming 16% EtOH, whereas increments in rectal and skin temperatures during treadmill exercise were unaffected. Although hematocrit and plasma protein levels were unaltered, plasma levels of the commonly reported indices of heat-exercise injury were exacerbated by consumption of increasing concentrations of EtOH. We concluded that ingestion of EtOH for 2 wk had minimal effects on thermoregulation and that the decrements in work capacity noted were probably the result of alterations in hepatic and muscle metabolism.

Alcohol Drinking↗
PubMed1981

Prostaglandin E1 hyperthermia: effects on ability to work in the heat.

To assess the effects of preinduced hyperthermia on the ability to exercise in the heat, prostaglandin E1 (PGE1) was administered intracerebroventricularly to male rats weighing 275-350 g. Following injection of PGE1, a fever of 2 degrees developed within 20-30 min, at which time a 1-ml blood sample was taken. When these animals exercised in the heat (37 degrees C) to hyperthermic exhaustion (42.5-43 degrees C), their endurance capacity was significantly reduced (P less than 0.001) when compared with controls. Exercise to hyperthermic exhaustion resulted in significantly (P less than 0.05, minimal) increased plasma levels of lactate, potassium, and urea nitrogen in both control animals and those receiving PGE1. However, PGE1 pretreatment did not exacerbate these increments. Plasma glucose and sodium levels were significantly (P less than 0.05) increased in PGE1-treated animals, whereas glucose levels were reduced significantly (P less than 0.05) in both groups postrun. We concluded that preinduced hyperthermia severely reduces the ability to work in the heat. Although the clinical chemical indices of heat injury are unaffected by PGE1 pretreatment, the effects of PGE1 administration on circulating levels of glucose and sodium require further study.

Animals↗
PubMed1980

5-Thio-D-glucose: hypothermic responses in mice.

Adult male mice were administered several doses of 5-thio-D-glucose (5-TG) at two environmental temperatures, 4 and 22 degrees C. Both intracerebroventricular (icv) and intraperitoneal (ip) administration of 5-TG resulted in significant (P < 0.05 to P < 0.001) decrements in rectal temperature (Tre) that were dose dependent. After 30 min, the hypothermic effects were significantly (P < 0.001, icv, 100 microgram) exacerbated by cold exposure (4 vs. 22 degrees C) and were likewise intensified significantly (P < 0.005, 45 min, fed vs. 18 h fasted) by food deprivation. These reductions in Tre were accompanied by significant (P < 0.001) increases in circulating levels of glucose. The present results indicate that 5-TG may be eliciting both central and peripheral cellular glucopenia concomitant with circulatory hyperglycemia; thus, the resultant hypothermia may be arising from competitive inhibition of glycolysis by 5-TG intermediates as well as reduced availability of tissue glucose.

Animals↗