Oxygen-induced alteration of ventilation-perfusion relationships in rats

Truog, William E.; Hlastala, M. P.; Standaert, T. A.; McKenna, Hannah; Hodson, W. Alan

doi:10.1152/jappl.1979.47.5.1112

Cited by 31 publications

(39 citation statements)

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“…Specifically, the residual sum of squares (RSS) must begin to rise to abnormal levels as SF6 (and/or enflurane, the other MIGET gas of high MW) are preferentially retained in the blood. Such has been indeed noted in several studies [16][17][18]. Given the very low (i.e., normal) RSS values in the present paper, the mechanism of inert gas diffusion limitation is therefore unlikely.…”

Section: Causes Of Hypoxaemia In This Patientsupporting

confidence: 82%

Impairment of gas exchange in liver cirrhosis

Wagner¹

1995

Eur Respir J

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even at rest when TL,CO falls below about 50% of predicted, and Agustí's patients did not have pulmonary vascular malformations. Perhaps the subject of Crawford's study has lung disease in addition to vascular malformations, and both contribute to the hypoxaemia. Interpretation of radiolabelled particle distributionThe authors used albumin aggregates whose diameters were stated to range from 15 µm to 50 µm. Assuming radioactivity relates to particle mass, not diameter, 50 µm particles would be 37 times hotter than 15 µm particles ((50/15) 3 = 37). If the abnormal vascular channels at their narrowest exceeded 50 µm diameter, this inhomogeneity of size may have posed no problem. If any were less than 50 µm but greater than 15 µm, the hottest particles would have been preferentially caught in the lungs. Thus, without knowing the anatomy of the abnormal vessels or the distribution of particle sizes between 15 and 50 µm, there is a potential interpretative limitation on using the radioactive particle data to quantitatively assess the vascular shunts. Of interest, this would if anything underestimate the shunt, already computed to be about 40%. Interpretation of inert gas (MIGET) dataSeveral issues arise. The authors argue that the room air data suggest diffusion limitation for O 2 because the inert gases, generally considered to be invulnerable to diffusion limitation, predict a higher arterial oxygen tension (Pa,O 2 ) than was measured [13]. This result agrees with EDELL et al. [8] and CASTAING and MANIER [14] (and many other MIGET-based studies in other settings). The low TL,CO is consistent with this. However, whether the dilated vascular channels are the site of this limitation is uncertain. It is hard to imagine how these channels reduce total lung TL,CO to 34% of predicted if indeed the alveolar parenchyma is otherwise normal. Thus, hypothetically abnormal parenchyma could explain the observations rather than limited O 2 exchange across the abnormal vessels. There are thus two competing hypotheses and it would seem that they cannot be distinguished from the present data.The 100% O 2 breathing data are particularly intriguing and the higher measured-than-MIGET-predicted Pa,O 2 is used by the authors as evidence of diffusion limitation of the inert gases, especially the least soluble gas, sulphur hexafluoride (SF6). However, while the diffusion Eur Respir J, 1995, 8, 1993 DOI: 10.1183 ISSN 0903 -1936 The paper in this issue by CRAWFORD et al..08121993 Printed in UK -all rights reserved Copyright ©ERS Journals Ltd 1995 European Respiratory Journal[1] addresses a problem that has vexed clinicians and physiologists for many years: In cirrhosis, the presence and mechanisms of hypoxaemia, usually more severe in the upright posture, and without evidence of classical lung disease, such as obstructive or restrictive syndromes. Ever since abnormally dilated pulmonary blood vessels were first identified in such patients [2], studies have focused on the obvious potential connection between such functional shunts and hy...

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Section: Causes Of Hypoxaemia In This Patientsupporting

confidence: 82%

Impairment of gas exchange in liver cirrhosis

Wagner¹

1995

Eur Respir J

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“…The study was performed on 19 male Wistar rats, closely following an experimental protocol described earlier (Truog et al 1979). Briefly, rats were anaesthetized with urethane (1.5g/kg i.p., Fluka Chemie AG, Germany) and restrained in a supine position.…”

Section: Methodsmentioning

confidence: 99%

“…For such calculations, a mean QT value of 220 ml min -1 kg-1 for.rats breathing air and in similar experimental conditions was assumed (Truog et al 1979). 275 thoracic cavity was immediately opened and all the animals were verified with the intracardiac catheter correctly placed in the RV.…”

Section: Methodsmentioning

confidence: 99%

“…It has been applied successfully to human beings (Wagneret al 1985, Ballester et al 1989 as well as to several animal species, including dogs (Wagner et al 1975, Domino & Hlastala 1994 and geese (Powell & Wagner 1982). However, studies on small animals like rats are scarce in the literature (Truog et al 1979). The MIGET is based on the comparison of arterial (Pal, mixed venous blood (py) and mixed expired air partial pressures (PE) of six inert gases administered continuously through a peripheral vein (Wagner et al 1974b).…”

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confidence: 99%

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Blood sampled in rats from right ventricle may not always be truly representative of a mixed venous sample

et al. 1996

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SummaryBlood samples from the right ventricle (RV)in rats are usually assumed to be representative of mixed venous blood. However, results presented here suggest that this assumption may not be true in all experimental circumstances. Nineteen male Wistar rats were anaesthetized with urethane and mechanically ventilated. The six gases used in the multiple inert gas elimination technique (MIGETI were administered continuously and samples of mixed expired air and blood from the left carotid artery and RV were simultaneously withdrawn. While inert gas concentrations in arterial blood and mixed expired air were almost homogeneous, those obtained from RV blood showed a high variability, specially evident for the less soluble gases in blood. As inert gases are cleared in the lungs according to their solubility in blood and they are only replaced through the lower systemic circulation, higher or lower concentrations found in RV samples than those expected suggests a preferential collection of blood from the lower or upper systemic circulation, respectively. Gleeson et al. 1983, Hilty et al. 19891/respiratory (Truog et al. 1979, Cain & Bradley 1983, Pages et al. 1993, Alfaro et al. 1995 and metabolic data (Walsh et al. 1980, Souba et al. 1990, mainly on the basis of analysis of arterio-venous blood differencesCorrespondence to: Dr Vicente Alfaro, Departamento de Fisiologla, Facultad de Biologia, Avda. Diagonal 645, 08071 Barcelona, Spain, Fax: 34-3-4110358, Tel: 34-3-4021526 Accepted 27 November 1995 and application of the Fick principle to calculate metabolic rates or cardiac output (QTl. These studies are based on the assumption that analysis of blood samples withdrawn from the RV and/or right atrium (RA) are indicative of the composition of mixed venous blood, a fact that is supported by some experimental work. Thus, the study performed by Musch and Larach (1988) comparing the O 2 content from the pulmonary artery, the RV and the RA of anaesthetized rats did not show significant differences between blood samples.Data presented here were derived from the application of the multiple inert gas elimination technique (MIGETI on rats. The MIGET is a well-known method, published in 1974 (Wagner et al. 1974a, b), and used to provide

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“…The multiple inert gas elimination technique (12) was used as previously described (1,3) to assess intrapulmonary shunt and distribution of VA/Q ratios. A unitless index of overall ventilation perfusion heterogeneity, separate from shunt (perfusion to areas of zero ventilation) and dead space (ventilation to areas of zero perfusion) was assessed using the derived variable SDQ, (13,14). Special care was taken to maintain constant hematocrit and animal temperature during the experimental protocol in order to prevent fluctuations in the blood-gas partition coefficient for each inert gas (1 5).…”

Section: Methodsmentioning

confidence: 99%

Neonatal Group B Streptococcal Sepsis: Effects of Late Treatment with Dazmegrel

et al. 1988

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ABSTRACT. Neonatal group B streptococcal (GBS) sepsis produces pulmonary arterial hypertension and hypoxemia that are preventable by pretreatment with the selective thromboxane A2 synthase inhibitor, dazmegrel. In the present experiment we administered dazmegrel (8 mg/kg) 2 h after the initiation of a 2% h infusion of 5 x 10' GBS/ kg/h in ten 2-to 3-wk-old piglets. The multiple inert gas elimination technique was used to measure intrapulmonary shunt and alveolar ventilation to pulmonary perfusion mismatching. Thromboxane B2, the stable metabolite of thromboxane A2, and 6-keto-prostaglandin F,,, the stable metabolite of prostacyclin, were assayed in arterial blood. Pulmonary arterial pressure increased immediately after initiation of the GBS infusion, rising from 12 f 2 to 34 f 4 torr ( p < 0.02); pulmonary vascular resistance increased by 400% ( p < 0.01). Arterial hypoxemia developed ( p c 0.02) in association with an increase in the low ventilationperfusion ratio index but without a significant increase in intrapulmonary shunt. Thromboxane Bz levels increased 10-fold. Infusion of the carrier substance for dazmegrel after 2 h of GBS infusion produced no change in any variables. In contrast, infusion of the drug resulted in the return to pre-GBS infusion baseline values for both pulmonary arterial pressure and pulmonary vascular resistance. However, no improvement in arterial p 0 2 or in the low ventilation-perfusion ratio index occurred. Both pulmonary vascular resistance and pulmonary arterial pressure remained normal for 0.5 h after dazmegrel administration despite continued GBS infusion. Thromboxane Bz levels were decreased 30 min after dazmegrel ( p < 0.02), but remained greater than pre-GBS levels. Dazmegrel reversed pulmonary hypertension and elevated pulmonary vascular resistance, but did so without concomitant improvement in pulmonary gas exchange, when administered after 2 h of GBS infusion. (Pediatr Res 23: 352-356,1988 Intravenous infusion of GBS into a neonatal piglet results in acute derangements of both pulmonary gas exchange and pulmonary hemodynamics. An acute elevation in P,, and PVR develops with onset of GBS infusion (1-3). In addition, arterial hypoxemia develops because of mismatching of ventilation to perfusion characterized by increased Q, to low VA/Q areas (3) and from depression of total Q, . Vasoactive metabolites of AA help mediate these events (4, 5). The pulmonary hemodynamic response to GBS in neonatal animals has been blocked or blunted by pretreatment or immediate post-GBS infusion treatment by the nonspecific cyclooxygenase inhibitor indomethacin (2), by the specific T,A2 synthase inhibitor dazmegrel (I), and by a competitive antagonist of sulfidopeptide leukotriene products of the 5-lipoxygenase pathway of AA metabolism, FPL 557 12 (5).Presently unknown is the extent to which AA metabolites, or other vasoactive substances (6,7), sustain or aggravate the hemodynamic and gas exchange derangements during prolonged GBS infusion, and whether a thromboxane synthase inhibitor would al...

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Oxygen-induced alteration of ventilation-perfusion relationships in rats

Cited by 31 publications

References 0 publications

Impairment of gas exchange in liver cirrhosis

Impairment of gas exchange in liver cirrhosis

Blood sampled in rats from right ventricle may not always be truly representative of a mixed venous sample

Neonatal Group B Streptococcal Sepsis: Effects of Late Treatment with Dazmegrel

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