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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elderly adults are assumed to have an exaggerated ventilatory response to exercise. This study sought to examine this assumption by comparing the steady-state ventilatory and gas exchange responses of a group of elderly and younger humans. Steady-state ventilatory responses to moderate cycle ergometer exercise were measured in 14 elderly (71.0 +/- 1.3, mean +/- SEM years) and 14 younger (21.8 +/- 0.7 years) subjects. Compared with the younger group, the elderly had a significantly higher VE, VCO2, and VO2 at all work rates. In addition, delta VE/delta VCO2 was significantly higher for the elderly than for the younger subjects (31.07 +/- 1.34 vs 27.16 +/- 1.01, respectively; p less than .03), but the intercept with the ventilation axis was significantly lower (0.81 +/- 0.97 1.min-1 vs 4.15 +/- 0.77 1.min-1, respectively; p less than .015). Consequently, the VE-VCO2 relationships of the two groups crossed and the ventilatory equivalent for CO2 was similar for both groups. Thus, in these elderly subjects, the steeper delta VE/delta VCO2 was misleading because it was not associated with a greater ventilatory equivalent for CO2. In summary, although the ventilatory response of these elderly subjects to a given work rate was greater than that of the younger subjects, this was secondary to a greater metabolic requirement and cannot therefore be considered exaggerated. Furthermore, the data suggest that delta VE/delta VCO2 may be an inappropriate index of the ventilatory response to exercise in the elderly.
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PMID:A comparison of the ventilatory responses to exercise of elderly and younger humans. 162 90

We have previously observed correlations between placental glucose transfer and growth of fetuses of ethanol (EtOH)-fed and control rats. In the present study, whole mammalian embryos were used to define the interaction of glucose supply and the effects of EtOH on growth and differentiation. Rat embryos were cultured in 75% normal rat serum from day 9.5 to day 11.5 of gestation. EtOH produced dose-dependent reductions of embryo protein content (mean +/- SEM = 212 +/- 5, 171 +/- 11, 141 +/- 16, and 113 +/- 9 micrograms/embryo in the presence of 0, 25, 50, and 100 mM EtoH, respectively). Somite number was 25.7 +/- 0.3, 23.4 +/- 0.7, 21.8 +/- 0.7, and 21.1 +/- 0.4 under the same conditions. Exposure to ethanol during the first 24 hr in culture decreased embryo protein content to the same extent as exposure for the entire 48-hr culture period. After 46 hr in culture, control and ethanol-exposed embryos were incubated with 14C-glucose for 2 hr. Ethanol produced dose-dependent reductions of CO2 production, anabolic utilization, lactate release, and total glucose utilization. Glucose supplementation (300 mg/dl) significantly increased embryo protein content and each of these glucose utilization parameters. When glucose utilization was expressed relative to embryo protein content, incorporation of the label into embryonic tissues was significantly reduced by ethanol and increased by glucose supplementation. Embryo protein content correlated closely (r = 0.871, p less than 0.0001) with anabolic glucose utilization. Thus, ethanol directly affects embryo glucose utilization, both as an energy source and as a synthetic substrate, in addition to its effects on placental glucose transfer.
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PMID:Effects of ethanol on glucose utilization by cultured mammalian embryos. 162 46

The cardiopulmonary, anesthetic, and postanesthetic effects of an IV infusion of the hypnotic agent propofol were assessed in 6 Greyhounds and 7 non-Greyhounds. After IM injection of acetylpromazine and atropine, a bolus injection of propofol sufficient to allow endotracheal intubation (mean +/- SEM = 4.0 +/- 0.3 mg/kg of body weight in Greyhounds; 3.2 +/- 0.1 mg/kg in non-Greyhounds) was administered, followed by continuous infusion at a rate of 0.4 mg/kg/min for 60 minutes, during which time dogs breathed 100% oxygen. In 23% of all dogs (3 of 13), apnea developed after initial bolus administration of propofol. Arterial blood pressure was well maintained in all dogs, but heart and respiratory rates were decreased significantly (P less than 0.05) during the infusion in Greyhounds. In Greyhounds, mild respiratory acidosis developed after 45 minutes, whereas arterial carbon dioxide tension was increased at all times after propofol administration in non-Greyhounds. In all dogs, PCV and total plasma proteins were unaffected by propofol. Rectal temperature decreased during treatment. Muscle tremors were observed in approximately 50% of dogs (in 3 of 6 Greyhounds and 3 of 7 non-Greyhounds) during and after infusion of propofol. Non-Greyhounds lifted their heads, assumed sternal recumbency, and stood 10 +/- 1, 15 +/- 3, and 28 +/- 5 minutes, respectively, after the end of the infusion; in Greyhounds, the corresponding times were 36 +/- 4, 43 +/- 6, and 63 +/- 7 minutes.
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PMID:Cardiopulmonary, anesthetic, and postanesthetic effects of intravenous infusions of propofol in greyhounds and non-greyhounds. 162 71

The purpose of this study was to evaluate a new method to measure closing volume (CV). This new method does not require oxygen or inert gases to be inhaled to obtain the onset of phase 4. Because there are regional differences in the concentrations of the resident alveolar gases (O2, CO2, and N2), there should be an abrupt change in the concentration of these gases at the terminal portion of a prolonged expired vital capacity (VC) that marks the onset of phase 4. Nine normal healthy subjects, 30 to 65 years of age, inspired room air from residual volume (to mimic the maneuver of the standard single breath N2 (SBN2) washout test) to total lung capacity. During the expiration (flow constant at 250 ml.s-1) following a 10-s breath hold at total lung capacity, the exhaled gas was analyzed with a mass spectrometer for fractions of O2, CO2, and N2. Although the onset of phase 4 can be shown as the change in concentration of any of the three alveolar resident gases, oxygen was selected because (1) it demonstrates a greater apex to base concentration gradient than that found with CO2 and N2, and (2) a clear identification of the onset of phase 4 (minimum value of O2 fraction). With this method, the mean +/- SEM of CV was 16.8 +/- 1.52 percent (CV x 100/VC). No significant difference was found among the room air method, SBN2 method, and the helium bolus technique.
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PMID:Single-breath, room-air method for measuring closing volume (phase 4) in the normal human lung. 164 29

Short-term triglyceride (TG) synthesis was measured over 48 h in four healthy males from the incorporation rate of deuterium in body water into plasma TG. Subjects drank 0.7 g D2O kg-1 estimated body water (99.8 atom% excess), followed by water containing 1.4 g D2O kg-1 water to maintain plasma deuterium enrichment at plateau. Blood samples (20 ml) were obtained before dosing and every 4 h thereafter. Subjects self-selected three meals each day. TG from each time point were separated from plasma lipids by thin-layer chromatography and combusted to water and CO2. Combustion water was vacuum distilled into Zn-containing Pyrex tubes, reduced to hydrogen gas, and analyzed for deuterium enrichment by isotope ratio mass spectrometry. Deuterium enrichment of TG increased over the 48 h study period for all four subjects studied. Superimposed on this increase were short-term non-periodic fluctuations in enrichment reflecting dietary influx and intra-individual differences in TG metabolism. The TG fractional synthetic rate (FSR) was calculated using linear and mono-exponential models. Triglyceride FSR of the subjects over the first 24 h of the study was 0.0702 +/- 0.0048 day-1 (mean +/- SEM) by the linear model and 0.0728 +/- 0.0051 day-1 by the exponential model. Deuterium enrichment reached a plateau on day 2, indicative of continuing TG synthesis in a saturated body water pool. These results are consistent with the notion of meal-dependent variability in TG synthesis into a small rapid turnover plasma TG pool.
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PMID:Measurement of triglyceride synthesis in humans using deuterium oxide and isotope ratio mass spectrometry. 165 17

The quantification of adenine nucleotides released from the heart is hampered by their rapid dephosphorylation to adenosine in the extracellular space catalyzed by highly active ectonucleotidases. To determine the total release of adenine nucleotides from isolated Langendorff-perfused guinea pig hearts, ecto 5'-nucleotidase was effectively blocked by infusion of alpha, beta-methylene-ADP (AOPCP, 50 microM). Adenine nucleotides were measured in the coronary venous effluent by the luciferin-luciferase method after enzymatic rephosphorylation to ATP. In hearts perfused at a constant flow rate (10 ml/min) with normoxic buffer (95% O2, 5% CO2) the release +/- SEM of adenine nucleotides and adenosine was 0.06 +/- 0.01 (n = 11) and 0.04 +/- 0.01 (n = 13) nmol/min. In the presence of AOPCP, the release of adenine nucleotides increased to 0.43 +/- 0.04 nmol/min (n = 9; p less than 0.05), whereas adenosine remained unchanged. Hypoxic perfusion (10% O2, 85% N2, 5% CO2) caused a threefold increase in adenine nucleotide release but a 40-fold increase in adenosine. In contrast, global ischemia (30 seconds) caused adenine nucleotide and adenosine release to rise to similar values of 1.06 +/- 0.10 and 0.80 +/- 0.14 nmol/min (n = 9). Stimulation of hearts with isoproterenol (4 nM) likewise increased the release of adenine nucleotides (0.50 +/- 0.04 nmol/min) and adenosine (0.87 +/- 0.21 nmol/min) (n = 6). To determine the cellular source of adenine nucleotides released from the heart, the coronary endothelial adenine nucleotide pool was selectively prelabeled by [3H]adenosine. Global ischemia increased the specific radioactivity of released adenine nucleotides by 57%. The findings indicate that 1) adenine nucleotides and adenosine are released at the same order of magnitude from the well-oxygenated heart; 2) beta-adrenergic stimulation and ischemia stimulate the release of adenine nucleotides and adenosine, both purines reaching vasoactive concentrations in the effluent perfusate; 3) during hypoxic perfusion only the release of adenosine is greatly enhanced; and 4) the coronary endothelium preferentially contributes to the ischemia-induced adenine nucleotide release.
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PMID:Adenine nucleotide release from isolated perfused guinea pig hearts and extracellular formation of adenosine. 174 67

The purpose of this study was to determine the effect of fitness and work level on the O2 uptake and CO2 output kinetics when the increase in work rate step is adjusted to the subject's maximum work capacity. Nine normal male subjects performed progressive incremental cycle ergometer exercise tests in 3-min steps to their maximum tolerance. The work rate step size was selected so that the symptom-limited maximum work rate would be reached in four steps at 12 min in all subjects. Oxygen consumption (VO2) and carbon dioxide production (VCO2) were calculated breath by breath. For the group, the time (mean, SEM) to reach 75% of the 3-min response (T0.75) for VO2 increased significantly (P less than 0.01) at progressively higher work rate steps, being 53.3 (5.5) s, 63.5 (4.6) s, 79.5 (5.0) s, and 94.5 (5.8) s, respectively. In contrast, T0.75 for VCO2 did not change significantly [74.9 (7.4) s, 75.6 (5.0) s, 85.1 (5.3) s, and 89.4 (6.3) s, respectively]. VCO2 kinetics were slower than VO2 kinetics at the low fractions of the subjects' work capacities but were the same or faster at the high fractions because of the slowing of VO2 kinetics. The first step showed the fastest rise in VO2. While VO2 kinetics slowed at each step, they were faster at each fraction of the work capacity in the fitter subjects. The step pattern in VO2 disappeared at high work rates for the less fit subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of fitness on VO2 and VCO2 kinetics in response to proportional step increases in work rate. 174 11

Extracted third molars were used to study the effect of Nd:YAG laser irradiation combined with CO2 laser beam on dental hard tissues. The specimens were studied with SEM after lasing and the size of the impact areas and beam penetration into enamel and dentin were planimetrically analyzed. High-energy CO2 laser (e.g. 10 s irradiation with 10 W output energy) penetrated all enamel and dentin. The simultaneous addition of Nd:YAG irradiation to the CO2 beam was found to increase the effect of CO2 laser, while Nd:YAG irradiation alone, used with equivalent energy densities, did not cause any effect on enamel surface. Thus, Nd:YAG laser was found to potentiate statistically significantly the effect of CO2 irradiation, but the morphologic alterations on dental hard tissues, such as crater formation at the beam focus site, appeared to be due to CO2 irradiation alone.
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PMID:Irradiation of human dental tissues with CO2-, Nd:YAG-, and CO2-Nd:YAG combination laser. 176 82

The contribution of insulin (3.6 pmol.kg body mass-1.min-1) to adrenaline-induced (0.164 nmol.kg fat free mass-1.min-1) thermogenesis was studied in ten postabsorptive healthy volunteers using two sequential protocols. Variables considered were oxygen consumption as well as carbon dioxide production, heart rate, blood pressure, plasma concentrations of glucose, insulin, glycerol, free fatty acids, beta-HO-butyrate and lactate. Adrenaline increased plasma concentrations of glucose, glycerol, free fatty acids, and beta-HO-butyrate, and heart rate and metabolic rate during normo-insulinaemia [61.3 (SEM 6.6) pmol.l-1]. Similar effects were observed during hyperinsulinaemia [167.9 (SEM 18.7) pmol.l-1], but the effect of adrenaline on oxygen consumption was reduced. On average, metabolic rate increased by 12.9% during normo-insulinaemia and by 8.9% during hyperinsulinaemia. We concluded that relative hyperinsulinaemia resulted in decreased adrenaline-induced thermogenesis and therefore increased whole body anabolism.
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PMID:Thermogenic effect of adrenaline: interaction with insulin. 176 54

Carbon monoxide (CO) 1% was administered to anaesthetised rabbits for 15 minutes. Despite a 28% +/- 5.8 (SEM) fall in mean arterial blood pressure during the CO exposure, cerebral blood flow increased by 236% +/- 36.5 in the left and 287% +/- 28.9 in the right cortex. Cerebrovascular resistance was reduced by 70.6% +/- 2.8 in the left and by 76.2% +/- 3 in the right cortex. These changes were accompanied by an increase in intracranial pressure, a drop in body temperature and ventilation requirement, and a metabolic acidosis. When the CO was withdrawn all these parameters returned to normal over three hours. Hence, these vascular effects are reversible and consistent with the natural history of CO intoxication in humans. Carboxyhaemoglobin levels correlated well with hemispheric cerebral blood flow (r = 0.90; r = 0.98) and cerebrovascular resistance (r = 0.87; r = 0.97).
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PMID:Acute carbon monoxide exposure and cerebral blood flow in rabbits. 176 5


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