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At least 19 recordsLinked to original sources
PubMed2004

Effects of acute temperature changes on aerial and aquatic gas exchange, pulmonary ventilation and blood gas status in the South American lungfish, Lepidosiren paradoxa.

Lungfish (Dipnoi) are probably sister group relative to all land vertebrates (Tetrapoda). The South American lungfish, Lepidosiren paradoxa, depends markedly on pulmonary gas exchange. In this context, we report on temperature effects on aquatic and pulmonary respiration, ventilation and blood gases at 15, 25 and 35 degrees C. Lung ventilation increased from 0.5 (15 degrees C) to 8.1 ml BTPS kg(-1) min(-1) (35 degrees C), while pulmonary O(2)-uptake increased from 0.06 (15 degrees C) to 0.73 ml STPD kg(-1) min(-1) (35 degrees C). Meanwhile aquatic O(2)-uptake remained about the same ( approximately 0.01 ml STPD kg(-1) min(-1)) at all temperatures. Concomitantly, the pulmonary gas exchange ratio (R(E)) rose from 0.11 (15 degrees C) to 0.62 (35 degrees C), because a larger fraction of total CO(2) output became eliminated by the lung. Accordingly, PaCO(2) rose from 13 (15 degrees C) to 37 mm Hg (35 degrees C), leading to a significant decrease of pHa at higher temperature (pHa=7.58-15 degrees C; 7.33-35 degrees C). The acid-base status of L. paradoxa was characterized by a generally low pH (7.4-7.5), high bicarbonate level (20-25 mM) and PaO(2) ( approximately 80 mm Hg). The increased dependence on the lung at higher temperature parallels data for amphibians. Further, the effects of bimodal gas exchange on temperature-dependent acid-base regulation closely resemble those of anuran amphibians.

Animals↗
PubMed2000

Unilateral lung edema: effects on pulmonary gas exchange, hemodynamics, and pulmonary perfusion distribution.

Two types of unilateral lung edema in sheep were characterized regarding their effects on pulmonary gas exchange, hemodynamics, and distribution of pulmonary perfusion. One edema type was induced with aerosolized HCl (0.15 M, pH 1.0) and the other with NaCl (0.15 M, pH 7.4). Both aerosols were nebulized continuously for 4 h into left lungs. In HCl-treated animals, pulmonary gas exchange deteriorated [from a partial arterial O(2) pressure-to-inspired O(2) fraction ratio (Pa(O(2))/FI(O(2))) of 254 at baseline to 187 after 4 h HCl]. In addition, pulmonary artery pressure and total pulmonary vascular resistance increased (from 16 to 19 mmHg and from 133 to 154 dyn. s. cm(-5), respectively). In NaCl-treated animals, only the central venous pressure significantly increased (from 7 to 9 mmHg). Distribution of pulmonary perfusion (measured with fluorescent microspheres) changed differently in both groups. After HCl application, 6% more blood flow was directed to the treated lung, whereas, after NaCl, 5% more blood flow was directed to the untreated lung. HCl and NaCl treatment both induce an equivalent lung edema, but only HCl treatment is associated with gas exchange alteration and tissue damage. Redistribution of pulmonary perfusion maintains gas exchange during NaCl treatment and decreases it during HCl inhalation.

Aerosols↗
PubMed1989

Effects of altitude acclimatization on pulmonary gas exchange during exercise.

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

Acclimatization↗
PubMed1979

24-hour extracorporeal membrane oxygenation in the hypoxic dog: hemodynamics and pulmonary gas exchange.

Hemodynamic and pulmonary gas exchange values were investigated during 24-hour extracorporeal membrane oxygenation performed on 7 anesthetized dogs subjected to alveolar hypoxia. The chief effects of extracorporeal membrane oxygenation were demonstrated. The duration of the extracorporeal membrane oxygenation was associated with a progressive decline in the systemic arterial pressure and heart rate and a progressive increase in the pulmonary blood flow rate. Left-ventricular stroke work remained constant. The sum of the pulmonary and extracorporeal oxygen uptakes showed no change in spite of large variations in pulmonary flow rate.

Animals↗
PubMed1976

Effect of increased gas density on pulmonary gas exchange in man.

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and the improved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio (VA/Q) variance was reduced. Of several considered mechanisms, we favor one in which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows for observed increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregional VA/Q variance accounts for at least one-half of the resting AaDO2 in healthy supine young men.

Blood Gas Analysis↗
PubMed1993

In vivo quantitation of carbonic anhydrase and band 3 protein contributions to pulmonary gas exchange.

The contributions to pulmonary gas exchange of red blood cell (RBC) membrane band 3 protein HCO3(-)-Cl- exchange and carbonic anhydrase- (CA) catalyzed HCO3- dehydration have never been determined directly in the whole animal. We utilized an experimental and model approach to measure these by analysis of phase III exhaled CO2 and O2 profiles in anesthetized dogs. In this method, we inhibit RBC membrane band 3 protein and cytoplasmic CA in RBCs passing the pulmonary capillaries and lung vascular luminal membrane-bound CA during a single ventilatory cycle. This is achieved with appropriately timed right atrial infusions of 4,4'-dinitrostilbene-2,2'-disulfonate (DNDS) to inhibit band 3 protein, ethoxzolamide (a lipophilic CA inhibitor with rapid membrane penetrance) to inhibit RBC and lung tissue CA, and benzolamide (an extremely hydrophilic CA inhibitor with virtually no penetrance into RBC cytoplasm) to inhibit only lung vascular luminal membrane CA. DNDS caused a 15% reduction in CO2 production (VCO2) without any change in O2 consumption (VO2). The addition of benzolamide to DNDS did not cause any further decrease in VCO2. Inhibition of RBC CA by ethoxzolamide caused a 67% reduction in VCO2 and a 11.5% reduction in VO2. Inhibition of lung vascular CA by benzolamide alone caused no statistically significant changes in either VCO2 or VO2. These results are in general agreement with in vitro data and model calculations. The only exceptions are the higher than predicted effect of RBC CA inhibition on VO2 (Bohr effect) and the lack of any contribution to CO2 transfer in the dog by lung vascular CA with access to plasma as a possible consequence of an endogenous plasma CA inhibitor.

Acetylene↗
PubMed1986

Pulmonary gas exchange during hemodialysis.

UNLABELLED: Pulmonary gas exchange was continuously measured in 13 mechanically ventilated patients during 24 hemodialyses for acute renal failure. Minute-ventilation was maintained constant by controlled ventilation and gas exchange was continuously measured by a mass-spectrometer system. Three groups were compared: a cuprophan membrane with an acetate dialysate; a polyacrilonitrile membrane (PAN) with an acetate dialysate; and PAN with a bicarbonate dialysate. Arterial PO2 and the O2 alveolar-arterial gradient were the same regardless of the membrane used. [H+] mildly decreased with all dialysates used. Arterial PCO2 decreased only with the acetate dialysate. O2 consumption increased, up to 20 +/- 5% of the initial values during hemodialysis, and remained increased during the two hours following the hemodialysis. Respiratory exchange ratio was lower after than before the hemodialysis. IN CONCLUSION: the maintenance of a constant minute ventilation prevented hemodialysis induced hypoxemia. VO2 increased during hemodialysis.

Acute Kidney Injury↗
PubMed1991

Pulmonary gas exchange in acute myocardial infarction with low pulmonary capillary wedge pressure.

To evaluate the clinical characteristic of pulmonary gas exchange in patients with low pulmonary capillary wedge pressure (PCW less than 18 mmHg) in the early phase of acute myocardial infarction, we investigated 48 patients admitted within 24h from the onset of chest pain. The alveolar-arterial oxygen tension difference (AaDO2) and arterial blood gas parameters were obtained while breathing room air on admission. The disturbance of pulmonary gas exchange, as revealed by the high value of AaDO2, existed without left ventricular dysfunction, and AaDO2 had no significant relationship with any of the hemodynamic parameters including the difference between plasma colloid osmotic pressure and PCW. Multiple regression analysis was performed using 9 variables related to pulmonary gas exchange, to identify those which were important. As a result, QRS score (p less than 0.01) and age (p less than 0.05) were identified as significant variables related to AaDO2. Thus, the disturbance of pulmonary gas exchange in patients with low PCW was caused by mechanisms other than left ventricular failure which may reflect the extent of ischemic myocardium.

Aged↗
PubMed1971

Gas exchange in renal failure. II. Pulmonary gas exchange during peritoneal dialysis.

Blood gas analysis studies have been made in patients undergoing peritoneal dialysis. It has been shown that oxygen tensions are reduced when fluid has been run into the peritoneal cavity and that this fall in Pao(2) is reversed after running out the dialysate. The change in Pao(2) is greater with 2-litre than with 1-litre cycles.

Carbon Dioxide↗
PubMed1989

Pulmonary gas exchange in panting dogs.

Pulmonary gas exchange during panting was studied in seven conscious dogs (32 kg mean body wt) provided with a chronic tracheostomy and an exteriorized carotid artery loop. The animals were acutely exposed to moderately elevated ambient temperature (27.5 degrees C, 65% relative humidity) for 2 h. O2 and CO2 in the tracheostomy tube were continuously monitored by mass spectrometry using a special sample-hold phase-locked sampling technique. PO2 and PCO2 were determined in blood samples obtained from the carotid artery. During the exposure to heat, central body temperature remained unchanged (38.6 +/- 0.6 degrees C) while all animals rapidly switched to steady shallow panting at frequencies close to the resonant frequency of the respiratory system. During panting, the following values were measured (means +/- SD): breathing frequency, 313 +/- 19 breaths/min; tidal volume, 167 +/- 21 ml; total ventilation, 52 +/- 9 l/min; effective alveolar ventilation, 5.5 +/- 1.3 l/min; PaO2, 106.2 +/- 5.9 Torr; PaCO2, 27.2 +/- 3.9 Torr; end-tidal-arterial PO2 difference [(PE' - Pa)O2], 26.0 +/- 5.3 Torr; and arterial-end-tidal PCO2 difference, [(Pa - PE')CO2], 14.9 +/- 2.5 Torr. On the basis of the classical ideal alveolar air approach, parallel dead-space ventilation accounted for 54% of alveolar ventilation and 66% of the (PE' - Pa)O2 difference. But the steepness of the CO2 and O2 expirogram plotted against expired volume suggested a contribution of series in homogeneity due to incomplete gas mixing.

Acepromazine↗
PubMed1996

Effects of cardiopulmonary bypass temperature on pulmonary gas exchange after coronary artery operations.

BACKGROUND: Pulmonary dysfunction is one aspect of the postoperative morbidity associated with cardiopulmonary bypass. Normothermic systemic perfusion can result in shorter intubation times, which have been attributed to improved pulmonary gas exchange, but the influence of perfusion temperature on pulmonary gas exchange itself is not known. METHODS: Pulmonary gas exchange was assessed using alveolar-arterial oxygen pressure gradients in 45 patients undergoing routine coronary revascularization who were randomized to undergo cardiopulmonary bypass at 28 degrees C, 32 degrees C, or 37 degrees C. This was part of a more comprehensive study of the effects of temperature on bodily systems. The gradients were estimated preoperatively with the patients breathing air, again over a period between 2 and 4 hours postoperatively during mechanical ventilation with three different oxygen concentrations (30%, 40%, and 60%), and again 1 hour after extubation while breathing the same three oxygen concentrations. RESULTS: Preoperative alveolar-arterial oxygen pressure gradients on air were 24.4 +/- 8.2 mm Hg (mean +/- standard deviation) (28 degrees C), 24.5 +/- 20.4 mm Hg (32 degrees C), and 20.5 +/- 9.5 mm Hg (37 degrees C). Postoperatively, during ventilation and after rewarming, the gradients increased with the increase in inspired oxygen fraction concentrations (30% to 60%) from 67.1 +/- 12.0 mm Hg to 193.1 +/- 30.5 mm Hg (28 degrees C), from 76.4 +/- 20.6 mm Hg to 246.7 +/- 47.7 mm Hg (32 degrees C), and from 79.0 +/- 18.0 mm Hg to 222.9 +/- 40.5 mm Hg (37 degrees C), respectively. A similar pattern was noted 1 hour after extubation, when the gradients increased from 72.4 +/- 12.5 mm Hg to 256.6 +/- 26.5 mm Hg (28 degrees C), from 75.7 +/- 13.9 mm Hg to 252.7 +/- 38.3 mm Hg (32 degrees C), and from 69.1 +/- 19.3 mm Hg to 253.1 +/- 33.0 mm Hg (37 degrees C). There were no significant differences in alveolar-arterial oxygen pressure gradient between the three groups during ventilation or after extubation. CONCLUSIONS: Cardiopulmonary bypass perfusion temperature does not influence alveolar-arterial oxygen pressure gradients in the first 12 hours after routine coronary artery bypass grafting in patients with uncompromised pulmonary and left ventricular function.

Carbon Dioxide↗
PubMed1985

Pulmonary gas exchange and exercise performance in pulmonary hypertension.

Patients with pulmonary hypertension have disordered pulmonary gas exchange and impaired exercise tolerance. The hypoxemia is due to mild ventilation-perfusion (VA/Q) inequality exaggerated by the presence of a low mixed venous PO2 (PvO2) and is accentuated during exercise due to a further fall in PvO2. This in turn may be worsened by vasodilators which increase the degree of VA/Q inequality. Decreased exercise tolerance is due predominantly to cardiac limitation, and thus an improvement in cardiac function subsequent to successful vasodilation can be assessed by improved exercise performance.

Humans↗