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Biomedical subjects

W Schaffartzik

Publications and source records attributed to W Schaffartzik.

48 records · Page 3Linked to original sources
PubMed1993

Effect of reduced hemoglobin concentration on leg oxygen uptake during maximal exercise in humans.

Maximum oxygen uptake (VO2max) is affected by hemoglobin concentration ([Hb]). Whether this is simply due to altered convection of O2 into the muscle microcirculation or also to [Hb]-dependent diffusive transport of O2 out of the muscle capillary is unknown in humans. To examine this, seven healthy volunteers performed four maximal cycle exercise bouts at sea level immediately after 8 wk at altitude (3,801 m, barometric pressure 485 Torr), a sojourn designed to increase [Hb]. The first two bouts were at ambient [Hb] of 15.9 +/- 0.7 g/100 ml breathing 21 or 12% O2 in random order. [Hb] was then decreased to a prealtitude level of 13.8 +/- 0.6 g/100 ml by venesection and isovolemic replacement with 5% albumin in 0.9% saline, and the exercise bouts were repeated. At whole body VO2max, PO2, PCO2, pH, and O2 saturation were measured in radial arterial and femoral venous blood. Femoral venous thermodilution blood flow was determined for calculation of leg VO2. Mean muscle capillary PO2 and muscle diffusing capacity (DO2) were computed by Bohr integration between measured arterial and femoral venous PO2. Averaged over both fractional concentrations of inspired O2, leg VO2 at maximum decreased by 17.7 +/- 4.3% as [Hb] was lowered while leg O2 delivery decreased by 17.5 +/- 2.6% and DO2 decreased by 10.7 +/- 2.7% (all P < 0.05). The relative contributions of decreases in leg O2 delivery and DO2 to the decrease in VO2max were computed to be 64 and 36%, respectively. These findings suggest that [Hb] is an important determinant of O2 diffusion rates into working muscle in humans. Possible mechanisms include 1) dependence of DO2 on intracapillary red blood cell spacing, 2) changes in the total rate of dissociation of O2 from [Hb], and 3) increased red blood cell flow heterogeneity as [Hb] is reduced.

Adolescent↗
PubMed1993

Pulmonary interstitial edema in the pig after heavy exercise.

During exercise (especially in hypoxia), the alveolar-arterial O2 tension difference increases. This impairment of pulmonary gas exchange is caused partly by diffusion disequilibrium, but it has also been shown that an exercise-induced increase in ventilation-perfusion (VA/Q) inequality develops. Possible explanations of increased VA/Q mismatch include nonuniform pulmonary vasoconstriction, reduced gas mixing in the large airways, airway obstruction, and the development of interstitial pulmonary edema. To directly determine whether the latter develops in high-intensity short-term exercise, we exercised pigs on a motor-driven treadmill at the highest speed that they could sustain for 6-7 min. Heart rate reached 274 +/- 5 min-1 in the exercised group, confirming that the pigs reached a near-maximal level of exercise. While running, the pigs were killed by an intravenous overdose of pentobarbital. Postmortem, the lungs were immediately removed, drained of blood, weighed, and then airway fixed with 10% formaldehyde. Four tissue blocks of the right lung of each pig were taken from the ventral and dorsal areas of the upper and lower lobes, respectively. They were stained with hematoxylin and eosin and prepared for histological examination by light microscopy. There was no difference in the lung-to-body weight ratio between exercised pigs (7.72 +/- 0.87 g/kg) and a nonexercised control group (7.70 +/- 0.68 g/kg). However, we found a significantly higher percentage of pulmonary arteries with perivascular edema in exercised (33.8 +/- 3.4%) than in nonexercised pigs (20.0 +/- 4.0%; P < 0.02). Thus, perivascular edema (and thus possibly also parenchymal interstitial edema) can occur during short-term heavy exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of hyperoxia on maximal leg O2 supply and utilization in men.

We studied O2 transport in the leg to determine if hyperoxia will increase the maximal rate of O2 uptake (VO2max) in exercising muscle. An increase in inspired O2 fraction (FIO2) from 0.21 to 1.00 was postulated to have the following effects: 1) increase the leg VO2max by approximately 5-10%, 2) increase the maximal O2 delivery [arterial O2 concentration.flow (CaO2.Q] by approximately 10%, and 3) raise the leg VO2max in proportion to both the femoral venous PO2 and mean leg capillary PO2. To test these hypotheses, 11 men performed cycle exercise to the highest work rates (WRmax) they could achieve while breathing 100% O2 (hyperoxia), 21% O2 (normoxia), and 12% O2 (hypoxia). Leg VO2 was derived from duplicate measurements of femoral venous blood flow and CaO2 and femoral venous blood O2 concentrations (CVO2) at 20, 35, 50, 92, and 100% WRmax in each FIO2. Femoral venous leg Q (Qleg) was measured by the constant-infusion thermodilution technique, and leg O2 uptake (VO2) was determined by the Fick principle [VO2 = Qleg(CaO2-CVO2)]. Leg VO2max was the mean of duplicate values of VO2 at 100% WRmax for each FIO2. Hyperoxia increased leg VO2max by 8.1% (P = 0.016) and maximal O2 delivery by 10.9% (P = 0.05) without changing Qleg. There was a significant increase in femoral venous PO2 (P < 0.001) that was proportionally greater than the increase in leg VO2max. The results support our first and second hypotheses, providing direct evidence that in normal subjects leg VO2max is limited by O2 supply during normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Methods of interpreting pulmonary gas exchange].

When arterial and mixed venous blood gas tensions, inspired and expired O2 and expired CO2 concentrations are known, it is possible to calculate the alveolar-arterial PO2 difference, intrapulmonary right-to-left shunt and dead space ventilation. However, because arterial hypoxemia is caused by ventilation/perfusion mismatching in most cases, a method allowing analysis of ventilation/perfusion ratios is needed. The "multiple inert gas elimination technique" (MIGET) is a powerful method that is useful for this purpose. This technique is based on measurements of arterial, venous and expired levels of inert gases spanning a wide range of solubility and analysis of the lung for the ventilation/perfusion ratios from true shunt to dead space ventilation. True shunt, with ventilation/perfusion ratios of 0, can be differentiated from ventilation/perfusion ratios of 0.005, and dead space ventilation can be distinguished from ventilation/perfusion ratios over 10 and under 100. Ventilation/perfusion ratios between these extremes can also be differentiated. It is not unusual for results yielded by MIGET to differ from those obtained with O2-dependent methods: O2 shunt generally exceeds MIGET shunt, for example, because O2 shunt includes low ventilation/perfusion units.

Animals↗
PubMed1992

Ventilation-perfusion relationships in the lung during head-out water immersion.

Water immersion can cause airways closure during tidal breathing, and his may result in areas of low ventilation-perfusion (VA/Q) ratios (VA/Q less than or equal to 0.1) and/or shunt and, ultimately, hypoxemia. We studied this in 12 normal males: 6 young (Y; aged 20-29 yr) with closing volume (CV) less than expiratory reserve volume (ERV), and six older (O; aged 40-54 yr) with CV greater than ERV during seated head-out immersion. Arterial and expired inert gas concentrations and dye-dilution cardiac output (Q) were measured before and at 2, 5, 10, 15, and 20 min in 35 degrees C water. During immersion, Y showed increases in expired minute ventilation (VE; 8.3-10.3 l/min), Q (6.1-8.2 l/min), and arterial PO2 (PaO2; 91-98 Torr; P less than or equal to 0.05). However, O2 uptake (VO2), shunt, amount of low-VA/Q areas (% of Q), and the log standard deviation of the perfusion distribution (log SDQ) were unchanged. During immersion, O showed increases in shunt (0.6-1.8% of Q), VE (8.5-11.4 l/min), and VO2 (0.31-0.40 l/min) but showed no change in low-VA/Q areas, log SDQ, Q, or PaO2. Throughout, O showed more VA/Q inequality (greater log SDQ) than Y (O, 0.69 vs. Y, 0.47).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of inspired CO2, hyperventilation, and time on VA/Q inequality in the dog.

In a recent study by Tsukimoto et al. (J. Appl. Physiol. 68: 2488-2493, 1990), CO2 inhalation appeared to reduce the size of the high ventilation-perfusion ratio (VA/Q) mode commonly observed in anesthetized mechanically air-ventilated dogs. In that study, large tidal volumes (VT) were used during CO2 inhalation to preserve normocapnia. To separate the influences of CO2 and high VT on the VA/Q distribution in the present study, we examined the effect of inspired CO2 on the high VA/Q mode using eight mechanically ventilated dogs (4 given CO2, 4 controls). The VA/Q distribution was measured first with normal VT and then with increased VT. In the CO2 group at high VT, data were collected before, during, and after CO2 inhalation. With normal VT, there was no difference in the size of the high VA/Q mode between groups [10.5 +/- 3.5% (SE) of ventilation in the CO2 group, 11.8 +/- 5.2% in the control group]. Unexpectedly, the size of the high VA/Q mode decreased similarly in both groups over time, independently of the inspired PCO2, at a rate similar to the fall in cardiac output over time. The reduction in the high VA/Q mode together with a simultaneous increase in alveolar dead space (estimated by the difference between inert gas dead space and Fowler dead space) suggests that poorly perfused high VA/Q areas became unperfused over time. A possible mechanism is that elevated alveolar pressure and decreased cardiac output eliminate blood flow from corner vessels in nondependent high VA/Q regions.

Animals↗
PubMed1992

VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema.

Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.

Acid-Base Equilibrium↗
PubMed1992

Relationship between body and leg VO2 during maximal cycle ergometry.

It is not known whether the asymptotic behavior of whole body O2 consumption (VO2) at maximal work rates (WR) is explained by similar behavior of VO2 in the exercising legs. To resolve this question, simultaneous measurements of body and leg VO2 were made at submaximal and maximal levels of effort breathing normoxic and hypoxic gases in seven trained male cyclists (maximal VO2, 64.7 +/- 2.7 ml O2.min-1.kg-1), each of whom demonstrated a reproducible VO2-WR asymptote during fatiguing incremental cycle ergometry. Left leg blood flow was measured by constant-infusion thermodilution, and total leg VO2 was calculated as the product of twice leg flow and radial arterial-femoral venous O2 concentration difference. The VO2-WR relationships determined at submaximal WR's were extrapolated to maximal WR as a basis for assessing the body and leg VO2 responses. The differences between measured and extrapolated maximal VO2 were 235 +/- 45 (body) and 203 +/- 70 (leg) ml O2/min (not significantly different). Plateauing of leg VO2 was associated with, and explained by, plateauing of both leg blood flow and O2 extraction and hence of leg VO2. We conclude that the asymptotic behavior of whole body VO2 at maximal WRs is a direct reflection of the VO2 profile at the exercising legs.

Adult↗
PubMed1991

Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Relationship among cardiac output, shunt, and inspired O2 concentration.

In comparing gas exchange responses of the methacholine- (MCh) challenged mongrel dog with leukotriene receptor blockers and placebo at different inspiratory O2 fractions (FIO2), we previously noted systematically different values of cardiac output as a function of drug administration and/or FIO2. This confounds identification of the effects of FIO2 and/or drugs on gas exchange, because shunt is well known to vary directly with cardiac output when other factors are equal. Accordingly, in six dogs we examined the dependence of combined shunt and low ventilation-perfusion (VA/Q) blood flow ("shunt") on cardiac output in the MCh-challenged mongrel dog. Two dogs breathed 100% O2, another two breathed room air, and the final pair breathed 12% O2 while cardiac output was altered several times by sequentially opening and closing arteriovenous fistulas every 10 min for approximately 90 min after a standard MCh challenge. On 100% O2, shunt increased by 11.0% of the cardiac output per 1-l/min increase in cardiac output. On room air, the value was 7.4%. With 12% O2 breathing shunt rose by only 2.2% per 1-l/min rise in blood flow. This FIO2 -dependent behavior of the shunt-cardiac output relationship was highly reproducible, both within and between animals. It suggests that the increase in shunt with cardiac output depends more on vascular tone of noninjured areas than on tone of the low VA/Q regions (which are hypoxic at all FIO2 values).

Animals↗
PubMed1990

Effect of common dead space on VA/Q distribution in the dog.

Several previous studies have shown worsening ventilation-perfusion (VA/Q) relationships in humans during heavy exercise at sea level. However, the mechanism of this deterioration remains unclear because of the correlation with ventilatory and circulatory variables. Our hypothesis was that the decrease in the series dead space-to-tidal volume ratio during exercise might be partly responsible because mixing in the common dead space can reduce apparent inequality. We tested this notion in 10 resting anesthetized normocapnic dogs passively hyperventilated by increase tidal volume and a) inspired CO2 or b) external dead space. We predicted less apparent VA/Q inequality in condition b because of mixing in the added dead space. After base-line measurements, conditions a and b were randomly assigned, and after a second set of base-line measurements they were repeated in the reverse order in each dog. VA/Q inequality was measured by the multiple inert gas elimination technique. Comparison of conditions a and b demonstrated that additional external dead space improved (P less than 0.001) the blood flow distributions as hypothesized [log standard deviation of perfusion = 0.49 +/- 0.02 (SE) in condition b and 0.61 +/- 0.03 in condition a with respect to 0.52 +/- 0.03 at base line]. This study suggests that the increased tidal volume during exercise could uncover VA/Q inequality not evident at rest because of the higher ratio of common dead space to tidal volume at rest.

Animals↗