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S C Hempleman

Publications and source records attributed to S C Hempleman.

34 records · Page 2Linked to original sources
PubMed1991

Respiratory system mechanical behavior in the chicken.

We evaluated whether the avian respiratory system displays the same fundamental mechanical behavior during external forcing as found in mammals. We measured airway flow and pressures in the trachea, air sacs and thoracoabdominal cavity in 4 anesthetized-paralyzed roosters during sinusoidal volume oscillations at the trachea in the normal range of euthermic breathing frequency, f(0.2 to 1.0 Hz), and tidal volume, VT (10-50 ml). From the pressure and flow waveforms, we calculated resistance (R) and elastance (E) of the total respiratory system and its major compartments (lungs, air sacs and chest wall). E of the chest wall was minimum (147 cmH2O.L-1 +/- 7 SE) at 0.2 Hz-50 ml and was consistently, slightly lower than E of the total respiratory system over the entire range studied. Both elastances showed the same dependence on f and VT, increasing slightly with increasing f and decreasing with increasing VT. R of the chest wall was maximum (35.6 cmH2O.L- 1.sec-1 +/- 2.2 SE) at 0.2 Hz-10 ml and decreased with increasing f and VT, although the VT effect diminished at the higher f. E and R of the air sacs were much smaller than those of the chest wall, but showed similar f and VT dependencies. R of the lungs, due to resistance of the airways, was minimum (6.8 cmH2O.L-1.sec-1 +/- 1.5 SE) at 0.2 Hz-10 ml and increased with both f and VT. Total respiratory R reflected R of the air sacs and chest wall at low f and R of the lungs at high f. The f and VT dependencies of E and R in the chicken were strikingly similar to those measured in various types of mammalian respiratory tissues (Stamenović et al. (1990) J. Appl. Physiol. 69: 973-988. We conclude that, despite important anatomical differences between species, avian and mammalian respiratory tissues exhibit fundamentally similar mechanical behavior.

Airway Resistance↗
PubMed1990

Temperature and the oxygen-hemoglobin dissociation curve of the harbor seal, Phoca vitulina.

To determine the effect of temperature and pH on oxygen-hemoglobin affinity of the harbor seal, we measured 61 biotonometric oxygen-hemoglobin dissociation curves on blood from 5 seals at 3 temperatures and a range of pH values. The average (+/- SEM) hemoglobin concentration was 3.44 +/- 0.15 mM, nearly 50% greater than found in normal humans. At pH 7.4 the P50 (partial pressure of O2 at 50% hemoglobin saturation) +/- SEM values were 22.4 +/- 0.6,25.3 +/- 0.5, and 28.5 +/- 0.4 Torr at 33, 37 and 41 degrees C, respectively. The effect of temperature on oxygen-hemoglobin affinity, (delta log P50/delta T) was 0.014 +/- 0.001 at pH 7.4, significantly lower than that observed in human and dog blood. This low temperature sensitivity may facilitate oxygen off-loading from hemoglobin when temperature gradients exist within the animal or as tissue temperature decreases during a dive. Temperature did not significantly affect the Hill coefficient 'n' (shape) of the dissociation curve which averaged 2.43 +/- 0.04 at 37 degrees C. The fixed-acid Bohr coefficient (delta log P50/delta pH) was -0.606 +/- 0.032 at 37 degrees C and increased with temperature. This relatively large value for the Bohr coefficient was similar to those previously reported for the Northern Elephant, Bladdernose, and Weddell Seals, and may facilitate oxygen off-loading as acidosis develops during a dive.

Animals↗
PubMed1989

Amplitude dependency of regional chest wall resistance and elastance at normal breathing frequencies.

Current methods for measurement of chest wall properties assume that resistance (R) and elastance (E) are independent of the volume breathed. In six healthy subjects relaxed at functional residual capacity, we measured total and regional R and E of the chest wall within the range of normal breathing frequencies (0.2 to 0.6 Hz) and tidal volumes (250 to 750 ml), using volume forcing at the mouth as previously described. With these methods, esophageal and gastric pressures are compared with surface displacements measured with inductance plethysmographic belts to calculate R and E of rib cage and diaphragm-abdomen "pathways." Rib cage R and E were 25 to 30% higher than that of the total chest wall at each frequency and volume, whereas diaphragm-abdomen R and E were at least five times higher. R of the chest wall and each of the pathways decreased by about 70% with increasing frequency and by about 30% with increasing tidal volume. E of the chest wall and each of the pathways also decreased by about 30% with increasing tidal volume but was independent of frequency in this range. These results are consistent with nonlinear, viscoplastic models presented elsewhere. We conclude that: (1) despite the great structural differences between the rib cage and diaphragm-abdomen, each exhibits nonlinear behavior similar to that of the total chest wall; (2) chest wall R and E depend importantly on frequency and tidal volume.

Adult↗
PubMed1988

Estimating steady-state DLO2 with nonlinear dissociation curves and VA/Q inequality.

A DLO2 estimate which accounts for the nonlinearity of the oxygen dissociation curve using the Kelman blood gas routines is presented here. The simultaneous differential equations that describe O2 and CO2 diffusion between alveolar gas and pulmonary capillary blood in lung compartments with different VA/Q ratios were solved numerically with a Runge-Kutta algorithm. These integrated estimates were compared to DLO2 estimates that assume the oxygen dissociation curve is linear. In 140 gas exchange data sets from 18 healthy male subjects previously collected at rest and during exercise it was found that DLO2 estimates based on linear dissociation curves exceeded integrated DLO2 estimates by 14, 31, and 55 percent when the PIO2 was 80, 100, and 148 Torr, respectively. We conclude that the linear approximation is accurate when PIO2 is less than 100 Torr but that comparisons of DLO2 estimates at different levels of inspired oxygen must allow for the difference in curvature of the oxygen dissociation curve as a function of PIO2.

Algorithms↗
PubMed1987

Oxygen diffusing capacity estimates derived from measured VA/Q distributions in man.

Data from eighteen subjects, studied in hypoxia (minimum PIO2 = 80 Torr) both at rest and during exercise, were analyzed using computer models which estimate O2 diffusing capacity from measured VA/Q distributions (obtained using the multiple inert gas elimination technique 'MIGET') and measured O2 exchange. Two of these models assigned the distribution of the diffusing capacity (D) in proportion to either the perfusion (DLO2-Qwt) or ventilation (DLO2-Vwt) distributions from MIGET, and thus modeled the effects of VA/Q and D/Q beta (where Q beta is the perfusive conductance) inequalities respectively. The third model (DLO2-3C) assigned all the diffusing capacity to a single homogeneous compartment. At rest DLO2 was 41.1 +/- 4.8, 41.1 +/- 5.4 and 30.2 +/- 2.1 ml X min-1 X Torr-1 for the Qwt, Vwt and 3C models respectively. These rose to 93.7 +/- 2.6, 109.3 +/- 4.5 and 81.1 +/- 1.9 ml X min-1 X Torr-1 respectively at maximal exercise, all significantly different from rest (P less than 0.001 for each). The effects of measured VA/Q and theoretical D/Q beta inhomogeneities on diffusing capacity estimates were significant even in normal lungs. Both types of inequality caused an appreciable underestimation of DLO2. These multi-compartment model estimates, using real data, are consistent with published theoretical predictions of the effects of V, Q and D inequalities. The results during exercise come close to morphometric predictions of maximal oxygen diffusing capacity in man.

Blood Gas Analysis↗
PubMed1986

Computer simulation of mammalian gas-exchange.

Gas exchange efficiency is dependent upon the distribution of ventilation to perfusion throughout the lung, as well as the position and shape of the oxygen and carbon dioxide dissociation curves, and the composition of mixed venous blood. Computer simulation has allowed practical investigation of these relationships. A BASIC program suitable for small microcomputers is presented which calculates the arterial blood gases and gas transport corresponding to an arbitrary VA/Q distribution and mixed venous composition. The needed theory and equations are developed, the program is discussed, and an example is presented.

Carbon Dioxide↗
PubMed1986

Influence of pulmonary blood flow and O2 flux on DO2 in avian lungs.

O2 diffusing capacity (DO2) was measured in anesthetized, unidirectionally ventilated ducks during hypercapnic hypoxia. DO2 averaged 78.2 mumol X (min X Torr)-1. This value increased to 97.3 mumol X (min X Torr)-1 after correction for ventilation-perfusion inequality. DO2 increased when pulmonary O2 exchange (MO2) and pulmonary blood flow (Q) were increased by either 2,4 dinitrophenol (DNP,ca. 5 mg/kg i.v.) or temporary unilateral pulmonary artery occlusion (TUPAO). DO2 increased with MO2 42.4 mumol X (mmol X Torr)-1 (R = 0.664), and with Q 80.3 mumol X (L X Torr)-1 (R = 0.895). Since there is evidence against expansion of membrane diffusing capacity through recruitment and distention of pulmonary capillaries in avian lungs, we suggest that the close coupling of DO2 to Q reflects a reduction of functional lung heterogeneity at higher blood flows, perhaps due to better matching of V to D, or D to Q.

2,4-Dinitrophenol↗
PubMed1986

Sensitivity of avian intrapulmonary chemoreceptors to venous CO2 load.

To investigate the response of individual intrapulmonary chemoreceptors (IPC) to venous CO2 loads approximating moderate muscular exercise, we recorded vagal discharge from 33 IPC arising from the left lungs of 9 anesthetized, unidirectionally ventilated Pekin ducks. Each IPC was studied during control conditions (PECO2 = 29.0 +/- 0.8 Torr, PVCO2 = 30.2 +/- 0.6 Torr) and during venous CO2 load (PECO2 = 29.5 +/- 0.7 Torr, PVCO2 = 51.5 +/- 1.4 Torr). Venous loading was produced by increasing the percentage of CO2 in the gas ventilating the right lung from 0 to 9-25% CO2. The flow of 1% CO2 through the left lung was adjusted to keep the left lung PECO2 constant. During venous loading, discharge frequencies indicated that the PCO2 at the receptive sites fell, on the average, 1.6 +/- 0.8 Torr.

Action Potentials↗
PubMed1985

Comparison of intrapulmonary chemoreceptor response to PCO2 in the duck and chicken.

Intrapulmonary chemoreceptors (IPC) in the burrowing owl are reported to be much less sensitive to PCO2 than IPC in the chicken. This blunted IPC sensitivity has been suggested to be a physiological adaptation to hypercapnic subterranean environments. To investigate the natural variation IPC responses in non-burrowing species, stimulus-response characteristics of 87 IPC in 22 anesthetized Pekin ducks were recorded and compared to those from 54 previously reported chicken IPC. Average logarithmic stimulus response curves were described by slopes of - 11.2 and - 10.7 imp X (sec X InPCO2)-1 for duck and chicken, respectively. Each had slopes steeper than the - 6.87 imp X (sec X InPCO2)-1 slope reported for the burrowing owl. As with chicken IPC, slopes and intercepts of the individual curves were highly correlated in the duck. It appears that a general mechanism of receptor transduction exists in birds, with some quantitative interspecies variation.

Animals↗
PubMed1985

Sources of carbon dioxide in penguin air sacs.

CO2 tensions in the caudal air sacs of birds cannot be quantitatively predicted by current models of avian respiration, mainly because the contribution of neopulmonic parabronchial gas exchange has not been determined. To overcome this problem we studied penguins that have purely paleopulmonic lungs. Three penguins were anesthetized, intubated, and ventilated at a constant respiratory rate and different tidal volumes (VT). PO2 and PCO2 were measured in arterial blood and end-expired, mixed-expired, interclavicular air sac, and caudal thoracic air sac gas. Interclavicular air sac and end-expired gas had similar compositions. Caudal thoracic air sac gas was intermediate in composition to end-expired and inspired gas, and its PCO2 was 1.5-3.5 times greater than the value predicted from reinhaled dead space. This difference between measured and predicted caudal thoracic air sac PCO2 increased with VT but showed no relationship to changes in dead space-to-VT ratio. The difference is not explained by stratification or diffusive gas exchange across air sac walls. The results can be explained by postulating that inspired gas passes over exchange surfaces on its path to caudal air sacs. This is unexpected in the purely paleopulmonic lungs of penguins and suggests that airflow may not be caudocranial in all paleopulmonic parabronchi.

Air Sacs↗
PubMed1984

Receptive fields of intrapulmonary chemoreceptors in the Pekin duck.

Reflex experiments indicate a uniform distribution of CO2 chemosensitivity in avian lungs, but neural recording experiments suggest a non-uniform distribution of intrapulmonary chemoreceptor (IPC) endings. To reconcile these observations, blood gases and PECO2 were measured while recording discharge frequencies of 32 IPC innervating the unidirectionally ventilated lungs of 14 Pekin ducks. IPC discharge frequencies, recorded from the left vagus, were determined while ventilating the perfused left lung with caudocranial and craniocaudal flows of 1% CO2 in air, and then while ventilating the unperfused left lung with known levels of CO2 in air. Lung PCO2 profiles were predicted using an eight-compartment computer model of cross-current gas exchange with log-normal ventilation-perfusion inequality and shunt. The PCO2 profiles and IPC discharge frequencies were used to calculate receptor location. At the 99% confidence limit, estimates of IPC location changed significantly in all but 7 IPC when the direction of ventilation was reversed, indicating many IPC have multiple endings. Eighteen of 32 IPC had receptive fields extending at least 50% of the parabronchial length, which may explain the uniform reflex chemosensitivity to intrapulmonary CO2 noted by others.

Animals↗
PubMed1983

Effect of temperature on the CO2 sensitivity of avian intrapulmonary chemoreceptors.

We determined linear regressions of discharge frequency on ln PCO2 of 23 intrapulmonary chemoreceptors (IPC) from eight hyperthermic, adult cockerels. At low PCO2, IPC in hyperthermic cockerels discharged slower than IPC measured in euthermic cockerels; above 25 torr PCO2, however, they discharged faster than euthermic IPC. Thus, IPC were less sensitive to PCO2 during hyperthermia. We calculate that a 1 degree C increase in the temperature of the lung (TL) causes the slope of the linear regression of discharge frequency on ln PCO2 to be less negative by 1.5 +/- 0.5 imp (sec X ln PCO2)-1 and that, for any increase in TL above normal (41.5 degrees C), the average IPC discharge frequency equals (-10.7 + 1.5 (TL -41.5] X (ln (PCO2/25.0] + 3.7. This relationship may be partly responsible for the increased tidal volume and decreased respiratory frequency observed when body temperature increases during constant PaCO2.

Alkalosis, Respiratory↗
PubMedDate not supplied

A model of regional ventilation-perfusion inhomogeneity in the avian lung. Implications for gas exchange and intrapulmonary chemoreceptor microenvironment.

We recorded discharge frequencies of 32 intrapulmonary chemoreceptors (IPC) during caudocranial and craniocaudal ventilation in the perfused duck lung. Blood gases, ventilatory gas flow, inspired PCO2 and PO2, and expired PCO2 measured simultaneously were used to predict regional CO2 and O2 gradients within the lung. Gas exchange was modelled in 7 log normal ventilation-perfusion compartments using mass balance differentials with an adjustable step size. CO2 and O2 interactions during exchange were modelled using the Bohr effect, P50, blood acid-base status, and the CO2 dissociation relationship. Close agreement (+/- 1.0 Torr) between simulated arterial and expired PCO2 and observed values was achieved after forcing simulated PaO2 to converge on observed PaO2 by an iterative adjustment of the perfusive shunt or the log standard deviation of the ventilation-perfusion distribution. Using the IPC static CO2 sensitivity measured in the non-perfused lung and the CO2 gradients generated by the model, we have found evidence for a distributed multi-ending receptor system in the duck lung.

Animals↗
PubMedDate not supplied

Effects of normobaric and hypobaric hypoxia on ventilation and arterial blood gases in ducks.

We measured ventilation (V1) and arterial blood gases in awake Pekin ducks exposed to normoxia at sea level, normobaric hypoxia achieved by lowering FIO2 at normal barometric pressure (NORMO), and hypobaric hypoxia achieved with a low pressure chamber and 21% O2 (HYPO). Average normoxic values were: V1 = 0.46 L . (kg.min)-1, PaO2 = 99.7 Torr, PaCO2 = 30.1 Torr. At PIO2 = 90 Torr, NORMO and HYPO measurements were not significantly different (P greater than 0.05). At PO2 = 46 Torr, NORMO V1 was less than HYPO V1 but blood gases were not significantly different: VI = 1.00 vs 1.45 L . (kg.min)-1; PaO2 = 31.3 vs 33.0 Torr; PaCO2 = 11.5 vs 10.6 Torr. Although both tidal volume (VT) and respiratory frequency (fR) were greater in HYPO, similar blood gases with NORMO and HYPO suggest similar parabronchial ventilation. The results suggest increased physiologic dead space, caused by reduced efficacy of aerodynamic valving, with reduced gas density in hypobaria.

Air Pressure↗