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Biomedical subjects

C V Gisolfi

Publications and source records attributed to C V Gisolfi.

At least 37 records · Page 2Linked to original sources

Gastrointestinal permeability following aspirin intake and prolonged running.

We sought to evaluate the effects of exercise and aspirin on gastroduodenal and intestinal permeability. Seven volunteers (age = 29 +/- 3 yr, VO2max = 56.8 +/- 4.1 ml.kg-1.min-1) rested or performed treadmill exercise (60 min at approximately 68% VO2max), with or without aspirin ingestion. Placebo (glucose) or aspirin (1.3 g) was taken the night before and prior to rest or exercise (total 2.6 g). A permeability test solution (approximately 1300 mOsm.kg-1), containing 10 g lactulose (L), 5 g mannitol (M), and 10 g sucrose (S), was ingested prior to rest or exercise. Urinary excretion rates (6.h-1), expressed as a percentage of ingested dose, were used to quantify intestinal (L/M ratio) or gastroduodenal (S) permeability. Ingestion of aspirin before running increased (P < 0.05) intestinal permeability compared to placebo+running and placebo+rest, but not compared to aspirin+rest; mean (+/-SE) values for the L/M ratio were 0.248 +/- 0.046, 0.029 +/- 0.012, 0.012 +/- 0.004, and 0.104 +/- 0.057, respectively. Gastroduodenal permeability following aspirin+running (3.25 +/- 1.21%) was also elevated (P < 0.05) compared to placebo+running (0.43 +/- 0.15%) and placebo+rest (0.24 +/- 0.11%), but not compared to aspirin+rest (0.66 +/- 0.27%). Neither running nor aspirin ingestion was associated with gastrointestinal (GI) complaints. Thus, GI permeability while running can be markedly elevated by aspirin ingestion.

Adult↗

Reexamination of tympanic membrane temperature as a core temperature.

Controversies surrounding tympanic temperature (Tty) itself and techniques for measuring it have dampened the potential usefulness of Tty in determining core temperature (operationally defined here as the body temperature taken at a deep body site). The present study was designed to address the following questions. 1) Can a tympanic membrane probe be made that is safer and more reliable than its predecessors? 2) Why is the effect of facial cooling and heating on Tty so inconsistent in reports from different laboratories? 3) Is Tty still useful as a measure of core temperature? Data from this study, obtained with a modified thermocouple probe, suggest that the widely reported facial skin cooling effect on Tty is most probably due to thermal contamination from the surrounding ear canal wall and/or suboptimal contact of the probe sensor with the tympanic membrane because 1) Tty that fell during facial cooling was increased to the precooling level by the repositioning of the probe sensor; 2) Tty determined by using a probe with a larger sensor area (the sensor soldered to a steel wire ring)tended to fall in response to facial cooling, whereas Tty determined with a thermally insulated probe ring did not; and 3) Tty obtained under careful positioning of the insulated probe was relatively insensitive to facial cooling or heating. Because Tty was practically identical to esophageal temperature (Tes) in the steady state, i.e., 36.83 +/- 0.20 (SD) degrees C for Tty and 36.87 +/- 0.16 degrees C for Tes at room temperature (n = 11), and because facial cooling had little effect on both Tty and Tes (36.86 +/- 0.17 degrees C for Tty and 36.86 +/- 0.26 degrees C for Tes during facial or scalp skin cooling), we support the postulate that Tty is a good measure of core temperature. The temperature transient in response to foot warming was detected 5 min (n = 2) faster with Tty than with Tes. Thus, with further improvements in the design of the probe. Tty can become a standard for determination of core body temperature.

Adult↗

Glucagon-like peptide-1(7-36)amide induces the release of aspartic acid and glutamine by the ventromedial hypothalamus of the conscious rat.

Glucagon-like peptide-1(7-36)amide (GLP-1(7-36)amide) and its own receptor have been found in the hypothalamus and brain stem of the rat. In an attempt to gain further insight into the role of this peptide in brain functioning we investigated the effects of GLP-1 (7-36)amide on the release of excitatory amino acid neurotransmitters by the ventromedial hypothalamus using an experimental microdialysis approach. GLP-1(7-36)amide produced an immediate increase in the extracellular concentrations of aspartic acid and glutamine, p < 0.01 and p < 0.05, respectively. By contrast, extracellular concentrations of glutamic acid, alanine, threonine, and tyrosine were unaffected. The results of this study show a stimulatory effect of GLP-1(7-36)amide on the release of aspartic acid and glutamine by the ventromedial hypothalamus of the rat.

Animals↗

Tissue-specific HSP70 response in animals undergoing heat stress.

Heatstroke is a multisystem disorder that can result in death. Activities that increase the rate of heat storage predispose an organism to thermal injury. Using a 72-kDa heat shock protein (HSP72) as a marker of thermal injury, we determined 1) which organs synthesize HSP in animals after hyperthermia and 2) whether a high heating rate (HHR) resulted in more HSP72 than a low heating rate (LHR). Rats were assigned to either control, HHR (0.166 degrees C/min), or LHR (0.045 degrees C/min) groups. Heat exposure ended when colonic temperature (Tc) reached 42 degrees C. Total time in the heat and thermal load (measured as the time an animal maintained a Tc > 40.4 degrees C) were significantly lower in HHR compared with LHR animals. Hyperthermia resulted in a tissue-specific increase in HSP72 in the liver, small intestine, and kidney, but not in the brain or quadriceps muscles. In addition, HHR animals showed significantly greater accumulation of HSP72 in the liver compared with animals in the LHR group. Thus HSP72 synthesis is tissue specific at high physiological temperatures and may identify a critical target tissue susceptible to early thermal damage.

Animals↗

Responses of rat mesenteric arteries to norepinephrine during exposure to heat stress and acidosis.

Both cardiovascular abnormalities and metabolic acidosis can be prominent in heat stroke and may contribute to morbidity and mortality in heat stroke victims. Thus the effects of heat stress and/or low pH on the responses of rat mesenteric arteries (approximately 300 microns) to norepinephrine (NE; 10(-8)-10(-5) M) and acetylcholine (ACh; 10(-5) M) were examined. Arteries (5-7/group) were isolated, cannulated with micro-pippettes, placed under constant intraluminal pressure (50 mmHg), and then examined during 60-min exposures to either 1) 37, 42, or 43 degrees C or 2) 37 or 42 degrees C under conditions of low pH (pH = 7.0 by addition of 1 N HCl). Contractile responses to NE remained unaltered during exposure to 42 and 43 degrees C. When arteries were returned from that elevated temperature back to 37 degrees C for 30 min, enhanced (P < 0.05) contractile responses to NE were observed. Exposure to low pH depressed contractile responses to NE to a similar extent in arteries tested at 37 or 42 degrees C. Dilations to ACh were not altered by exposure to 42 degrees C, regardless of pH conditions, but were progressively reduced during the 43 degrees C (P = 0.09) exposure. Arteries exposed to NE demonstrated vasomotion. The NE-induced vasomotion, while maintained at 37 degrees C, was reduced (P < 0.05) by exposure to 43 degrees C. In conclusion, the contractile response to NE in mesenteric arteries was not altered by heat stress per se (up to 43 degrees C) but was depressed by low pH. The latter response was not potentiated by heat stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

Sympathetic nerve responses to hyperthermia in the anesthetized rat.

The aim of the present study was to characterize the sympathetic nerve responses to hyperthermia in chloralose-anesthetized rats. Discharges were recorded from the renal, lumbar, and splanchnic sympathetic nerves. Mean arterial pressure, heart rate, and sympathetic nerve discharge (SND) were recorded continuously during progressive increases in core body temperature (Tc) from 38.0 to 41.0 degrees C. The following observations were made: 1) significant increases in renal, lumbar, and splanchnic SND were observed during hyperthermia; 2) autospectral analysis of renal and lumbar SND revealed that the frequency distribution of SND can be altered during progressive increases in Tc; and 3) increases in splanchnic SND to acute heating were similar in baroreceptor-innervated and -denervated rats. We conclude that 1) hyperthermia is a potent stimulus to the sympathetic nervous system and increases the activity in three sympathetic nerves that innervate different regional arterial beds, 2) acute heating influences the neural circuits involved in generating SND as evidenced by changes in the basic pattern of renal and lumbar SND, and 3) the increase in splanchnic SND during hyperthermia is not opposed by the arterial and cardiopulmonary baroreceptors.

Animals↗

Effect of sodium concentration in a carbohydrate-electrolyte solution on intestinal absorption.

Intestinal absorption during infusion (15 ml.min-1) of a 6% carbohydrate (2% glucose and 4% sucrose) solution containing either 0, 25 or 50 mEq.l-1 Na+ was measured by segmental perfusion with a triple lumen tube in males (age 24.3 +/- 1.6) at rest in a neutral environment (22 degrees C). Infusion of the 25 and 50 mEq.l-1 Na+ solutions was performed using a balanced design on the same day, separated by a 1-hr period of no infusion. Infusion of 0 mEq.l-1 Na+ solution was performed on a separate day. A 45-min equilibration period preceded a 90-min test session. Water and solute fluxes were determined from differences in concentration of polyethylene glycol and solute across a 40-cm intestinal segment of the duodenojejunum. A two-factor repeated measures ANOVA indicated no differences (P > 0.1) over time for water, Na+, or glucose flux for all solutions. Plasma volume increased (P < 0.01) approximately 5% over time for all solutions. We conclude that Na+ concentrations of 0, 25, or 50 mEq.l-1 in a 6% carbohydrate solution have similar effects on the absorption of water, Na+, and glucose from the duodenojejunum. Glucose in the infusion solution is the more important factor determining intestinal water absorption than Na+. This study suggests that adding Na+ to fluid replacement beverages may not be a factor in fluid absorption.

Adult↗

Effects of carbohydrate type and concentration and solution osmolality on water absorption.

We studied intestinal absorption of solutions containing either one (glucose, Glu, or maltodextrin, Mal) or two (fructose, Fru, and Glu or sucrose, Suc) transportable carbohydrate (CHO) substrates using segmental perfusion technique in eight healthy male subjects. These CHO were either free or directly transportable monosaccharides (Glu, Fru), bound as the disaccharide (sucrose, Suc), or as oligomers (maltodextrins, Mal). [CHO] was varied from 6% to 8% (120-444 mmol.1(-1)). All solutions contained low [Na+] (15-19 mEq) and [K+] (3-4 mEq). Solutions osmolalities varied from 165 to 477 mOsm.kg(-1). Osmolalities in the test segment ranged from 268 to 314 mOsm.kg(-1). The regression line of osmolality with water absorption differed for single as compared with multiple substrate solutions. The significantly different intercepts of these two regression lines suggest that solutions with multiple substrates produce greater water absorption at a given osmolality than those with one. Comparing all solutions, test segment solute flux (partial r = 0.69) was more important than mean osmolality (partial r = 0.32). In conclusion, solutions with multiple substrates stimulate several different solute absorption mechanisms yielding greater water absorption than solutions with only one substrate.

Amino Acids↗

Hyperthermia stimulates nitric oxide formation: electron paramagnetic resonance detection of .NO-heme in blood.

Previous experiments from our laboratory have demonstrated that severe hyperthermia results in a selective loss of splanchnic vasoconstriction. Using electron paramagnetic resonance spectroscopy to scan whole blood samples collected in vivo from the portal vein and femoral artery of conscious unrestrained rats, we observed an increase in the concentration of spectroscopy-detectable species in portal venous blood of all heat-stressed animals. These spectra consisted of at least three distinct species: one with a broad feature having an effective g factor for the unpaired electron (g) of 2.06 assigned to the copper-binding acute phase protein ceruloplasmin, and two with narrower features that evolved at core temperatures > 39 degrees C representing a semiquinone radical and .NO-heme. This heat-induced signal displays the classic nitrogen triplet hyperfine structure (nitrogen hyperfine splitting constant = 17.5 gauss, centered at g = 2.012) that is consistent with a five-coordinate heme complex and is characteristic of an unpaired electron coupled to nitrogen in the ferrous .NO-heme adduct [(alpha 2+NO) beta 3+]2. The intensity of this signal increased approximately twofold as core temperature rose to > 39 degrees C, peaking 1 h post-heat exposure at greater than threefold basal concentration. This species was not seen in corresponding arterial blood samples. This is the first demonstration that whole body hyperthermia produces increased concentrations of radicals and metal binding proteins in the venous blood of the rat and suggests that severe hyperthermia stimulates an enhanced local release of .NO within the splanchnic circulation.

Animals↗

Effects of solution osmolality on absorption of select fluid replacement solutions in human duodenojejunum.

These experiments examined relationships between initial osmolality and carbohydrate (CHO) composition of an infused solution and osmolality and water and CHO absorption in a test segment. A triple-lumen tube with a 10-cm mixing segment and a 40-cm test segment was passed into the duodenojejunum. The infusion port was approximately 10 cm beyond the pyloric sphincter. Perfusion solutions were hypotonic (186 mosmol/kg; solution A), isotonic (283 mosmol/kg; solution B), and hypertonic (403 mosmol/kg; solution C). All solutions contained 18 meq Na+ and 3 meq K+. In the mixing segment, osmolality increased 83 mosmol/kg and decreased 90 mosmol/kg for solutions A and C, respectively. Corresponding changes in the test segment were an increase of 60 mosmol/kg and a decrease of 34 mosmol/kg. The osmolality of solution B did not change. In the test segment, mean osmolality and water and total solute fluxes were not significantly different among solutions, but solution C produced 27% greater fluid absorption than did solution A. When net fluid movement from mixing and test segments was determined, solution A produced 17% greater fluid absorption than did solution C. The mean increases in plasma and urine volumes over the 80-min test period were not significantly different. In the test segment, water flux correlated with CHO and Na+ fluxes but not with osmolality. In conclusion, 1) significant differences in solution osmolality were eliminated within the proximal duodenum and 2) perfusing 6% CHO solutions with osmolalities ranging from 186 to 403 mosmol/kg did not produce significant differences in fluid homeostasis (plasma volume) at the end of an 80-min test period.

Body Water↗

Heat stress does not sensitize rats to the toxic effects of bacterial lipopolysaccharide.

To determine whether heat stress sensitizes rats to lipopolysaccharide (LPS), four groups were examined: saline, LPS, heat stressed+saline, and heat stressed+LPS treated rats. Saline or LPS (Escherichia coli, 5 mg.kg-1 body weight, i.v.) was given after exposure to heat and at the same time of day for nonheated rats. Survival was monitored for 24 or 48 h; samples of liver and small intestine were obtained at 24 h for histological analysis. Thermal responses were similar (P > 0.05) for the heat stressed saline and LPS treated rats: mean values for maximum colon temperature were 43.0 +/- 0.1 and 42.9 +/- 0.1 degrees C, respectively. Mortality was similar for rats exposed to heat stress+saline (11%, 2/19) and heat stress+LPS (32%, 6/19). No lethality was observed in nonheated rats given saline or LPS. Tissue damage was similar in heat stress+saline and heat stress+LPS treated rats. Liver showed mild to severe degrees of coagulative necrosis while duodenum exhibited damage to the villous tips. These findings show that severe heat stress does not markedly sensitize the rat to the lethal activity of LPS.

Analysis of Variance↗

Intestinal absorption during rest and exercise: implications for formulating an oral rehydration solution (ORS). Proceedings of a roundtable discussion. April 21-22, 1993.

Formulation of oral rehydration solutions (ORS) is reviewed in the context of methods for measuring absorption of water and component substrates, transport mechanisms of substrates and water, requirements of the athlete, and effects of exercise on absorption. The triple lumen tube intubation perfusion method is the optimal technique for obtaining absorption data from the human small intestine during rest and exercise. Factors that must be considered when interpreting absorption data obtained by this technique include the role of the mixing segment in altering composition of the infused solution, defining optimal segment length, effects of ORS osmolality, and absorption of "nonabsorbed" indicators. Absorption data are applicable only to the test segment and may lack relevance to ORS transport proximal and distal to the test segment. Absorption rate of an ORS measured by perfusion may not correlate with absorption rate following ingestion. Transport of water, electrolytes, carbohydrates, and other solutes including glutamine and amino acids is considered in relation to ORS formulation. Factors affecting absorption of an ORS including the unstirred layer, motility, intestinal blood flow, and maximal absorptive capacity of the alimentary tract are considered. Exercise per se at 30-70% VO2max for 60-90 min probably has minimal effects in limiting absorption of an ORS. Consideration relevant to supplying needs of the athlete during prolonged exercise in relation for ORS formulation are discussed.

Animals↗

Effects of carbonated and noncarbonated beverages at specific intervals during treadmill running in the heat.

Eight male runners performed four 2-hr treadmill runs at 65% VO2max in the heat (35 degrees C, 15-20% RH). A different beverage was offered each trial and subjects drank ad libitum for 2 min every 20 min. The beverages were, 6% carbohydrate (CHO) solution (NC 6), 6% carbonated-CHO solution (C 6), 10% CHO solution (NC 10), and 10% carbonated-CHO solution (C 10). NC 6 and C 6 contained 4% sucrose and 2% glucose. NC 10 and C 10 contained high fructose corn syrup. Subjects drank more NC 6 than C 6. Fluid consumption was not different among other trials. During all trials, volume consumed and % delta PV declined while heart rate and rectal temperature increased (p < 0.05). No significant differences occurred between beverages for these variables. Percent body weight lost was greater (p < 0.05) for the C 10 trial compared to the NC 6 trial. Neither sweat rate, percent fluid replaced, plasma [Na+], [K+], osmolality, percent of drink volume emptied from the stomach, or glucose concentration differed among trials. Plasma [K+] and osmolality increased (p < 0.05) over time. Ratings of fullness and thirst were not different among beverages, although both perceptions increased (p < 0.05) with time. It is concluded that (a) carbonation decreased the consumption of the 6% CHO beverage; (b) fluid homeostasis and thermo-regulation were unaffected by the solutions ingested; and (c) fluid consumption decreased with time, while ratings of fullness and thirst increased.

Adult↗

Thermal effects of prolonged treadmill exercise in the heat. 1974.

Six trained men 21-38 yrs old ran 19-29 km (1.5 to 2.5 hrs) approximately 75% of their VO2 max on a level treadmill in the heat (33.5/21.5 degrees C db/wb, wind velocity 36 m/min). Every 20 min while running they (a) drank 200 ml of 10 degrees C water, (b) drank 200 ml of water at core body temperature, or (c) sponged their faces, arms, and trunks for 2 min with a towel soaked in 10 degrees C water. In another series of experiments each subject (d) hydrated 30 min before the run by drinking 1 liter of water, (e) hydrated and performed (a) above, and (f) hydrated and performed (b) above. Rectal temperature (Tre) and body weight loss (WL) were determined every 30 min and metabolism at 45 min of running. Terminal Tre after (a) through (f) averaged 39.1, 39.3, 39.9, 39.7, 39.1, and 39.3 degrees C respectively. During a control run the corresponding mean Tre was 39.9 degrees C. In a 66.7 kg man with a body weight/surface area (BW/SA) ratio of 37.5 and running at 74% of his VO2 max, Tre rose 0.4 degrees C/1% WL with increasing WL's greater than 2.0% of his initial body weight regardless of the intervention imposed. In another subject weighing 70 kg with a BW/SA ratio of 38.8 and running at 83% of his VO2 max, Tre rose 0.49 degrees C/1% WL over the entire range of WL's.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Temperature↗

Acute heat stress protects rats against endotoxin shock.

The purpose of this study was to determine 1) whether prior (24-h) heat stress could render rats cross-resistant to the lethal activity of bacterial lipopolysaccharide (LPS) and 2) whether this acquired state of resistance is associated with endotoxemia during the heat stress event. Four groups (n = 7/group) of rats were examined: 1) saline treated, 2) LPS treated, 3) heat stressed and saline treated, and 4) heat stressed and LPS treated. Saline or LPS (Escherichia coli, serotype 0111:B4, 20 mg/kg body wt) was given intravenously 24 h after exposure to heat (ambient temperature 47-50 degrees C, relative humidity 30%) for heat-stressed rats and at the same time of day for nonheated rats; survival was monitored for 48 h. Thermal responses were similar (P > 0.05); values for maximum core temperature (Tc) and time above Tc of 40 degrees C were 42.7 +/- 0.1 and 42.6 +/- 0.1 degrees C (SE) and 44.0 +/- 2.1 and 47.9 +/- 3.7 (SE) min for the heat-stressed saline-treated and heat-stressed LPS-treated rats, respectively. Administration of LPS to nonheated rats resulted in 71.4% (5 of 7 rats) lethality. In contrast, all (7 of 7) rats subjected to a single nonlethal heat stress event 24 h before LPS treatment survived (P < 0.05). Endotoxin was not detected in arterial plasma immediately after heat stress in rats (n = 6) exposed to a Tc of 42.9 +/- 0.1 degrees C. These findings demonstrate that acute heat stress can protect rats from the lethal activity of LPS.

Animals↗

Intestinal water absorption from select carbohydrate solutions in humans.

Eight men positioned a triple-lumen tube in the duodenojejunum. By use of segmental perfusion, 2, 4, 6, or 8% solutions of glucose (111-444 mM), sucrose (55-233 mM), a maltodextrin [17-67 mM, avg. chain length = 7 glucose units (7G)], or a corn syrup solid [40-160 mM, avg. chain length = 3 glucose units (3G)] were perfused at 15 ml/min for 70 min after a 30-min equilibration period. All solutions were made isotonic with NaCl, except 6 and 8% glucose solutions, which were hypertonic. An isotonic NaCl solution was perfused as control. Water absorption (range: 9-15 ml.h-1.cm-1) did not differ for the 2, 4, and 6% CHO solutions but was greater (P < 0.05) than absorption from control (3.0 +/- 2.2 ml.h-1.cm-1). The 8% glucose and 3G solutions reduced (P < 0.05) net water flux compared with their 2, 4, and 6% solutions, but 8% sucrose and 8% 7G solutions promoted water absorption equivalent to lower CHO concentrations. Water absorption was independent of [Na+] in the original solution. In the test segment, 1) Na+ flux correlated with net water flux (r = 0.72, P < 0.01), K+ (r = 0.78, P < 0.01), and [Na+] (r = 0.68, P < 0.001); 2) Na+ absorption occurred at luminal [Na+] as low as 50 mM; 3) glucose transport increased linearly over the luminal concentration range of 40-180 mM; and 4) net water flux was similar over a range of glucose-to-Na+ concentration ratios of 0.4:1 to 3.5:1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗