Effect of lung volume reduction surgery on gas exchange and pulmonary hemodynamics at rest and during exercise

The present study was an investigation of the regulation of anion secretion across cultured mouse endometrial epithelium by prostaglandin E2 (PGE2) using the short-circuit current (ISC) technique. The cultured endometrial monolayers responded to both apical and basolateral application of PGE2 with a sustained rise in ISC in a concentration-dependent manner. However, the potencies of apical and basolateral addition of PGE2 were different, with apparent EC50 of 200 and 4 nM, respectively. Replacement of Cl- or HCO3- in the bathing solution significantly reduced the ISC responses to both apical and basolateral addition of PGE2; however, the apical response exhibited greater dependence on HCO3- . Pretreatment with diphenylamine 2,2'-dicarboxylic acid, a Cl- channel blocker, significantly reduced both PGE2-induced ISC responses, while pretreatment with amiloride, a Na+ channel blocker, did not exert any effect. Forskolin, an adenylate cyclase activator, and 3-isobutyl-dihydro-testosterone-1-methyl-xanthine, a cAMP phosphodiesterase inhibitor, mimicked the ISC response to PGE2 while MDL12330A, an adenylate cyclase inhibitor, completely abolished the PGE2-induced ISC. The results of the present study indicate that the anion secretion across the mouse endometrial epithelium may be regulated by PGE2 involving a cAMP-dependent mechanism predominantly. The differential responses to apical and basolateral challenge with PGE2 also suggest that PGE2 of different origins may play different roles in uterine function.     

The efficacy of pulmonary thromboendarterectomy on long-term gas exchange

It has not been delineated in detail how pulmonary thromboendarterectomy (PTE) affects gas exchange through long-term follow-up. In Japan, this surgery has been undertaken in a limited number of institutions, and the results of PTE have not been well publicized. A total of 25 patients were operated on during the period from 1985 to 1996 at our institution, and the overall mortality rate was 16%. Our criteria for PTE were based on the following: 1) thrombi surgically accessible as judged by angiographic study; 2) mean pulmonary arterial pressure > or = 30 mmHg. The efficacies of PTE were analysed on haemodynamics as well as gas exchange at one month postsurgery and during follow-up (6-24 months). Significant haemodynamic improvement was obtained as early as 1 month after surgery. Improvement of gas exchange lagged, but was then observed during follow-up, and the improvement level of pulmonary haemodynamics was sustained. The early postoperative restrictive impairment and ventilation-perfusion abnormality on lung perfusion scan resolved during the follow-up period. It was concluded that the early postoperative efficacy of pulmonary throm-boendarterectomy was mainly achieved due to the reduction of pulmonary hypertension, whereas improvement in gas exchange was obtained over the longer term.     

Effect of pulmonary hypertension on gas exchange

This paper reviews the effects of pulmonary artery hypertension on gas exchange by exploring three different issues, namely: 1) how does gas exchange behave in diseases characterized by increased vascular tone (primary pulmonary hypertension (PPH), chronic obstructive pulmonary disease (COPD) and interstitial pulmonary fibrosis (IPF)) or decreased vascular tone ("hepatopulmonary syndrome"); 2) how does exercise, as a non-pharmacological tool of increasing pulmonary blood flow, modify gas exchange in these diseases; and 3) how do several drugs that lower (vasodilators) or increase (almitrine) the active component of pulmonary hypertension interact with gas exchange. Available data show that: 1) in PPH a high pulmonary vascular tone enhances gas exchange and when it is lowered, either by oxygen or vasodilators, ventilation perfusion (VA/Q) distributions deteriorate; 2) in COPD a lowered (vasodilators) or augmented (almitrine) active vascular tone is almost invariably paralleled by a deterioration or enhancement of ventilation-perfusion matching, respectively; 3) in IPF an adequate active response of the pulmonary vasculature is essential to maintain gas exchange, both at rest and during exercise; and 4) in patients with liver cirrhosis a low pulmonary vascular tone induces an abnormal VA/Q distribution. In summary, these data show that any situation and/or therapeutic intervention that lowers the active vascular tone deteriorates VA/Q relationships and vice versa. The final effect of pulmonary vascular tone on arterial oxygen tension (PaO2) is less predictable. The reason for this uncertainty is that the actual PaO2 value depends on the interplay of the intra- and extrapulmonary factors that control gas exchange in humans, and not only on the degree of VA/Q mismatching.     

Mechanisms of worsening gas exchange during acute exacerbations of chronic obstructive pulmonary disease

This study was undertaken to investigate the mechanisms that determine abnormal gas exchange during acute exacerbations of chronic obstructive pulmonary disease (COPD). Thirteen COPD patients, hospitalized because of an exacerbation, were studied after admission and 38+/-10 (+/-SD) days after discharge, once they were clinically stable. Measurements included forced spirometry, arterial blood gas values, minute ventilation (V'E), cardiac output (Q'), oxygen consumption (V'O2), and ventilation/perfusion (V'A/Q') relationships, assessed by the inert gas technique. Exacerbations were characterized by very severe airflow obstruction (forced expiratory volume in one second (FEV1) 0.74+/-0.17 vs 0.91+/-0.19 L, during exacerbation and stable conditions, respectively; p=0.01), severe hypoxaemia (ratio between arterial oxygen tension and inspired oxygen fraction (Pa,O2/FI,O2) 32.7+/-7.7 vs 37.6+/-6.9 kPa (245+/-58 vs 282+/-52 mmHg); p=0.01) and hypercapnia (arterial carbon dioxide tension (Pa,CO2) 6.8+/-1.6 vs 5.9+/-0.8 kPa (51+/-12 vs 44+/-6 mmHg); p=0.04). V'A/Q' inequality increased during exacerbation (log SD Q', 1.10+/-0.29 vs 0.96+/-0.27; normal < or = 0.6; p=0.04) as a result of greater perfusion in poorly-ventilated alveoli. Shunt was almost negligible on both measurements. V'E remained essentially unchanged during exacerbation (10.5+/-2.2 vs 9.2+/-1.8 L x min(-1); p=0.1), whereas both Q' (6.1+/-2.4 vs 5.1+/-1.7 L x min(-1); p=0.05) and V'O2 (300+/-49 vs 248+/-59 mL x min(-1); p=0.03) increased significantly. Worsening of hypoxaemia was explained mainly by the increase both in V'A/Q' inequality and V'O2, whereas the increase in Q' partially counterbalanced the effect of greater V'O2 on mixed venous oxygen tension (PV,O2). We conclude that worsening of gas exchange during exacerbations of chronic obstructive pulmonary disease is primarily produced by increased ventilation/perfusion inequality, and that this effect is amplified by the decrease of mixed venous oxygen tension that results from greater oxygen consumption, presumably because of increased work of the respiratory muscles.     

Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans

The activation of MAPKs is controlled by the balance between MAPK kinase and MAPK phosphatase activities. The latter is mediated by a subset of phosphatases with dual specificity (VH-1 family). Here, we describe a new member of this family encoded by the puckered gene of Drosophila. Mutations in this gene lead to cytoskeletal defects that result in a failure in dorsal closure related to those associated with mutations in basket, the Drosophila JNK homolog. We show that puckered mutations result in the hyperactivation of DJNK, and that overexpression of puc mimics basket mutant phenotypes. We also show that puckered expression is itself a consequence of the activity of the JNK pathway and that during dorsal closure, JNK signaling has a dual role: to activate an effector, encoded by decapentaplegic, and an element of negative feedback regulation encoded by puckered.     

Effect of prolonged heavy exercise on pulmonary gas exchange in horses

During short-term maximal exercise, horses have impaired pulmonary gas exchange, manifested by diffusion limitation and arterial hypoxemia, without marked ventilation-perfusion (VA/Q) inequality. Whether gas exchange deteriorates progressively during prolonged submaximal exercise has not been investigated. Six thoroughbred horses performed treadmill exercise at approximately 60% of maximal oxygen uptake until exhaustion (28-39 min). Multiple inert gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained at rest and 5-min intervals during exercise. Oxygen uptake, cardiac output, and alveolar-arterial PO2 gradient were unchanged after the first 5 min of exercise. Alveolar ventilation increased progressively during exercise, from increased tidal volume and respiratory frequency, resulting in an increase in arterial PO2 and decrease in arterial PCO2. At rest there was minimal VA/Q inequality, log SD of the perfusion distribution (log SDQ) = 0.20. This doubled by 5 min of exercise (log SDQ = 0.40) but did not increase further. There was no evidence of alveolar-end-capillary diffusion limitation during exercise. However, there was evidence for gas-phase diffusion limitation at all time points, and enflurane was preferentially overretained. Horses maintain excellent pulmonary gas exchange during exhaustive, submaximal exercise. Although VA/Q inequality is greater than at rest, it is less than observed in most mammals and the effect on gas exchange is minimal.     

Lung aeration and pulmonary gas exchange during lumbar epidural anaesthesia and in the lithotomy position in elderly patients

We investigated a total of 36 subjects with a mean (SD) age of 65 (13) years, during baseline conditions (supine, before any anaesthesia), and then during one of the following protocols: (1) lithotomy positioning (n = 12), (2) epidural anaesthesia (n = 12), (3) general anaesthesia in the supine position (n = 12). Lung aeration, ventilation/perfusion matching, gas exchange and functional residual capacity were measured. Lung aeration was normal during baseline assessment with almost no regions with poor aeration and no substantial dependent densities. Shunt and perfusion of poorly ventilated regions were minor. Lithotomy positioning did not reduce functional residual capacity and did not affect aeration of the lung or ventilation/perfusion matching. Epidural anaesthesia, in general, had no effect on aeration, ventilation/perfusion matching or gas exchange, regardless of whether the patient was in the supine or lithotomy position. General anaesthesia, however, caused significant increases in poorly aerated lung regions and in dependent densities (interpreted as atelectasis). In conclusion, no or little impairment of lung aeration and ventilation/perfusion matching was caused by the lithotomy position and/or epidural anaesthesia, contrary to the effects seen during general anaesthesia. However, our findings also suggest that being overweight is a factor that may cause impairment of lung aeration.     

Prevention of hypothermia by cutaneous warming with new electric blankets during abdominal surgery

We have evaluated the efficacy of new electric warming blankets, which meet the requirements of the international standard for perioperative electrical and thermal safety, in preventing intraoperative hypothermia. We studied 18 patients undergoing abdominal surgery, allocated to one of two groups: in the control group, there was no prevention of intraoperative hypothermia (n = 8) and in the electric blanket group, two electric blankets covered the legs and upper body (n = 10). Anaesthesia duration was similar in the two groups (mean 201 (SEM 11) min), as was ambient temperature (20.5 (0.1) degrees C). Core temperature decreased during operation by 1.5 (0.1) degrees C in the control group, but only by 0.3 (0.2) degree C in the electric blanket group (P < 0.01). Five patients shivered in the control group compared with one in the electric blanket group (P < 0.05). We conclude that cutaneous warming with electric blankets was an effective means of preventing intraoperative hypothermia during prolonged abdominal surgery.     

Influence of feed deprivation on ventilation and gas exchange in broilers: relationship to pulmonary hypertension syndrome

Fast-growing broiler chickens not uncommonly exhibit elevated pulmonary vascular resistance that leads to pulmonary hypertension and right ventricular failure. We tested the hypothesis that a distended gastrointestinal tract in these full-fed birds results in an abnormally low tidal volume and minute ventilation that could lead to pulmonary hypoxia, pulmonary arterial vasoconstriction, right ventricular failure, and ascites. Tidal volume, respiratory frequency, heart rate, percentage saturation of hemoglobin with oxygen (HbO2), O2 consumption, and carbon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volume of full-fed birds was not abnormally low despite HbO2 values varying from above 80% to nearly 60%. Importantly, HbO2 was found to be markedly increased in the hypoxemic birds at and beyond a 3-h period without feed, despite a reduction in minute ventilation. This response was not caused by a decrease in O2 consumption. Thus, limitation of gas intake at the mouth was not the cause of the hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.     

The relation of passage of gas an abdominal bloating to colonic gas production

OBJECTIVE: To determine the relation of gas passage and abdominal bloating to the production of gas in the colon. DESIGN: Randomized, double-blind, crossover study of gaseous symptoms during a 1-week period. SETTING: A Veterans Affairs medical center. PARTICIPANTS: 25 healthy medical center employees. INTERVENTION: Participants' diets were supplemented with either a placebo (10 g of lactulose, a nonabsorbable sugar), psyllium (a fermentable fiber), or methylcellulose (a nonfermentable fiber). MEASUREMENTS: All participants were polled for gaseous symptoms (including number of gas passages, impression of increased rectal gas, and abdominal bloating), and five were examined for breath hydrogen excretion. RESULTS: Participants passed gas 10 +/- 5.0 times per day (mean +/- SD) during the placebo period. A significant increase in gas passages (to 19 +/- 12 times per day) and a subjective impression of increased rectal gas were reported with lactulose but not with either of the two fiber preparations. Breath hydrogen excretion, an indicator of hydrogen production in the colon, did not increase after ingestion of either of the fibers. However, a statistically significant (P < 0.05) increase in feelings of abdominal bloating (which the participants perceived as excessive gas in the bowel) was reported with both fiber preparations and with lactulose. CONCLUSIONS: The physician should distinguish between excessive gas (which indicates excessive gas production) and feelings of bloating (which are usually unrelated to excessive gas production). Treatment of the former consists of limiting the supply of fermentable material to the colonic bacteria. Symptoms of bloating usually indicate the irritable bowel syndrome, and therapy should be directed accordingly.     

Effects of cardioselective beta blockers on ventilation and gas exchange in patients with heart disease during ramp treadmill testing

The effects of cardioselective beta blockade on ventilation and gas exchange were investigated in 12 male subjects with coronary artery disease during ramp treadmill testing. Patients were able to maintain much of their functional capacity as measured by oxygen consumption in the beta-blocked condition, and also maintained minute ventilation by increasing respiratory rate despite a decrease in tidal volume.     

Effects of human atrial natriuretic peptide on hemodynamics and pulmonary gas exchanges in cardiac surgery patients

We investigated the effects of human atrial natriuretic peptide (hANP) on hemodynamics and pulmonary gas exchanges in 22 cardiac surgery patients without pulmonary hypertension. In 10 patients, hANP was infused at a rate of 0.2 microgram.kg-1.min-1 throughout the surgery (hANP group), while in other 12 patients hANP was not infused at all (control group). Before cardiopulmonary bypass (CPB), mean arterial pressure and systemic vascular resistance decreased and cardiac output increased significantly in hANP group as compared with those in control group. After weaning from CPB and at the completion of surgery there was no significant difference in these hemodynamic variables between the two groups. Mean pulmonary arterial pressure, pulmonary vascular resistance, arterial pH, arterial oxygen tension, arterial carbon dioxide tension and shunt ratio did not show any significant difference between the two groups throughout surgery. These findings indicate that hANP infusion causes greater systemic vasodilation with less pulmonary vasodilation, and suggest that this systemic vasodilating effect contributes to the improvement of left ventricular function in patients undergoing open heart surgery.     

Respiratory gas exchange. Anesthesia with enflurane or isoflurane in nitrous oxide during spontaneous and controlled ventilation

The estimation of oxygen consumption and carbon dioxide elimination is essential for predicting the metabolic activity and needs of any patient having anaesthesia. During anaesthesia oxygen consumption can be measured and compared to a predicted value. However, oxygen uptake is affected by anaesthetic agents, which complicates the interpretation of measured oxygen uptake rate. The purpose of this study was to investigate whether there are any differences in respiratory gas exchange during anaesthesia with enflurane and isoflurane and also to assess the effects of spontaneous versus controlled ventilation. METHODS. Forty orthopedic patients were randomized to enflurane or isoflurane anaesthesia in nitrous oxide with either spontaneous or controlled ventilation. A fresh low-gas-flow technique was used. Inspiratory oxygen and end-tidal carbon dioxide concentrations and expiratory minute ventilation were measured in a circle absorber system between the y-piece and the endotracheal tube with a sampling analyser. Between the mixing box and the absorption canister, carbon dioxide concentration was continuously measured. The carbon dioxide elimination was calculated from mixed expired concentration and expiratory minute ventilation. Excess gas was collected every 10 min in a non-permeable mylar plastic bag connected to the excess valve. The excess gas flow was calculated and the oxygen uptake rate was assumed to be the difference between the oxygen fresh gas flow and the oxygen excess gas flow. RESULTS. The grand mean oxygen uptake rate was 2.5 ml.kg-1 x min-1 or 100 ml.min-1 x m-2. There were no statistically significant differences in oxygen uptake between enflurane and isoflurane anaesthesia or between spontaneous and controlled ventilation. The mean oxygen uptake rate at 10 min was between 2.0 and 2.2 ml.kg-1 x min-1 in all groups. At 30 min the mean oxygen uptake rates were 2.6 to 2.8 ml.kg-1 x min-1. Carbon dioxide elimination was closely associated with expired minute ventilation, with a carbon dioxide excretion of about 30 ml per litre gas exhaled, irrespective of ventilatory mode employed.