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Biomedical subjects

G Basset

Publications and source records attributed to G Basset.

At least 19 recordsLinked to original sources
PubMed1991

Low molecular weight hydroxyethyl starch 6% compared to albumin 4% during intentional hemodilution.

Intentional normovolemic hemodilution was chosen as the model to compare a 6% low molecular weight hydroxyethyl starch (LMW HES) to 4% albumin. The study ran over the plasma exchange period for 24 h. Nine patients, scheduled for abdominal aortic surgery, were included in each group. After basal measurements, blood was withdrawn and simultaneously replaced by either 4% albumin (Group 1) or 6% LMW HES (Group 2) to achieve a final hematocrit of approximately 30%. Hemodynamic blood oxygen gas and hormonal plasma levels were determined before hemodilution then at 30 min, 1, 2, 3, and 24 h after the end of hemodilution. Basal value for total blood volume was 4377 +/- 162 ml in group 1 and 4138 +/- 315 ml in group 2. As in both groups the decrease in blood cell volume was exactly compensated by the increase in plasma volume, no significant change in total blood volume (respectively 4432 +/- 159 and 4305 +/- 267 ml) was observed. Throughout the study, in both groups, no significant change in mean arterial and right atrial pressures was observed. In group 2 (LMW HES), a significant increase of pulmonary capillary wedge pressure was noted 120 min after hemodilution. After hemodilution, despite a significant decrease in arterial oxygen O2 content, systemic oxygen transport did not significantly vary until 24 h in relation to the increased cardiac index. An increase in O2 extraction was observed after the exchange but no further increase was observed until the 24 h. No significant changes either in global O2 consumption or in lactate concentration were detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Glucose, K+, and albumin concentrations in the alveolar milieu of normal humans and pulmonary sarcoidosis patients.

Some properties of the alveolar epithelial barrier during transalveolar transport of water and solutes were studied in normal humans and patients with sarcoidosis by means of the transalveolar capillary concentration gradients of various solutes. A total of 9 normal control subjects (Group A) and 60 sarcoidosis patients, 52 with an evolving disease (Group B) and 8 recovered (Group C), underwent bronchoalveolar lavage (BAL). The second aliquot of fluid was used to measure urea, glucose, potassium, and albumin, which were also investigated in plasma. Urea was used to determine the volume of alveolar epithelial lining fluid (AELF volume). Results are expressed as the ratio of solute concentration in AELF over that in plasma (A/P ratio). In Group A there were clear concentration gradients of glucose, potassium, and albumin between the AELF and plasma, as the A/P ratios of glucose, potassium, and albumin were 0.02 +/- 0.006 (mean +/- SEM), 3.2 +/- 0.34, and 0.04 +/- 0.008, respectively. In Group B the A/P ratios of glucose (0.21 +/- 0.02, p less than 0.001) and albumin (0.17 +/- 0.02, p less than 0.001) were significantly increased but that of potassium remained unchanged (2.9 +/- 0.2). The A/P ratios of these various solutes were independent of chest x-ray typing. The albumin but not the glucose A/P ratio was correlated with the percentage of lymphocytes recovered from BAL (p less than 0.02); however, there was no correlation between the albumin A/P ratio and the CD4+/CD8+ T lymphocyte ratio. In group C there was a striking contrast between the albumin A/P ratio, which was normal, and the glucose A/P ratio, which was clearly elevated despite a normal lymphocyte count.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Endothelial and epithelial permeabilities to antipyrine in rat and dog lungs.

Temperature effects on the permeabilities of the structured endothelium and epithelium to antipyrine (AP) have been determined with the indicator dilution technique in isolated rat and dog lungs perfused between 38 and 8 degrees C. Permeability coefficients of the endothelium to AP [Pendo(AP)] from the Crone equation are smaller than values for isolated endothelial cells but close to the permeability coefficient of the interstitial epithelial plasmalemma [Pepi(AP)] obtained from physical and mathematical models. In these, tracer water is flow limited at the endothelium and the epithelium at all temperatures; AP is flow limited at the endothelium at T greater than 20 degrees C but barrier limited at the endothelium for T less than 20 degrees C and at the epithelium at all temperatures. At T less than 20 degrees C, log Pendo(AP) decreases regularly with 1/T, with a slope close to that found in cultured bovine pulmonary artery endothelial cells. At 15 degrees C, Pendo(AP) for the endothelial plasmalemma in situ is 30 X 10(-5) cm/s and is 56 X 10(-5) cm/s for the isolated cells in support of transcellular rather than paracellular passage. At T greater than 20 degrees C, log Pepi(AP) in situ decreases slightly with 1/T, with a discontinuity at T = 20 degrees C, and for T less than 20 degrees C, decreases with 1/T with a slope close to that of Pendo(AP). At 15 degrees C, Pepi(AP) is 2.8 X 10(-5) cm/s. The discontinuity may represent a change in the physical state of lipids in the interstitial plasmalemma of the epithelial cells.

Animals↗
PubMed1989

Cellular effects of beta-adrenergic and of cAMP stimulation on potassium transport in rat alveolar epithelium.

Alveolar fluid absorption is greatly enhanced by cAMP and by beta-adrenergic agonists via an increase in Na+ transport. Little is known about K+ homeostasis under these circumstances. We studied K+ transport across alveolar epithelium in isolated perfused rat lungs stimulated either by dibutyryl-cAMP or isoproterenol. K+ fluxes and the apparent permeability of 86Rb across the epithelium (alveoli to plasma) were interpreted according to a model involving two types of cells, B and L, distinguished by the location of Na+-K+-ATPases (basal and luminal). Water is considered to be absorbed by B cells in a solute-coupled process energized by a basolateral Na+-K+-ATPase that is stimulated by isoproterenol and cAMP. K+ transport out of the alveoli is due to the activity of a Na+-K+-ATPase located in the apical membrane of L cells. In the present study net transport rate of K+ was -0.5 +/- 0.15 nmol/s, n = 20 (out of alveoli) in control conditions. When the epithelium was stimulated by dibutyryl-cAMP (10(-4) mol/l) net absorption of K+ reversed to net 'secretion' into alveoli (3.2 +/- 0.31 nmol/s), fluid absorption was not stimulated. K+ 'secretion' was abolished by apical Ba2+, indicating it was due to opening of apical K+ channels. Basolateral ouabain reversed net K+ 'secretion' to net absorption indicating that K+ entry into alveoli was dependent on activity of B cell basolateral Na+-K+-ATPase (masking simultaneous K+ removal by apical L cell Na+-K+-pump). When larger concentrations of dibutyryl-cAMP (10(-3) mol/l) or when isoproterenol were used to stimulate the epithelium there was a tripling of fluid absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1988

Apical sodium-sugar transport in pulmonary epithelium in situ.

The presence of an apical sodium-coupled transport system for D-glucose in lung alveolar epithelial cells has been demonstrated in lungs instilled with Ringer's fluid and perfused with either blood or Ringer's fluid (Basset et al. (1987) J. Physiol. 384, 325-345). The direction of transport is from alveoli towards interstitium. The characteristics of the system were evaluated in similar preparations by use of sugar analogues such as alpha-methyl-glucopyranoside, 2-deoxyglucose, 3-O-methylglucose and L-glucose. The main finding was the presence of a transport system for alpha-methylglucopyranoside and 2-deoxyglucose in the apical cell membrane. This system was unaffected by phloretin. Both alpha-methylglucopyranoside and 2-deoxyglucose transports were inhibited by phloridzin and by the presence of glucose (10(-2) mol.l-1). Competition was demonstrated between D-glucose and alpha-methylglucopyranoside or 2-deoxyglucose, but not for 3-O-methylglucose or L-glucose. 3-O-Methylglucose was cleared as slowly as L-glucose. The results comply partly with those known from intestinal epithelium and kidney proximal tubular epithelium, but the handling of 3-O-methylglucose was different. The relative transport rates of Na+ and glucose are compatible with a Na+: glucose coupling ratio larger than one.

Animals↗
PubMed1988

Potassium transport across rat alveolar epithelium: evidence for an apical Na+-K+ pump.

1. Experiments were performed on rat lungs into which various solutions were instilled whilst the lungs were perfused with either whole blood or Ringer solution. Instillation of ion-free glucose solution led to a net flux of fluid and ions into the alveolar spaces. K+ ions entered faster than Na+ ions and reached a concentration about twice that in the perfusate. Ouabain in the perfusate (basolateral side) prevented the rise in alveolar K+ concentration above that in the perfusate, indicating a transcellular pathway. Ba2+ in the instillate (apical side) hindered the entry of K+ into alveoli, suggesting the presence of apical K+ channels. 2. When Ringer solution was instilled, K+ was continuously removed from the alveoli and the K+ concentration in the instillate remained constant or decreased slightly depending on the rate of fluid absorption. The net K+ efflux from alveoli to blood was 0.23 pmol/(cm2 s). When Ba2+ was added to the instillate the net K+ efflux increased to 0.36 pmol/(cm2 s). Apical ouabain reversed the K+ flux resulting in a net K+ flux of 0.19 pmol/(cm2 s) into the alveoli. This suggests the presence of an Na+-K+-ATPase located in the apical membrane of some alveolar cells. 3. The K+ transport from instillate (Ringer solution) to perfusate was traced by means of 86Rb which was added to the instillate. Ouabain in the instillate did not affect fluid absorption but reduced the apparent 86Rb permeability by 50% although the paracellular permeability (estimated with [3H]mannitol) was unaffected. This also indicates the presence of an apical Na+-K+-ATPase. When ouabain was added to the perfusate, the apparent 86Rb permeability doubled. These findings indicate that recirculation of 86Rb (and K+) occurs due to the activity of both apical and basolateral Na+-K+-ATPases. 4. When ouabain was placed on both sides of the epithelium, preventing transcellular transport, the passive 86Rb permeability was 10.3 x 10(-8) cm/s (assuming an alveolar surface area of 5000 cm2). This value agrees with the passive permeabilities for mannitol, Na+ and Cl- suggesting that the paracellular pathway acts as a water-filled neutral channel. 5. We conclude that K+ is 'secreted' into the alveoli and is also removed from the alveoli, both processes being energized by Na+-K+-ATPases placed on the basolateral and apical sides, respectively. It is likely that two functionally different cell types exist in the alveolar membrane. One type ('B cell') has a Na+-K+-ATPase located at the basolateral membrane and K+ channels situated luminally.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗
PubMed1988

High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure.

The respective roles of high pressure and high tidal volume to promote high airway pressure pulmonary edema are unclear. Positive end-expiratory pressure (PEEP) was shown to reduce lung water content in this type of edema, but its possible effects on cellular lesions were not documented. We compared the consequences of normal tidal volume ventilation in mechanically ventilated rats at a high airway pressure (HiP-LoV) with those of high tidal volume ventilation at a high (HiP-HiV) or low (LoP-HiV) airway pressure and the effects of PEEP (10 cm H2O) on both edema and lung ultrastructure. Pulmonary edema was assessed by extravascular lung water content and microvascular permeability by the drug lung weight and the distribution space of 125I-labeled albumin. HiP-LoV rat lungs were not different from those of controls (7 cm H2O peak pressure ventilation). By contrast, the lungs from the groups submitted to high volume ventilation had significant permeability type edema. This edema was more pronounced in LoP-HiV rats. It was markedly reduced by PEEP, which, in addition, preserved the normal ultrastructural aspect of the alveolar epithelium. This was in striking contrast to the diffuse alveolar damage usually encountered in this type of edema. To our knowledge, this constitutes the first example of a protective effect of PEEP during permeability edema.

Animals↗
PubMed1987

cAMP and beta-adrenergic stimulation of rat alveolar epithelium. Effects on fluid absorption and paracellular permeability.

The absorption of fluid (bicarbonate-buffered Ringer with 10 mmol/l glucose) instilled into rat lungs is a Na+-coupled process that takes place through two apical transport systems: an amiloride-sensitive Na+ transport and a Na+-glucose co-transport. Fluid absorption in isolated, perfused rat lungs and the permeability to 3H-mannitol of alveolar epithelium were studied in control conditions and during stimulation of the alveolar epithelium by cAMP or isoproterenol. cAMP led to a threefold increase in the rate of fluid absorption and to an increase in the paracellular permeability. A similar response was found following beta-adrenergic stimulation obtained with isoproterenol in the perfusate. The increase in fluid transport was due to enhancement of the amiloride-sensitive component of Na+ transport. The Na+-glucose co-transport which accounts for about 60% of fluid absorption in control conditions was depressed, possibly as a consequence of a depolarization of the apical alveolar cell membrane. Fluid absorption was reduced by 40% by apical amiloride (10(-4) mol/l) in control lungs and to an even larger extent in isoproterenol-stimulated lungs; it was completely abolished by amiloride in cAMP stimulated lungs. Since the Na+-glucose co-transport was still operative, this suggests that a secretory process was triggered. This was confirmed in experiments in which both kinds of transport were inhibited with a combination of amiloride and glucose-free Ringer. In these conditions fluid balance was zero in unstimulated lungs whilst fluid entry into alveoli was observed in isoproterenol and cAMP stimulated lungs.

Absorption↗
PubMed1987

Significance of active ion transport in transalveolar water absorption: a study on isolated rat lung.

1. Experiments were performed on isolated rat lungs perfused with Ringer solutions containing red cells. The goal was to clarify the role of active transport of Na+ for the absorption of fluid across the alveolar membrane, and to characterize active and passive pathways. 2. Partially degassed lungs were filled with 5 ml of an isotonic Ringer solution containing 125I-labelled albumin in order to calculate the fluid movement, and 22Na+ or 36Cl- for measurement of ion fluxes. Passive non-electrolyte permeability was determined in all experiments using [3H]mannitol. 3. The average rate of fluid absorption in phosphate-buffered instillates was 134 nl/s (S.E., 18.5; n = 14). With ouabain (10(-4) M) in the perfusate the fluid absorption rate fell to 57 nl/s (S.E., 8.2; n = 18). Amiloride (10(-3)-10(-4) M) in the instillate reduced the absorption to 75 nl/s (S.E., 8.6; n = 16). These results show that fluid absorption depends on transcellular transport of Na+ and that alveolar epithelial cells have a Na+ entry system in the luminal membrane and a Na+-K+ pump in the abluminal membrane. 4. The transcellular ion transport operates in parallel with a paracellular, passive leak that allows mannitol to pass with a permeability surface area product of 1.2 X 10(-4) ml/s, corresponding to a permeability coefficient of 2.4 X 10(-8) cm/s, assuming an alveolar surface area of 5000 cm2. 5. The passive fluxes of Na+ were 9.4 pmol/(cm2s) (S.E., 1.3; n = 25) in the direction from alveoli to perfusate and 8.0 pmol/(cm2s) (S.E., 0.86; n = 6) from perfusate to plasma. The passive fluxes of Cl- in the two directions were not significantly different either. Thus the transalveolar electrical potential difference is too small to affect ion movements measurably. 6. The passive permeability to Na+ was 6.7 X 10(-8) cm/s and to Cl- was 10.2 X 10(-8) cm/s (alveolar surface area assumed to be 5000 cm2). The ratio of the permeabilities is close to the ratio of the diffusion coefficients in free solution, suggesting a neutral or weakly charged paracellular channel. 7. We conclude that the alveolar epithelium performs solute-coupled fluid transport from alveoli to plasma, and that it shows many features that are common to other fluid-transporting epithelia; with an approximate surface area of 100 m2 in humans it constitutes one of the largest epithelial surfaces in the body.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗
PubMed1987

Fluid absorption by rat lung in situ: pathways for sodium entry in the luminal membrane of alveolar epithelium.

1. The purpose of the investigation was to characterize the luminal membrane and the paracellular pathway of rat lung alveolar epithelium. Experiments were performed on lungs in situ instilled with isotonic, buffered Ringer solution and perfused with blood from a donor rat using cross-circulation technique. 2. The rate of active Na+ transport was 4.4 pmol/(cm2s). The fluid absorption was 156 nl/s, and was unaffected by the presence of protein in the instillate (166 nl/s). In the absence of Na+, fluid absorption was zero. Amiloride (10(-3) M) reduced fluid absorption by 60%. Amiloride, combined with absence of D-glucose, arrested fluid absorption completely. Phloridzin at the luminal side reduced fluid absorption whilst phloretin had no effect. Amiloride together with phloridzin (10(-3) M) also arrested absorption. Thus, there are two entry systems for Na+ in the luminal membrane: Na+ channels and a Na+-D-glucose symport. These results show that alveolar fluid absorption is due to cellular activity. 3. Substitution of Cl- with gluconate not only stopped fluid absorption, but led to slight reversal of net fluid movement. 4. Passive unidirectional flux of Na+, determined with 22Na+, was 9.9 pmol/(cm2s) and that of Cl-, determined with 36Cl-, was 12.4 pmol/(cm2s). These fluxes were based on an assumed alveolar surface area of 5000 cm2. Transference numbers calculated from these figures are close to those in free solution, suggesting a neutral or weakly charged intercellular junctional pathway. The D-mannitol permeability in the paracellular pathway was 1.7 X 10(-8) cm/s. 5. It is a consequence of the proposed mechanism for fluid absorption that it becomes inoperative if the normally high reflexion coefficients for Na+ and Cl- are lowered in pathological states. In such conditions pulmonary oedema may develop depending on the net balance of passive mechanical and colloid-osmotic forces. 6. An explanation of the reversal of fluid transport at the time of birth is presented.

Absorption↗
PubMed1987

Pulmonary disposition of roxithromycin (RU 28965), a new macrolide antibiotic.

The penetration of roxithromycin (RU 28965), an ether oxime derivative of erythromycin, into the cells and fluid lining the epithelial surface of the lower respiratory tract was studied by performing fiber-optic bronchoscopy with bronchoalveolar lavage on eight patients who had received roxithromycin at 300 mg perorally every 12 h for 5 days. The apparent volume of epithelial lining fluid recovered by bronchoalveolar lavage was determined by using urea as an endogenous marker. There was a significant relationship (r = 0.75; P less than 0.02) between roxithromycin levels in plasma and epithelial lining fluid, with a correlation whose slope suggested that the level of drug penetration into the lining fluid was 0.2. Concentrations of the antibiotic in cells recovered by bronchoalveolar lavage (21 +/- 10 micrograms/ml) were 2 and 10 times higher than in plasma (11.4 +/- 5.7 micrograms/ml) and epithelial lining fluid (2.0 +/- 1.7 micrograms/ml), respectively. Thus, when administered perorally in humans, roxithromycin is markedly accumulated by resident alveolar macrophages in concentrations largely exceeding the MBCs of the drug for most facultative intracellular pathogens including Legionella pneumophila, despite low concentrations in the epithelial lining fluid.

Bronchitis↗
PubMed1986

Estimation of volume of epithelial lining fluid recovered by lavage using urea as marker of dilution.

Bronchoalveolar lavage is a powerful technique for sampling the epithelial lining fluid (ELF) of the lower respiratory tract but also results in a significant dilution of that fluid. To quantify the apparent volume of ELF obtained by bronchoalveolar lavage, urea was used as an endogenous marker of ELF dilution. Since urea diffuses readily through the body, plasma and in situ ELF urea concentrations are identical; thus ELF volume can be calculated using simple dilution principles. Using this approach, we determined that with a standard lavage procedure, the volume of ELF recovered from a normal human is 1.0 +/- 0.1 ml/100 ml of recovered lavage fluid. Time course experiments in which the saline used for lavage was permitted to remain in the lower respiratory tract for various "dwell times" suggested that diffusion of urea from sources other than recovered ELF can contribute to the total urea recovered resulting in an overestimate of the volume of ELF recovered. Thus, while reasonably accurate, the volume of ELF determined by urea must be considered an overestimate, or "apparent" volume. The ELF albumin concentration based on the apparent ELF volume was 3.7 +/- 0.3 mg/ml, a value that is in good agreement with direct measurements made by other techniques in experimental animals. The density of all inflammatory and immune effector cells on the epithelial surface of the lower respiratory tract, based on the apparent ELF volume, was 21,000 +/- 3,000 cells/microliter, a value that is twofold greater than that in blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1985

Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats.

The mechanisms by which intermittent positive-pressure ventilation with high inflation pressure (HIPPV) induces pulmonary edema remain uncertain. In this study we investigated the physiologic and anatomic changes related to HIPPV at 45 cmH2O peak inspiratory pressure in rats. Edema was quantified by the extravascular lung water obtained from postmortem weighing and by 22Na distribution space. Pulmonary microvascular permeability was assessed by dry lung weight and fractional albumin uptake. After only 5 min of HIPPV, there was a significant increase in Na space, dry lung weight, and fractional albumin uptake when compared with that in control rats mechanically ventilated at 7 cmH2O peak inspiratory pressure. These changes suggest that edema may be due at least in part to alterations in microvascular permeability. Moderate peribronchovascular edema was present. At the ultrastructural level, some endothelial cells were found detached from their basement membrane. This lesion has been previously described in other types of pulmonary microvascular injury. The above findings remained almost unchanged after 10 min of HIPPV. After 20 min of HIPPV, we observed the outpouring of a high protein content alveolar flooding accompanied by a further significant increase in fractional albumin uptake and dry lung weight. Additional anatomic damage appeared including epithelial lesions and hyaline membranes. Thus, HIPPV edema presents all the features of high permeability edema. These results may be of concern in the ventilatory management of patients with acute respiratory failure in order to avoid additional damages induced by local overinflation.

Animals↗
PubMed1984

[Diagnostic, prognostic and developmental value of serum angiotensin converting enzyme in sarcoidosis].

Two hundred ninety three patients with mediastinal and pulmonary sarcoidosis were assayed one or more than one time for seric angiotensin converting enzyme (SACE) using the method of Cushman and Cheung (substrate hippuryl-histidyl-leucin). Seventy one normal subjects and 163 patients with various broncho-pulmonary diseases excluding sarcoidosis were used as control. SACE is elevated in 67.2 p. 100 of the patients with sarcoidosis and reflects the intra and extrathoracic extend of the granuloma. Elevated levels of SACE in pneumoconiosis diminishes the diagnostic value of this test (as well as the presence of a normal SACE level in some sarcoid patients). There is no correlation between SACE and the percentage of lymphocytes in bronchoalveolar lavage fluid. SACE returns to normal in cases with spontaneous radiological improvement, and reaches more elevated levels in cases with worsening. An initial low level of SACE is usually a sign of a future good evolution. An initial high level is an argument for starting on steroid treatment. Repeated dosages of SACE are useful for monitoring the steroid posology at the end of the treatment and for deciding to stop it. Persistence of low levels allows to stop the treatment. Re-elevation of SACE may correspond to a radiological and clinical relapse or to an isolated and resolvent rebound.

Adolescent↗
PubMed1982

[Characteristics, assay and semeiologic value of angiotensin converting enzyme (ACE)].

Serum angiotensin conversion enzyme (serum ACE) is a dipeptidylcarboxypeptidase which activates angiotensin I to angiotensin II and inactivates bradykinine. It is a glycoprotein with an MW of 126,000 to 480,000. It is produced by all endothelial cells, and is located on the cell membrane. It is inhibited by EDTA (chelator of Zn-- cofactor), teprotide (snake venom nonapeptide) and captopril. Estimation of ACE has greatly benefitted from the use of synthetic tripeptides. An example is the method of Cushman and Cheung using hippuryl histidyl leucine. A raised serum ACE level in sarcoidosis has been demonstrated by Liebermann in 1975. The diagnostic value is limited by the existence of high levels in other pulmonary diseases (asbestosis, silicosis). Serum ACE levels in sarcoidosis are all higher when the disease is diffuse from a pulmonary and extrapulmonary standpoint. They decrease when the disease regresses spontaneously and rise if it worsens. Radiological improvement in pulmonary sarcoid lesions under the influence of corticosteroid therapy is accompanied by a fall in serum ACE levels. Persistence of this normalization as the dose is decreased is a favourable sign, whilst the reappearance of a high serum level may either reflect simple and isolated biological "rebound" or may accompany a recurrence of signs of the disease. Serum ACE measurement is thus an important factor in the surveillance of cases of treated sarcoidosis when the dose of corticosteroids is to be reduced.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1981

Simultaneous detection of deuterium oxide and indocyanine green in flowing blood.

A spectrophotometer designed to measure simultaneously traces of deuterium oxide (12 mg.1-) and indocyanine green (0.12 mg.1-1) in flowing blood is described. Its symmetrical four-beam design enabled direct readings in optical density units to be obtained in the infrared region without interference due to atmospheric CO2 and water. This system was validated by the measures of pulmonary extravascular water in the rat in heart-lung preparations and in whole animals. An example of its application showed that, with this system, it was possible to evaluate correctly an alloxan edema in the rat a short time (105 min) after its induction. In these experiments lung water calculated by indicator curves represented 80% of the lung water content (r = 085, n = 10).

Animals↗