Search PubMed⌕ Search

Biomedical subjects

F L Powell

Publications and source records attributed to F L Powell.

At least 55 records · Page 3Linked to original sources
PubMed1992

CO2 and avian eggshell formation at high altitude.

We tested the hypothesis that altitude-induced hypocapnia in hens reduces eggshell conductance to water vapor (GH2O). Seven laying hens (Gallus domesticus) native to 1200 m were chronically exposed to high altitude (3800 m), and then to high altitude with sufficient inspired CO2 to relieve hypocapnia (3800 m + CO2). Egg GH2O was measured gravimetrically, shell thickness was measured with a micrometer, and aggregate pore area was calculated from measured values using Fick's law. Comparing results at 1200 m (n = 118) and 3800 m (n = 102), GH2O was reduced from 13.9 +/- 0.2 to 12.6 +/- 0.2 mg/(d.Torr)(mean +/- SE), shell thickness was reduced from 0.297 +/- 0.003 mm to 0.287 +/- 0.003 mm, and calculated aggregate pore area per egg was reduced from 1.97 +/- 0.03 mm2 to 1.72 +/- 0.03 mm2. When hypocapnia was relieved at 3800 m + CO2 (n = 82), GH2O was reduced even further to 11.1 +/- 0.2 mg/(d.Torr), shell thickness increased to 0.305 +/- 0.003 mm, and aggregate pore area was reduced to 1.61 +/- 0.03 mm2. Based on these results we reject our hypothesis. We conclude that hypocapnia is responsible for thin eggshells at altitude. Other physiological stimuli must cause the reductions in eggshell GH2O and pore area.

Altitude↗
PubMed1992

Effects of hypoxia and hypercapnia on cricothyroid muscle response to airway pressure.

We studied the effects of hypercapnia (FICO2 = 0.07) and hypoxia (FIO2 = 0.13) on the cricothyroid muscle response (peak integrated CT EMG) to graded inspiratory resistance (RI). Five anesthetized dogs spontaneously breathed through the upper airway (UAB) or a side arm of a tracheotomy cannula bypassing the larynx (TB). With room air UAB, graded increases in RI increased CT EMG, upper airway pressure change (Paw) and esophageal pressure change (Pes, indicating increased inspiratory drive), but decreased VT. For room air TB, the effects of RI were much less but still significant. Hypercapnia increased VT, fR, Pes, Paw and CT EMG for any given RI during UAB more than during TB. Hypoxia increased fR but did not increase VT, Pes, Paw, or CT EMG. The results are consistent with a model predicting CT activity as additive functions of inspiratory drive and laryngeal receptor stimulation by Paw and no direct effects of chemoreceptor stimulation on the CT, independent of those resulting from changes in inspiratory drive and upper airway pressure.

Airway Resistance↗
PubMed1992

Avian arterial chemoreceptor responses to steps of CO2 and O2.

The responses of avian arterial chemoreceptor preparations to 44-sec steps of inspired CO2 and O2 were quantified. Anesthetized ducks were unidirectionally ventilated, arterial pH was recorded with a fast responding indwelling electrode, and neural activity was recorded from 28 preparations consisting of dissected filaments of the vagus nerve (23 single-fibered, 5 few-fibered). We analyzed responses using cycle-triggered stimulus histograms of neural discharge, cross correlation analysis, and analysis of variance. Average responses of the chemoreceptor preparations to PaCO2 steps from 24 +/- 1 to 38 +/- 1 Torr were larger (per Torr), occurred faster, and appeared more rate sensitive than the responses to PaO2 steps from 101 +/- 3 to 56 +/- 2 Torr. Average responses to CO2 steps usually appeared more rate sensitive when measured during arterial hypoxia than during arterial normoxia. These characteristics are very much like those reported for mammalian arterial chemoreceptors, except that responses of avian chemoreceptor preparations to repetitive CO2 steps were highly variable according to statistical analysis.

Animals↗
PubMed1992

Augmented hypoxic ventilatory response in men at altitude.

To test the hypothesis that the hypoxic ventilatory response (HVR) of an individual is a constant unaffected by acclimatization, isocapnic 5-min step HVR, as delta VI/delta SaO2 (l.min-1.%-1, where VI is inspired ventilation and SaO2 is arterial O2 saturation), was tested in six normal males at sea level (SL), after 1-5 days at 3,810-m altitude (AL1-3), and three times over 1 wk after altitude exposure (PAL1-3). Equal medullary central ventilatory drive was sought at both altitudes by testing HVR after greater than 15 min of hyperoxia to eliminate possible ambient hypoxic ventilatory depression (HVD), choosing for isocapnia a P'CO2 (end tidal) elevated sufficiently to drive hyperoxic VI to 140 ml.kg-1.min-1. Mean P'CO2 was 45.4 +/- 1.7 Torr at SL and 33.3 +/- 1.8 Torr on AL3, compared with the respective resting control end-tidal PCO2 of 42.3 +/- 2.0 and 30.8 +/- 2.6 Torr. SL HVR of 0.91 +/- 0.38 was unchanged on AL1 (30 +/- 18 h) at 1.04 +/- 0.37 but rose (P less than 0.05) to 1.27 +/- 0.57 on AL2 (3.2 +/- 0.8 days) and 1.46 +/- 0.59 on AL3 (4.8 +/- 0.4 days) and remained high on PAL1 at 1.44 +/- 0.54 and PAL2 at 1.37 +/- 0.78 but not on PAL3 (days 4-7). HVR was independent of test SaO2 (range 60-90%). Hyperoxic HCVR (CO2 response) was increased on AL3 and PAL1. Arterial pH at congruent to 65% SaO2 was 7.378 +/- 0.019 at SL, 7.44 +/- 0.018 on AL2, and 7.412 +/- 0.023 on AL3.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Temperature effects on pulmonary receptor responses to airway pressure and CO2 in Alligator mississippiensis.

The effects of body temperature (Tb) on pulmonary stretch receptor (PSR) and CO2-sensitive intrapulmonary chemoreceptor (IPC) response characteristics may have important effects on ventilatory control in reptiles. In this study, three questions were addressed: (1) what are the effects of Tb on PSR and IPC responses to airway pressure (Paw) and lung CO2 (PCO2); (2) what are the effects of acute (less than 12 h) vs chronic (greater than 1 week) changes in Tb on both receptor groups; and (3) can predicted changes in the fractional dissociation of imidazole (alpha im), calculated via independent changes in Tb and PCO2, explain the CO2-sensitivity of either IPC or PSR? Single fiber PSR and IPC responses to Paw, PCO2 and Tb were determined in 11 anesthetized Alligator mississippiensis (pentobarbital; 30 mg/kg), acclimated at 20 degrees C (N = 5) or at 30 degrees C (N = 6). PSR activity increased as Paw increased at both Tb, but PSR activity and sensitivity to Paw were lower at 20 degrees C. The average Q10 was 2.1. Increasing inhaled CO2 from 1 to 7% decreased PSR activity by 27 +/- 6% at 20 degrees C and 18 +/- 5% at 30 degrees C. IPC activity decreased as PCO2 increased at both Tb, but IPC activity and sensitivity were reduced at 20 degrees C. The average Q10 was 3.2. Increasing Paw from 2 to 10 cm H2O had inconsistent effects on IPC activity. There were no differences between the effects of acute or chronic changes in Tb on either PSR or IPC responses. Predicted changes in alpha im could not explain the CO2-sensitivity of either IPC or PSR. We conclude that PSR and IPC adapt rapidly to Tb changes. The larger Q10 of IPC suggests that the relative role of IPC vs PSR in ventilatory control may be greater at elevated body temperatures.

Alligators and Crocodiles↗
PubMed1989

Ventilation-perfusion relationships in alligators.

We measured V/Q distributions with the multiple inert gas elimination technique in five anesthetized artificially ventilated American alligators at 24 degrees C. The overall V/Q was relatively high (2.0 to 7.2) because of continuous artificial ventilation. The V/Q distributions were usually unimodal (log standard deviation of Q distribution averaged 0.47 +/- 0.09 [SD] and there was considerable shunt (28.5 +/- 10.3% of cardiac output). The data are consistent with a pulmonary, rather than central cardiovascular shunt. We also detected a molecular weight dependent limitation to inert gas elimination. The difference in error of fit to enflurane and cyclopropane retentions was significantly greater than predicted from experimental error. The estimated stratification diffusing capacity, a measure of this limitation, was 10% of the value estimated for mammals and similar to morphometric estimates of membrane diffusing capacity in alligators, which is comparatively low. Hence, even though the multicameral lungs of alligators are unevenly partitioned and have large gas phase diffusion spaces, V/Q matching and molecular weight dependent limitations are relatively small. Shunt, dead space and membrane diffusion resistances can be more important limitations of gas exchange.

Alligators and Crocodiles↗
PubMed1988

Effects of intrapulmonary CO2 and airway pressure on pulmonary vagal afferent activity in the alligator.

The effects of airway CO2 and pressure on pulmonary vagal afferent fibers were studied in seven anesthetized alligators Alligator mississippiensis, at room temperature (24 degrees C). Of 49 receptors which fired in phase with ventilation, 13 behaved like mammalian rapidly adapting pulmonary stretch receptors, 19 like mammalian slowly adapting pulmonary stretch receptors (PSR), and 17 like avian intrapulmonary CO2-sensitive chemoreceptors (IPC). PSR and IPC were positively localized to the lung by punctate stimulation or response to airway CO2 changes during pulmonary artery occlusion. PSR discharge frequency (fPSR) was measured at airway pressures (Paw) from 0 to 15 cm H2O at FICO2 = 0.01 in 14 receptors. fPSR increased in all receptors throughout the range of Paw studied. In 13 PSR, increasing FICO2 from 0.01 to 0.07 decreased fPSR 23 +/- 13% (+/- SEM) at Paw = 2 cm H2O and 14 +/- 7% at 15 cm H2O. IPC discharge frequency (fIPC) decreased as FICO2 increased and most discharged less than 1 sec-1 at FICO2 = 0.03. In 7 IPC at FICO2 = 0.01, increasing Paw from 2 to 15 cm H2O increased fIPC 17 +/- 5% after pulmonary artery occlusion demonstrating some mechanosensitivity in alligator IPC. Although both IPC and PSR showed mechanosensitivity and CO2-sensitivity, the two receptor types were distinct. PSR were 13 times more sensitive to Paw changes than IPC and IPC were 14 times more sensitive to FICO2 changes than PSR. We did not find any receptors with intermediate CO2- or mechanosensitivities that could represent a transitional form of receptor. These results predict that IPC and PSR may have different roles in reflex ventilatory control.

Alligators and Crocodiles↗
PubMed1987

High-frequency ventilation of ducks and geese.

We studied gas exchange in anesthetized ducks and geese artificially ventilated at normal tidal volumes (VT) and respiratory frequencies (fR) with a Harvard respirator (control ventilation, CV) or at low VT-high fR using an oscillating pump across a bias flow with mean airway opening pressure regulated at 0 cmH2O (high-frequency ventilation, HFV). VT was normalized to anatomic plus instrument dead space (VT/VD) for analysis. Arterial PCO2 was maintained at or below CV levels by HFV with VT/VD less than 0.5 and fR = 9 and 12 s-1 but not at fR = 6 s-1. For 0.4 less than or equal to VT/VD less than or equal to 0.85 and 3 s-1. less than or equal to fR less than or equal to 12 s-1, increased VT/VD was twice as effective as increased fR at decreasing arterial PCO2, consistent with oscillatory dispersion in a branching network being an important gas transport mechanism in birds on HFV. Ventilation of proximal exchange units with fresh gas due to laminar flow is not the necessary mechanism supporting gas exchange in HFV, since exchange could be maintained with VT/VD less than 0.5. Interclavicular and posterior thoracic air sac ventilation measured by helium washout did not change as much as expired minute ventilation during HFV. PCO2 was equal in both air sacs during HFV. These results could be explained by alterations in aerodynamic valving and flow patterns with HFV. Ventilation-perfusion distributions measured by the multiple inert gas elimination technique show increased inhomogeneity with HFV. Elimination of soluble gases was also enhanced in HFV as reported for mammals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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

Single breath CO2 measurements of deadspace in ducks.

We measured deadspace (VD) in ducks using CO2 expirograms (plots of expired PCO2 vs expired volume) obtained during artificial ventilation at different tidal volumes (VT) and respiratory system volumes (VRS). Conventional analysis of the expirograms for Bohr and Fowler VD indicated both were larger than anatomic VD. Most expirograms at VT less than or equal to 100 ml had terminal slopes greater than predicted for lung gas and violated the usual assumptions of the Fowler calculation. Bohr VD was not affected by VRS but increased with VT. This can be explained by expired PCO2 not reaching lung values at low VT and an expiratory mesobronchial ventilatory shunt. We propose a measure of mesobronchial shunt corresponding to a volume of gas exhaled in one breath from caudal air sacs through the mesobronchus (VM). VM/VT changes with pump vs constant flow ventilation indicating sensitivity of VM to flow pattern. We estimate mesobronchial shunting is greatest at the beginning of expiration and approaches zero only near the end of a 200 ml expiration with constant flow ventilation.

Animals↗
PubMed1986

Intrapulmonary and extrapulmonary shunt in ducks.

We measured shunt in seven anesthetized, mechanically ventilated Pekin ducks by the multiple inert gas elimination technique (MIGET) and by the oxygen method during 100% O2 breathing (O2 shunt). MIGET shunt measures only intrapulmonary shunt but O2 shunt measures intra- and extrapulmonary shunt (e.g. bronchial drainage). O2 shunt was calculated from oxygen contents of blood estimated from measured PO2 and standard O2 equilibrium curves at appropriate pH and hematocrit measured in 4 other ducks. In normal lungs MIGET shunt was 1.3 +/- 0.4 (mean +/- SEM) percent of cardiac output and O2 shunt was 6.3 +/- 1.3%. O2 shunt exceeded MIGET shunt by 5.4 +/- 1.4% which we attribute to extrapulmonary shunts. These include part of the bronchial circulation, thebesian veins and vertebral venous-pulmonary circulation connections. Both MIGET and O2 shunts increased when water was introduced into lungs. Overall, the relationship between % MIGET shunt and % O2 shunt was described by the equation: O2 shunt = 0.86 X MIGET + 5.67 (r = 0.96, n = 24).

Animals↗
PubMed1986

Physiological dead space and effective parabronchial ventilation in ducks.

Gas exchange in avian lungs is described by a cross-current model that has several differences from the alevolar model of mammalian gas exchange [e.g., end-expired PCO2 greater than arterial PCO2 (PaCO2)]. Consequently the methods available for estimating effective ventilation and physiological dead space (VDphys) in alveolar lungs are not suitable for an analysis of gas exchange in birds. We tested a method for measuring VDphys in birds that is functionally equivalent to the conventional alveolar VDphys. A cross-current O2-CO2 diagram was used to define the ideal expired point (PEi) and VDphys was calculated as from the equation, VDphys = [(PEiCO2--PECO2)/PEiCO2]. VT, where VT is tidal volume. In seven Pekin ducks VDphys was 13.8 ml greater than anatomic dead space and measured changes in the instrument dead space volume. VDphys also reflected changes in ventilation-perfusion inequality induced by temporary unilateral pulmonary arterial occlusion. Bohr dead space, calculated by substituting end-expired PCO2 for PEiCO2, was insensitive to such inhomogeneity. Enghoff dead space, calculated by substituting PaCO2 for PEiCO2, is theoretically incorrect for cross-current gas exchange and was often less than anatomic dead space. We conclude that VDphys is a useful index of avian gas exchange and propose a standard definition for effective parabronchial ventilation (VP) analogous to alveolar ventilation (i.e., VP = VE--VDphys, where VE is total ventilation).

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↗
PubMed1985

Pulmonary vascular resistance during unilateral pulmonary arterial occlusion in ducks.

We measured mean pulmonary arterial pressure (Ppa) during temporary unilateral pulmonary arterial occlusion (TUPAO) in 10 ducks. Ppa increased from 11.4 +/- 0.8 mmHg during control conditions to 18.8 +/- 1.8 during TUPAO. In 5 of the 10 ducks we also measured mean left atrial pressure (Pla) and cardiac output (Q). In these ducks Ppa significantly increased with TUPAO from 13.9 +/- 0.4 to 22.0 +/- 1.2 mmHg, whereas Pla and Q did not change significantly. Pulmonary vascular resistance (PVR) increased from 10.6 +/- 1.3 to 24.1 +/- 5.3 mmHg X min X 1(-1) on TUPAO. By assuming equal vascular resistance in either lung it can be calculated that the vascular resistance in only one lung was 22.5 +/- 3.5 mmHg X min X 1(-1) during control conditions. Thus doubling flow resulted in no significant change in one lung's vascular resistance. A morphometric study of both lungs of a domestic goose that were rapidly frozen during TUPAO indicated very little compliance in pulmonary blood capillaries. The relative volume of exchange tissue occupied by blood capillaries was 0.28 in the occluded lung and 0.36 in the perfused lung. Surface-to-volume ratios of blood capillaries were 12,524 cm-1 in the occluded lung and 11,056 cm-1 in the perfused lung. We conclude that PVR in birds is relatively insensitive to changes in Q, in contrast to mammals.

Animals↗
PubMed1985

Effects of acetone in heparin on the multiple inert gas elimination technique.

We have detected acetone in several brands of heparin. If uncorrected, this leads to errors in measuring acetone in blood collected in heparinized syringes, as in the multiple inert gas elimination technique for measuring ventilation-perfusion ratio (VA/Q) distributions. Error for acetone retention [R = arterial partial pressure-to-mixed venous partial pressure (P-V) ratio] is usually small, because R is normally near 1.0, and the error is similar in arterial and mixed venous samples. However, acetone excretion [E = mixed expired partial pressure (P-E)-to-P-V ratio] will appear erroneously low, because P-E is accurately measured in dry syringes, but P-V is overestimated. A physical model of a homogeneous alveolar lung at room temperature and without dead space shows: the magnitude of acetone E error depends upon the ratio of blood sample to heparinized saline volumes and acetone partial pressures, without correction, acetone E can be less than that of less soluble gases like ether, a situation incompatible with conventional gas exchange theory, and acetone R and E can be correctly calculated using the principle of mass balance if the acetone partial pressure in heparinized saline is known. Published data from multiple inert gas elimination experiments with acetone-free heparin, in our labs and others, are within the limits of experimental error. Thus the hypothesis that acetone E is anomalously low because of physiological mechanisms involving dead space tissue capacitance for acetone remains to be tested.

Acetone↗
PubMed1984

Steady-state discharge and bursting of arterial chemoreceptors in the duck.

The steady-state discharge of fourteen arterial chemoreceptor preparations were recorded from the left cervical vagi of unidirectionally ventilated, pentobarbitone anaesthetized ducks. All were excited by both hypoxia and hypercapnia and these stimuli interacted multiplicatively, as they do in mammals. We located the receptive fields of three preparations by observing their responses to i.v. injections of 2,4-dinitrophenol before, during and after occlusion of various arteries. The responses of two preparations were consistent with their location in the ipsilateral carotid body, but the responses of one, containing two active fibres, suggested that its discharge originated in aortic bodies. The discharge of eleven preparations was not random, but came in short high frequency bursts. As stimulus intensity was increased by either hypoxia or hypercapnia the average number of impulses per burst decreased. We have shown that the arterial chemoreceptors of the duck are sensitive to both hypoxia and hypercapnia. Because the steady-state stimulus-response characteristics are essentially the same as those of mammals we suppose that both mammalian and avian chemoreceptors are excited by the same basic mechanism. We also show that ducks have active extra-carotid arterial chemoreceptors.

Animals↗
PubMed1983

Morphometrics of rapidly frozen goose lungs.

To understand the structural basis of avian gas exchange better, we made a morphometric study of domestic and Canada goose lungs. The volume of glutaraldehyde-fixed domestic goose lungs (30 cm3/kg body weight) was similar to that determined from silicone casts of Canada goose lungs by Duncker (33 cm3/kg). To examine finer structures, we rapidly froze goose lungs under physiologic conditions, fixed tissue samples by a freeze substitution procedure and analyzed samples with stereological methods. From light micrographs we determined that about 55% of the lung is parabronchi in both species. Volume densities of air capillaries, blood capillaries and tissue and surface:volume ratios of these same structures were determined from electron micrographs. Our measurements agree with those from glutaraldehyde-fixed Canada goose lungs from other laboratories. Gas exchange surface area was largest in the good flier (Canada goose) but both birds had larger surface areas than comparably sized mammals. The harmonic mean blood-gas barrier thickness is smaller in both species of birds (0.3 microns) than in mammals. Thus, membrane diffusing capacities for gases should be larger in birds than in mammals. Pulmonary blood capillary transit time, as calculated from blood capillary volume and normal levels of cardiac output, are longer in birds than in mammals and should allow more time for blood-gas equilibrium. Pleats and folds were frequently observed in air and blood capillaries, suggesting that the avian lung may not be as rigid as was previously thought and that capillary volumes and surface areas may change under physiologic conditions.

Animals↗