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Biomedical subjects

J A Loeppky

Publications and source records attributed to J A Loeppky.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of pentoxifylline on pulmonary hemodynamics during acute hypoxia in anesthetized dogs.

The effects of pentoxifylline on pulmonary hemodynamics were studied in anesthetized dogs during acute alveolar hypoxia. In Series A, 7 dogs received pentoxifylline orally (18 mg/kg/day) for 11 wk and 7 untreated dogs served as control animals. During anesthesia and controlled ventilation, acute alveolar hypoxia was induced (10 to 13% inspired O2) and pulmonary and systemic hemodynamic and blood rheologic measurements were compared with normoxia. In control dogs, cardiac index did not change during hypoxia, but pulmonary vascular resistance index (PVRI) increased 79%, erythrocyte filterability decreased significantly (p less than 0.05), and relative viscosity of blood corrected for hematocrit did not change. In the pentoxifylline-treated dogs, cardiac index increased 28% and PVRI increased only 20%; in contrast to the control dogs, relative viscosity of blood was decreased by 18% and no significant changes in filterability were observed. The increase in PVRI in relation to the drop in arterial O2 saturation was significantly larger (p less than 0.05) in the control dogs. Pentoxifylline also increased P50 by 2.8 mm Hg (p less than 0.05). In Series B, hemodynamic measurements were made during variations in blood flow (induced by restricting venous return) in 3 treated (26 mg/kg/day for 3 wk) and 3 control dogs. In these experiments, pulmonary artery pressure was significantly lower at comparable flows during both normoxia and hypoxia. In both studies, the hemodynamic effects of the drug on the systemic circulation were less than on the pulmonary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1987

Acid-base status immediately following rapid changes of alveolar gas composition in awake dogs.

To study the interrelationship between blood O2, CO2, and acid-base status during rapid changes of alveolar gas composition unanesthetized dogs were made to inhale high CO2 gas mixtures following air breathing or to rebreathe high CO2 and O2 mixtures following hypoxia. Before and immediately after each change in alveolar gases, sequential blood samples were taken from the carotid artery for measurement of pH, PCO2 and PO2. In the experiments at normoxia the calculated base excess (BE) decreased by about 0.7 mmol/L after 10 sec and then returned to baseline level. A smaller decrease (averaging 0.4 mmol/L) was found with hyperoxia following hypoxia. The changes in BE can be attributed to bicarbonate (or H+) exchange between blood and tissue. Lung tissue is probably responsible for the rapid initial change in BE.

Acid-Base Equilibrium↗
PubMed1987

Sleep apnea and autonomic cerebrovascular dysfunction.

Changes in common carotid blood flow (CCF) and resistance index (RI), calculated from velocity waveforms by a noninvasive pulsed Doppler technique, were measured during apneic episodes and voluntary breath holding in five sleep apnea patients (SA) and during breath holding in five normal subjects (N). During apneic episodes averaging 27 s, CCF was reduced by 9% and RI increased by 4%, both trends being related to apneic duration. Internal carotid artery measurements in one SA indicated more dramatic changes in blood flow and RI than noted in CCF. During breath holding, CCF decreased significantly in SA but not in N, and RI showed a smaller reduction in SA. These changes in CCF and RI during sleep apnea are similar to those noted in anesthetized dogs where vasomotor waves and associated apneas were induced by elevating intracranial pressure. Previously reported recordings of ventilatory and systemic cardiovascular responses in SA are similar to these recordings in dogs, and it is therefore proposed that vasomotor responses to intermittent cerebral ischemia and hypercapnia may be the principle event in SA and periodic breathing only a secondary consequence of the prevailing autonomic dysfunction.

Animals↗
PubMed1987

The effects of head-down tilt on carotid blood flow and pulmonary gas exchange.

Common carotid artery blood flow (CCF), pulmonary gas exchange and ventilation were measured in six subjects in the supine posture (SUP I), serially during 20 min of head-down tilt at -30 degrees (HDT) and after returning to the supine posture (SUP II). CCF was approximately 6% lower during HDT, with a transient increase during the second minute, and was about 7% higher during SUP II than during SUP I. The transition from SUP I to HDT caused increases in O2 uptake (VO2), CO2 output, respiratory exchange ratio and tidal volume in the first minute. Similar responses were apparent following the HDT to SUP II transition, except for VO2, which changed little. Correction of VO2 for changes in estimated lung O2 stores indicated that about 200 ml of blood were shifted within the circulation by the tilt transitions which provided a ventilatory stimulus. HDT can cause a loss in blood and tissue O2 stores and gain in CO2 stores by shifting blood volume toward and blood flow away from the dependent headward vascular compartment and perhaps by producing ischemia in the elevated lower extremities. Cerebral venous congestion during HDT appears to cause periodic breathing and reduce CCF, the latter being partially offset by reduced flow resistance in the carotid artery.

Adult↗
PubMed1986

Validation and application of single breath cardiac output determinations in man.

Cardiac outputs by single breath (Qsb) and Fick (Qf) procedures were compared in five healthy males during supine rest and exercise with Qf ranging from 6-19 L X min-1. The prolonged exhalation (SB) was not controlled. The Qsb calculations incorporated an equation of the CO2 dissociation curve and a "moving spline" sequential curve-fitting technique to calculate the instantaneous R from points on the original expirogram. The resulting linear regression equation for all 38 comparisons obtained (r = +0.76, p less than 0.001, mean difference +/- S.D. = 2.93 +/- 2.72 L X min-1) indicated a 24% underestimation of Qf. A substantial portion of the variability during exercise (n = 28) was due to a difference in alveolar ventilation between the time of the mixed expired (E) gas collection and the SB maneuver. When Qsb was corrected (Qsb) by a linear regression based on the difference between Re and Rsb during exercise and by adding 2.44 L X min-1 at rest (the mean difference), the relationship was greatly improved (Qsb = 0.14 + 0.99 Qf, r = +0.93, mean difference +/- S.D. = 0 +/- 1.47 L X min-1). A subsequent study during upright rest and exercise to 80% of VO2max in 6 subjects indicated a close linear relationship between Q'sb and VO2 for all 95 values obtained (r = +0.94), with slope and intercept close to published studies utilizing invasive cardiac output measurements. Considerations of measured blood gases in relation to estimated values suggested that underestimates of Qf arose, at least in part, from arterial desaturation during the SB maneuver. Detailed computational procedures are provided for implementing this improved Qsb procedure.

Adult↗
PubMed1985

Transient PO2 and PCO2 differences between end-tidal gas and arterial blood during rebreathing in awake dogs.

O2 and CO2 partial pressures in end-tidal gas (PA) and carotid artery blood (Pa) were measured during non-steady-state gas exchange in unanesthetized dogs. In 5 experiments (A), low O2 breathing in open circuit preceded prolonged rebreathing during maintained normoxia. In 6 experiments (B), steady-state hypoxia and hypercapnia were followed by rebreathing CO2 in hyperoxia which caused PAO2 to rise and then fall while PACO2 increased. Negative (Pa-PA)CO2, averaging -5 torr, were observed 10 sec after starting rebreathing in B and values between -1 and -2 torr were noted later in A and B. (PA-Pa)O2 showed considerable transient increases for 2 min in A and 20 sec in B. This behavior of (PA-Pa)O2 could be explained by a lung model with unequal distribution of alveolar ventilation and perfusion to alveolar volume. The negative (Pa-PA)CO2 values observed during rebreathing with rapidly increasing PACO2 were in part attributable to such unequal distribution effects, in part to lung-to-carotid artery transit time effects.

Animals↗
PubMed1985

Arterial-alveolar CO2 equilibration in exercising dogs during prolonged rebreathing.

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30-68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.

Animals↗
PubMed1984

Comparison of noninvasive pulsed Doppler and Fick measurements of stroke volume in cardiac patients.

We compared simultaneous measurements of stroke volume by direct Fick (SVF) and noninvasive pulsed Doppler (SVD) techniques in 15 resting, supine cardiac patients. Doppler measurements of ascending aorta blood velocity were obtained from the suprasternal notch with a single crystal transducer. The systolic velocity integral of the spatial-average velocity waveform was multiplied by cross-sectional area from the systolic aortic diameter, obtained independently by M-mode echocardiography, to determine absolute values for SVD. The resulting linear regression equation was SVD = -1.14 + 0.95SVF, r = +0.91, p less than 0.0001. The mean SVD and SVF values were 68 and 73 cm3, respectively. These results in consecutive patients serve to validate empirically the pulsed Doppler method at rest. It is a convenient, safe, and painless procedure which appears appropriate for clinical diagnostic screening where serial measurements would be useful. However, this noninvasive technique does require technical experience and an understanding of anatomy and flow waveforms by the operator to obtain valid measurements.

Aged↗
PubMed1984

Abnormal cerebrovascular responses to CO2 in sleep apnea patients.

The responses of common carotid blood flow (CCF), pressure (BP), and resistance (R) to variations in respiratory gases were compared during waking periods in 10 sleep apnea patients (SA) and 10 healthy controls (N) of similar age. Respiratory gases were altered by 3-min CO2 rebreathing (RB), 3-min hyperventilation (HV), and 4-min hypoxia (HYP) procedures. CCF was measured continuously by a 5-MHz pulsed Doppler duplex scanner and R was calculated using brachial BP. During RB, which increased end-tidal PCO2 (PACO2) by 15 mm Hg, SA had a lower CCF and greater BP response and therefore a significantly different (positive) change in R compared with N. The ventilatory responses to CO2 were not significantly different. With HV the PACO2 fell by 13 mm Hg in both groups and CCF fell more markedly in SA than N with the same change in BP; therefore, R was increased significantly more in SA. The HYP results did not demonstrate a difference between groups. These results suggest that abnormal cerebrovascular responses to PACO2, initiated either by unusual vasoactive properties of cerebral resistance vessels or peculiar venous outlow patterns, may initiate or potentiate periodic breathing in SA by prolonging lung-to-brain circulation time.

Carbon Dioxide↗
PubMed1983

Quantitative description of whole blood CO2 dissociation curve and Haldane effect.

A simple procedure is presented to describe accurately the whole blood CO2 dissociation curve on linear content (CCO2) and pressure (PCO2) coordinates with an exponential equation (CCO2 = K . PCO2b). A single coordinate and the hemoglobin concentration, Hb, are required. Whole blood CCO2 can be calculated from values for pH, PCO2, Hb and O2 saturation by empirically accurate equations. The mathematical description of the CO2 curve was employed to quantitate the in vivo Haldane factor (fH) from simultaneous arterial and mixed venous blood samples in 20 healthy exercising subjects. The mean +/- SE was 0.28 +/- 0.03 (vol. % delta CCO2/vol. % delta HbO2). In 20 patients with severe obstructive lung disease fH was 0.29 +/- 0.08 when calculated from arterial samples while breathing air and 100% O2. Values for fH were not related significantly to acid-base status or Hb as suggested by previous workers. By assuming these or other values for fH, the in vivo change in blood PCO2 resulting from a given change in oxygenation can be predicted.

Absorption↗
PubMed1981

Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen.

Arterial (PaCO2), alveolar (PACO2), mixed expired (PECO2) CO2 pressures, CO2 production (VCO2) as well as arterial O2 saturation (SaO2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean PaCO2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in PACO2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. PECO2 remained essentially the same. There was a statistically significant correlation between the increase in PaCO2 on HO and the arterial unsaturation (100 - SaO2) on A and also between PaCO2 on A and its increment on HO. When the rise in PaCO2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygenation of hemoglobin on HO (Haldane effect), 78% of the observed change in PaCO2 could be accounted for. The deadspace/tidal volume ratio (VD/VT) increased from 0.59 on A to 0.64 and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in PaCO2, aADCO2 and VD/VT on transition from air to hyperoxia, particularly in patients with severe hypoxemia and hypercapnia.

Carbon Dioxide↗
PubMed1981

Beat-by-beat stroke volume assessment by pulsed Doppler in upright and supine exercise.

A 3.0 MHz pulsed Doppler echocardiography was used to estimate instantaneous stroke volume (SV) and cardiac output (Q) in eight men during steady-state supine (S) and upright (U) exercise at 300 kpm/min. The mean transients in heart rate (HR), SV, and Q for the first 20 s of exercise in each posture were then determined. Center-line blood velocities were obtained in the ascending aorta with the transducer positioned manually in the suprasternal notch. Mean supine values for SV and Q at rest and exercise were 111 ml and 6.4 1/min and 112 ml and 9.71/min, respectively. The corresponding results for U were 76 ml and 5.61/min and 92 ml and 8.41/min, respectively. These values compare favorably with previous studies utilizing invasive procedures. The transient response of Q following the onset of exercise in U was about twice as fast as in S because of the rapid and almost immediate upsurge in SV. In S, only HR served to augment Q, as SV initially fell. The faster rise in aortic flow in U with exercise represented an additional volume (184 ml) of blood passing through the aorta compared with S in the first 20s. This must be related to the rapid mobilization of pooled venous blood from the leg veins during U.

Adult↗
PubMed1980

Effect of lower body negative pressure release on hyperpnea induced by inhaled gas.

Transient breath-by-breath ventilation (VI) and end-tidal gases were measured on 6 men in response to: (1) the release of lower body negative pressure (LBR); (2) the one-min inhalation of a gas mixture (GAS) containing 5.4% CO2, 14% O2, balance N2; (3) the two combined (LBR + GAS) with LBR preceding GAS inspiration by 5 sec. With LBR a + 29% peak response in VI occurred after 20 sec whereas with GAS and LBR + GAS, VI tended to level off after 25 sec at + 100% and + 180%, respectively. Simultaneously, PETCO2 had risen 2, 5 and 8 mm Hg and PETO2 had fallen 7, 14 and 19 mm Hg, respectively. LBR accelerated and potentiated the VI response to GAS. Leg volume indicated that 50% of the pooled blood returned from the legs after 4 sec, presumably with high PCO2 and low PO2 contributing an endogenous respiratory stimulus to the exogenous one of GAS. VI with LBR + GAS was greater than the sum of each, suggesting an enhancement of the chemoreceptor response by returning pooled blood.

Adult↗
PubMed1980

Circulation and respiration response to arm exercise and lower body negative pressure.

The effects of supine arm exercise and lower body negative pressure (LBNP) were studied in six subjects with 10 min of LBNP at -40 mmHg (L), arm cranking for 8 min at a work load of 225 kpm/min (E) and both combined (L + E) preceded by 2 min of LBNP. Initial responses of ventilation (VI) and VO2 were curtailed and heart rate was significantly higher after the first min of L + E than E, reflecting the less accessible venous reservoir and reduced stroke volume due to L. Leg volume was significantly reduced after 30 s of E and continued to decline and remained below baseline during 6 min of recovery. With L + E, leg volume remained constant after E began, indicating both a shift of blood from legs to arms and reduced extra-vasation with LBNP. End-tidal PO2, VI and VI/VO2 were higher and PCO2 lower during the latter stages of L + E than during E, indicating less effective lung perfusion and greater alveolar deadspace caused by LBNP. The release of pooled blood from the lower body after L + E caused a greater VI, VO2 and lower RE than after E and produced marked transients in PCO2 and PO2, thereby slowing the recovery of gas exchange.

Adult↗