PubMed Health⌕ Search

Biomedical subjects

M Delcroix

Publications and source records attributed to M Delcroix.

At least 19 recordsLinked to original sources
PubMed1998

Effects of pulmonary embolism on pulmonary vascular impedance in dogs and minipigs.

Pigs have been reported to present with a stronger pulmonary vascular reactivity than many other species, including dogs. We investigated the pulmonary vascular impedance response to autologous blood clot embolic pulmonary hypertension in anesthetized and ventilated minipigs (n = 6) and dogs (n = 6). Before embolization, minipigs, compared with dogs, presented with higher mean pulmonary arterial pressure (Ppa; by an average of 9 mmHg), a steeper slope of Ppa-flow (Q) relationships, and higher 0-Hz impedance (Z0) and first-harmonic impedance (Z1), without significant differences in characteristic impedance (Zc), and a lower ratio of pulsatile hydraulic power to total hydraulic power. Embolic pulmonary hypertension (mean Ppa: 40-55 mmHg) was associated with increased Z0 and Z1 in both species, but the minipigs had a steeper slope of Ppa/Q plots and an increased Zc. At identical Q and Ppa, minipigs still presented with higher Z1 and Zc and a lower ratio of pulsatile hydraulic power to total hydraulic power. The energy transmission ratio, defined as the hydraulic power in the measured waves divided by the hydraulic power in the forward waves, was better preserved after embolism in minipigs. No differences in wave reflection indexes were found before and after embolism. We conclude that minipigs, compared with dogs, present with a higher pulmonary vascular resistance and reactivity and adapt to embolic pulmonary hypertension by an increased Zc without earlier wave reflection. These differences allow for a reduced pulsatile component of hydraulic power and, therefore, a better energy transfer from the right ventricle to the pulmonary circulation.

Animals↗
PubMed1997

Sympathetic modulation of hypoxic pulmonary vasoconstriction in intact dogs.

BACKGROUND: The effects of the sympathetic nervous system on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We studied the effects of adrenergic receptor blockade and epidural blockade on HPV in 32 pentobarbital-anaesthetised intact dogs. METHODS: Pulmonary arterial flow-pressure relationships were determined in hyperoxia and hypoxia, at baseline and after alpha-blockade (phentolamine 2 mg/kg + 50 micrograms.kg-1.-1), beta-blockade (propranolol 2 mg/kg), alpha beta-blockade, epidural blockade (lignocaine 20 mg/kg), and alpha beta-plus epidural blockade. RESULTS: At reference flow of 3.5 1.min-1.m-2, the mean hypoxic response (hypoxia-induced increase in transpulmonary pressure gradient, each n = 8) changed from 6.0 +/- 0.9 to 3.5 +/- 1.0 mmHg after alpha-blockade, from 5.8 +/- 0.9 to 0.7 mmHg after beta-blockade, from 4.1 +/- 0.8 to 0.9 +/- 1.4 mmHg after alpha beta-blockade from 3.4 +/- 1.0 to 4.3 +/- 0.9 mmHg after epidural blockade (all P < 0.05), and was not affected by epidural blockade after alpha beta-blockade. CONCLUSIONS: In pentobarbital-anaesthetised dogs, (1) HPV is attenuated by alpha- and enhanced by beta-, alpha beta- and epidural blockade, and (2) epidural blockade has no significant adrenergic-unrelated effect on the pulmonary vasculature.

Adrenergic alpha-Antagonists↗
PubMed1997

Comparison of the effects of isoflurane with those of propofol on pulmonary vascular impedance in experimental embolic pulmonary hypertension.

Inhaled but not i.v. anaesthetics are reported to decrease pulmonary vascular resistance. The aim of this study was to compare the effects of isoflurane with those of propofol on the interaction between right ventricular (RV) function and the pulmonary vascular system in embolic pulmonary hypertension. Nine dogs received in random sequence propofol 18 mg kg-1 h-1 and 1.4% end-tidal isoflurane. Pulmonary haemodynamic state was evaluated by pulmonary arterial pressure/flow (PAP/Q) plots and pulmonary vascular impedance (PVZ) spectra. Right ventricular function was assessed by total hydraulic power (Wtot), ratio of oscillatory power (Wosc) to Wtot, and dP/dtmax. Measurements were obtained, with both anaesthetics, before and after pulmonary embolic hypertension induced by autologous blood clots. Embolism increased PAP, 0 Hz and low frequency input impedance, displaced first minimum of PAP/Q moduli and zero crossing of phase to higher frequencies, decreased characteristic impedance, decreased Wosc/Wtot without affecting Wtot, and increased dP/dtmax. Compared with propofol, isoflurane at baseline did not affect PAP/Q plots, PVZ or hydraulic power data, but decreased dP/dtmax. After embolism, isoflurane shifted PAP/Q plots to lower PAP without affecting PVZ, did not affect hydraulic power data and decreased dP/dtmax. We conclude that in canine embolic pulmonary hypertension, isoflurane compared with propofol impeded RV vascular coupling caused by decreased RV contractility, while after-load remained unchanged despite some decrease in pulmonary vascular tone.

Anesthetics, Inhalation↗
PubMed1997

Role of macrophages during Theiler's virus infection.

Theiler's virus, a murine picornavirus, causes a persistent infection of the central nervous system with chronic inflammation and primary demyelination. We examined the nature of infected cells at different times postinoculation (p.i.) with a combined immunocytochemistry-in situ hybridization assay. The virus was found in the gray matter of the brain, mostly in neurons, during the first week p.i. During the following weeks, the virus was present in the spinal cord, first in the gray and white matter, then exclusively in the white matter. Approximately 10% of infected cells were astrocytes at any time during the study. Infected oligodendrocytes were first noticed on day 14 p.i. and amounted to approximately 6% of infected cells. The number of infected macrophages increased with time and reached a plateau by day 21 p.i., when at least 45% of infected cells were macrophages. The role of blood-borne macrophages during infection was studied by depleting them with mannosylated liposomes containing dichloromethylene diphosphonate. The virus did not persist in the majority of the mice treated with liposomes. These mice showed only minimal mononuclear cell infiltration and no demyelination.

Animals↗
PubMed1997

[Prenatal diagnosis of an intraspinal lipoma. A case report].

This report describes a prenatal diagnosis of intraspinal lipoma. This pathology, not well known by obstetricians, forms a part of neural tube defects. Echographic aspect, embryologic origin, differential diagnosis, neurosurgical prognosis and treatment are reviewed and discussed.

Adult↗
PubMed1996

Hypoxic pulmonary vasoconstriction and gas exchange in acute canine pulmonary embolism.

Hypoxic pulmonary vasoconstriction (HPV) is inhibited in several models of acute lung injury. Whether HPV is preserved in pulmonary embolism is unknown. We investigated the effects of a reduction in the fraction of inspired O2 (FIO2) on pulmonary hemodynamics and gas exchange in anesthetized dogs before and after autologous blood clot pulmonary embolism. In a first group of 14 dogs, stimulus-response curves for HPV were constructed as pulmonary arterial pressure (Ppa) vs. FIO2 varied between 1.0 and 0.06 at a cardiac output (Q) kept constant at 3.5 l.min-1.m-2. Gas exchange was evaluated by using the multiple inert-gas elimination technique at FIO2 of 1.0, 0.4, and 0.1. Embolism decreased the relative magnitude of HPV, expressed as the gradient between Ppa and pulmonary arterial occluded pressure in hypoxia divided by (Ppa-pulmonary arterial occluded pressure) at FIO2 of 1.0, from 1.8 to 1.2 (P < 0.05). Retention minus excretion gradients for sulfur hexafluoride and ethane were increased by decreased FIO2 (P < 0.005 and P < 0.05, respectively) before but not after embolism. Hypoxia-induced deterioration in gas exchange before embolism was related to the amount of baseline very low ventilation-perfusion (VA/Q) ratios. Similar results were obtained in a second group of seven dogs with Q decreased to maintain Ppa at the same average value as before embolism. However, gas exchange was not affected by inspiratory hypoxia before as well as after embolism in this group, which presented with a lesser amount of baseline very low VA/Q. In both groups of dogs, increase in the FIO2 from 0.4 to 1.0 did not affect gas exchange. We conclude that 1) pulmonary embolism is associated with a partial inhibition of HPV, 2) HPV does not contribute to preserve gas exchange in pulmonary embolism, and 3) a strong HPV may deteriorate gas exchange in severe hypoxia in the presence of minor very low VA/Q inequality.

Animals↗
PubMed1996

Effects of chronic dexfenfluramine treatment on pulmonary hemodynamics in dogs.

An epidemic of primary pulmonary hypertension occurred in Europe in the 1960s, after the introduction of the appetite suppressant aminorex. Recently, a cluster of cases of pulmonary hypertension was observed in France in relation to the intake of the appetite suppressant dexfenfluramine. We previously reported that intravenous dexfenfluramine enhances hypoxic pulmonary vasoconstriction in dogs. We therefore investigated the pulmonary hemodynamic effects of chronic oral intake of this drug. Twenty-four dogs with a strong (n = 12) and a weak hypoxic pulmonary vasoconstriction (n = 12) respectively were randomly allocated in a double blind manner to a twice daily oral intake of either a placebo or dexfenfluramine 1.5 mg/kg for 20 d. A strong hypoxic vasoconstriction was defined as a hypoxia-induced increase in pulmonary artery pressure by more than 3 mm Hg at a standardized cardiac output of 3 L/min/m2. Pulmonary hemodynamics were studied in hyperoxia (fraction of inspired O2 [F(I)O2] 0.4) and in hypoxia (F(I)O2 0.1) before and after treatment. Venous return was manipulated at post-treatment evaluation for isoflow comparisons of pulmonary vascular pressures. Dexfenfluramine had no effect on systemic hemodynamics or blood gases, but increased pulmonary vascular resistance from 155 +/- 17 to 192 +/- 14 dyne x s x cm(-5) in hyperoxia (mean +/- SE, p < 0.05) and from 237 +/- 27 to 293 +/- 47 dyne x s x cm(-5) in hypoxia (p < 0.01). Dexfenfluramine, and not placebo, increased the isoflow pulmonary vascular pressure gradient in hyperoxia and in hypoxia. This effect was unrelated to the magnitude of pretreatment hypoxic vasoconstriction. We conclude that the chronic intake of dexfenfluramine in dogs is associated with a moderate increase in pulmonary vascular resistance which is unrelated to pulmonary vasoreactivity to hypoxia.

Administration, Oral↗
PubMed1995

Starling resistor vs. distensible vessel models for embolic pulmonary hypertension.

We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065-1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15-26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.

Animals↗
PubMed1995

Pulmonary vascular impedance response to hypoxia in dogs and minipigs: effects of inhaled nitric oxide.

The pig has been reported to present with a stronger hypoxic pulmonary vasoconstriction (HPV) than many other species, including dogs. We investigated [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (Ppao)] vs. pulmonary blood flow (Q) relationships and pulmonary vascular impedance (PVZ) spectra in nine minipigs and nine weight-matched dogs. The animals were anesthetized and ventilated in hyperoxia [inspired O2 fraction 0.4] or hypoxia (inspired O2 fraction 0.12). PVZ was computed from the Fourier series for Ppa and Q. In hyperoxia, the pigs had a higher Ppa (26 +/- 1 vs. 16 +/- 1 mmHg), a higher first-harmonic impedance (Z1), and a more negative low-frequency phase angle but no different characteristic impedance (Zc) compared with the dogs at the same Q. Hypoxia in the dogs increased (Ppa-Ppao) at all levels of Q studied by an average of 2 mmHg but did not affect Z1 or Zc. Hypoxia in the pigs increased (Ppa-Ppao) at all levels of Q by an average of 13 mmHg and increased Z1 and Zc. Inhaled NO (150 ppm) reversed the hypoxia-induced changes in (Ppa-Ppao)/Q plots and PVZ in the dogs and pigs. However, differences in (Ppa-Ppao)/Q plots and PVZ between the dogs and pigs in hyperoxia and hypoxia were not affected by inhaled NO. We conclude 1) that minipigs present with an elevated pulmonary vascular resistance and impedance in hypoxia more than in hyperoxia and 2) that baseline differences in pulmonary hemodynamics between dogs and minipigs are structural rather than functional.

Administration, Inhalation↗
PubMed1995

Effects of dexfenfluramine on hypoxic pulmonary vasoconstriction and embolic pulmonary hypertension in dogs.

There has been suggestion of a possible relationship between the intake of the appetite suppressant dexfenfluramine and the development of primary pulmonary hypertension. We investigated the pulmonary vascular effects of acute intravenous dexfenfluramine in pentobarbital-anesthetized dogs ventilated in hyperoxia (fraction of inspired oxygen, FIO2, 0.4) and either challenged with a FIO2 of 0.1 to induce hypoxic pulmonary hypertension (n = 20) or given autologous blood clots to induce embolic pulmonary hypertension (n = 6). Pulmonary vascular tone was evaluated by multipoint (mean pulmonary artery pressure [Ppa] - pulmonary artery occluded pressure [Ppao])/cardiac output (Q) plots. Hypoxia increased Ppa - Ppao over the entire range of Q studied, from 1.5 to 4.0 L/min/m2, in 12 dogs (responders) and had no significant effect on (Ppa - Ppao)/Q plots in 8 other dogs (nonresponders). Dexfenfluramine did not affect (Ppa - Ppao)/Q plots in 6 responders but shifted (Ppa - Ppao)/Q plots to higher pressures in hypoxia in 6 nonresponders (p < 0.001). Dexfenfluramine had no effect on (Ppa - Ppao)/Q plots in the 6 dogs with embolic pulmonary hypertension. Because dexfenfluramine has serotoninergic properties, we compared the effects of ketanserin, a serotonin (5-hydroxytryptamine, 5-HT) S2 receptor antagonist, on naturally present versus dexfenfluramine-restored hypoxic pulmonary vasoconstriction. Ketanserin did not affect hyperoxic or hypoxic pulmonary vascular tone, neither in 6 responders nor in 2 nonresponders with dexfenfluramine-restored hypoxic vasoconstriction. We conclude that dexfenfluramine restores hypoxic pulmonary vasoconstriction in dogs with weak or absent hypoxic pressor response and that this effect is unlikely to be mediated by activation of 5-HT S2 receptors.

Animals↗
PubMed1994

Effects of endogenous nitric oxide on pulmonary vascular tone in intact dogs.

The interaction between inspiratory fraction of O2 (FIO2) and endogenous nitric oxide (NO) regulation of pulmonary vascular tone was examined in intact anesthetized dogs. Stimulus (FIO2 of 1, 0.4, 0.21, 0.12, and 0.1)-response (changes in pulmonary artery pressure minus pulmonary artery occlusion pressure) curves were constructed with cardiac output kept constant (by opening a femoral arteriovenous bypass or inflating an inferior vena cava balloon catheter), before and after administration of compounds acting at different levels of the L-arginine-NO pathway, NG-nitro-L-arginine (L-NNA, 10 mg/kg iv, n = 16), a NO synthase inhibitor, and methylene blue (8 mg/kg iv, n = 16), a guanylate cyclase inhibitor. L-NNA and methylene blue did not influence pulmonary vascular tone in hyperoxic and in normoxic conditions, but they increased it during hypoxia, thus enhancing the vasopressor response to hypoxia (from 4.5 +/- 0.9 to 10.4 +/- 1.2 mmHg and from 4.2 +/- 0.8 to 9 +/- 1.5 mmHg, respectively, both P < 0.01). Hypoxic pulmonary vasoconstriction was augmented in dogs with a baseline hypoxic response ("responders") and restored in dogs without hypoxic response ("nonresponders"). These results suggest that endogenous NO does not influence hyperoxic and normoxic pulmonary vascular tone, but that it inhibits hypoxic pulmonary vasoconstriction in intact anesthetized dogs.

Animals↗
PubMed1994

Increased left atrial pressure inhibits hypoxic pulmonary vasoconstriction.

An increase in left atrial pressure (Pla) has been reported to either inhibit or not affect hypoxic pulmonary vasoconstriction in intact dogs. We investigated mean pulmonary arterial pressure (Ppa)-flow (Q) relationships at low and high fixed Pla and Ppa-Pla relationships at fixed Q in piglets, which are known to present with a stronger hypoxic pulmonary pressor response than dogs. Seven piglets were anesthetized; equipped with balloon catheters in inferior vena cava and left atrium to control Q and Pla, respectively; and ventilated alternatively in hyperoxia [fractional concn of O2 in inspired air (FIO2) 0.4] and hypoxia (FIO2 0.12). In all experimental conditions, Ppa-Q plots were best described by a linear approximation with extrapolated pressure intercepts (Pi) not different from Pla. Hypoxia increased slope but not Pi of Ppa-Q plots. An increase in Pla from 8 to 17 mmHg induced a parallel shift of Ppa-Q plots to higher Ppa in hyperoxia but did not affect Ppa-Q plots in hypoxia. In hyperoxia, an increase in Pla at constant Q induced an approximately equal increase in Ppa, whereas in hypoxia there was no effect. The hypoxia-induced increase in Ppa was blunted by increased Pla at all levels of Q studied. We conclude that in anesthetized piglets at fixed Pla hypoxia increases the slope of Ppa-Q plots without affecting Pi and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. The results suggest that no closing pressure higher than normal Pla contributes to hyperoxic or hypoxic Ppa in the intact porcine pulmonary circulation.

Animals↗
PubMed1994

Stimulus-response curve of hypoxic pulmonary vasoconstriction in intact dogs: effects of ASA.

Hypoxic pulmonary vasoconstriction (HPV) has been reported to decrease during severe hypoxia in isolated lungs, but it remains unknown whether this decrease occurs in the intact animal and how it is affected by cyclooxygenase inhibition. We investigated the HPV stimulus-response relationship in eight pentobarbital sodium-anesthetized intact dogs with a naturally occurring response to hypoxia ("responders"). The pulmonary arterial minus wedge pressure difference (Ppa-Ppw) was measured at 11 inspired O2 fraction (FIO2) values between 0.40 and 0.04 while ventilation, cardiac output, and acid-base status were kept constant. Ppa-Ppw increased by 8 +/- 1 mmHg between FIO2 of 0.40 and 0.10 (alveolar PO2 of approximately 40 Torr) and decreased by 3 +/- 1 mmHg between FIO2 of 0.10 and 0.04. To assess the effects of cyclooxygenase inhibition, similar stimulus-response curves were obtained after administration of 20 mg/kg of acetylsalicylic acid (ASA) in 16 more dogs selected as either nonresponders or responders to hypoxia. ASA restored HPV in nonresponders and enhanced HPV in responders, with the difference between Ppa-Ppw at FIO2 of 0.10 and 0.40 increasing from 1 +/- 1 to 8 +/- 1 mmHg (P < 0.001) and from 7 +/- 1 to 10 +/- 1 mmHg (P < 0.05), respectively. In both groups, the shape of the stimulus-response curve after ASA was comparable to that of spontaneous HPV, with a maximum at FIO2 of 0.10 and a significant decrease at lower FIO2. We conclude that severe hypoxia attenuates HPV in the intact animal and that ASA restores or enhances HPV by affecting the magnitude of the hypoxic response and not the sensitivity to hypoxia.

Acid-Base Equilibrium↗
PubMed1994

[Urinary infection in the pregnant woman].

Urinary tract infections are common during pregnancy. When unrecognized, they can be responsible for complications such as threatened premature labour and impaired intra-uterine development. Detection and appropriate treatment are thus essential. This article reviews the pathophysiology of urinary tract infections during pregnancy and the three major entities involved--different but related to each other--are detailed (significant asymptomatic bacteriuria or SAB, acute cystitis and acute pyelonephritis), together with their specific treatment. SAB tends to persist during pregnancy, then leading in the absence of treatment to a potentially serious complication (acute pyelonephritis) in approximately one woman in five. SAB should be sought at the first prenatal visit by microscopic and bacteriological examination of a properly obtained urine specimen. Lower genital infections should also be sought and treated, without forgetting to remind the patient of preventive measures (adequate hygiene, sufficient urine output, post-coital micturition, regular bowel habit).

Anti-Bacterial Agents↗
PubMed1993

Embolus size affects gas exchange in canine autologous blood clot pulmonary embolism.

Embolic pulmonary hypertension is associated with alterations in gas exchange of variable severity, which we hypothesized to be related to embolus size. We therefore examined the effects of different-size autologous blood clot embolization on pulmonary arterial pressure-cardiac output relationships (Ppa/Q) and on the distribution of ventilation-perfusion ratios (VA/Q) in 18 intact anesthetized and ventilated (inspired fraction of O2 0.4) dogs. Multipoint Ppa/Q plots were generated by a manipulation of venous return before and 60 min after sufficient amounts of small (1 mm, n = 6 dogs), medium (5 mm, n = 6 dogs), or large (10 mm, n = 6 dogs) clots to increase Ppa to 50 mmHg. The distribution of VA/Q was determined by the multiple inert gas elimination technique at the same intermediate Q in each of these experimental conditions. All three sizes of emboli resulted in an 82-92% mean angiographic pulmonary vascular obstruction and increased both the extrapolated pressure intercepts and the slopes of the linear Ppa/Q plots. Gas exchange was altered the most after large clots, which were associated with lower arterial pH, higher physiological and inert gas dead spaces, higher dispersion of ventilation, and also lower mean VA/Q of perfusion distributions. In contrast, inert gas dead space was decreased after small clots. We conclude that, in autologous blood clot embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size but that gas exchange is affected differently, mainly in high-VA/Q regions and most often after the largest clots.

Angiography↗
PubMed1993

Mechanisms of improved arterial oxygenation after peripheral chemoreceptor stimulation during hypoxic exercise.

Almitrine, a peripheral chemoreceptor agonist, has been reported to increase arterial O2 saturation (SaO2) without changing minute ventilation (VE) during hypoxic exercise (Giesbrecht et al. J. Appl. Physiol. 70: 1770-1774, 1991). To explain this finding, we studied pulmonary hemodynamics (right heart catheterization) and gas exchange (multiple inert gas elimination technique) in six healthy volunteers at rest and during heavy exercise in normobaric normoxia (fractional concentration of O2 in inspired air 0.21) or hypoxia (fractional concentration of O2 in inspired air 0.125), before and after 75 mg of almitrine taken orally. During normoxic exercise, at a mean O2 uptake (VO2) of 4.0 l/min, almitrine increased arterial PO2 (PaO2) (P < 0.05), SaO2 (P < 0.01), and VE (P < 0.05) and decreased arterial PCO2 (P < 0.01), without affecting pulmonary hemodynamics or ventilation-perfusion distributions. During hypoxic exercise, at a mean VO2 of 3.0 l/min, almitrine increased SaO2 (P < 0.01) and VE (P < 0.01) and decreased arterial PCO2 (P < 0.05), with no effect on PaO2 or on ventilation-perfusion distributions and with a slight pulmonary vasoconstriction (P < 0.01). Almitrine during hypoxia did not affect cardiac output or calculated O2 diffusing capacity, but it did increase the slope of the VE/VO2 relationship (P < 0.01). We conclude that during hypoxic exercise, a pharmacological stimulation of the peripheral chemoreceptors improves SaO2 but not PaO2 by means of increased ventilation and an associated leftward shift of the oxyhemoglobin dissociation curve.

Adult↗