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Biomedical subjects

R Naeije

Publications and source records attributed to R Naeije.

At least 127 records · Page 7Linked to original sources
PubMed1987

Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man.

Blood gases, hemodynamics and ventilation were measured in 7 healthy volunteers at baseline while breathing room air (FIO2 0.21), during hypoxia (FIO2 0.125, 15 min) and after nifedipine 20 mg sublingually at FIO2 0.21 (45 min) and at FIO2 0.125 (15 min). Distributions of ventilation-perfusion ratios (VA/Q) were determined, using the multiple inert gas elimination technique, at baseline, during hypoxia, and again during hypoxia after nifedipine intake. Hypoxia was associated with an average increase in pulmonary vascular resistances by 104%, which was partially inhibited by nifedipine. The inert gas data showed a mild deterioration in the distribution of VA/Q ratios during hypoxia. However, when blood flow and ventilation were constrained to the baseline normoxic values in the distributions recovered during hypoxia ('normalization procedure') a slight improvement in VA/Q matching could be evidenced, which was blunted during hypoxia after nifedipine. This was interpreted as the functional effect of hypoxic pulmonary vasoconstriction (HPV). Using the 'normalized' distributions, we computed the relationship between the decrease in compartmental blood flow that occurred during hypoxia and the corresponding alveolar PO2, and calculated the gain due to HPV feedback using equations of the control theory. The contribution of HPV to the stability of compartmental VA/Q was greatest for alveolar PO2 values around 60 mm Hg, but at best the feedback had only a moderate efficiency.

Adult↗
PubMed1987

Influence of cyclo-oxygenase inhibition and of leukotriene receptor blockade on pulmonary vascular pressure/cardiac index relationships in hyperoxic and in hypoxic dogs.

Overall mean pulmonary arterial pressure (MPAP)/cardiac index (CI) relationships were investigated in 13 pentobarbital anaesthetized dogs ventilated consecutively with a fraction of inspired O2 (F1O2) of 0.4 and with a F1O2 of 0.1. This sequence of alternated F1O2 0.4 and F1O2 0.1 was repeated in the dogs with a strong pulmonary pressor response to hypoxia (more than 20% increase in pulmonary vascular resistance) (n = 6) under a continuous infusion of the leukotriene receptor blocker FPL 57231 (2 mg min-1 kg-1), and in the dogs with a weak pressor response to hypoxia (n = 7) after cyclo-oxygenase inhibition by acetylsalicylic acid (1 g intravenously). Five-point MPAP/CI plots were constructed by opening a femoral arteriovenous fistula or by stepwise inflations of an inferior vena cava balloon catheter. The MPAP/CI plots were rectilinear in all experimental conditions. In responders, hypoxia was associated with an increase in MPAP over the entire range of CI studied (1-5 litres min-1 m-2). Infusion of FLP 57231 abolished the vasoconstricting effect of hypoxia. In non-responders, MPAP was not affected by hypoxia over the entire range of CI. After acetylsalicylic acid administration, hypoxia resulted in a significant rise in MPAP from 2 to 5 litres min-1 m-2. Infusion of FLP 57231 decreased mean systemic arterial pressure at both F1O2 0.4 and F1O2 0.1, while acetylsalicylic acid had no effect on systemic haemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Pulmonary hemodynamic response to dopamine and dobutamine in hyperoxic and in hypoxic dogs.

The pulmonary hemodynamic response to dopamine and to dobutamine was investigated in dogs ventilated with hyperoxia (fraction of inspired O2 concentration [FIO2], 0.4 balance nitrogen) and challenged with short periods of inspiratory hypoxia (FIO2 0.125 or 0.1 for 10 min). Dopamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased cardiac index (CI) and pulmonary artery pressure (PAP) without change in indexed pulmonary vascular resistance (PVRI) at both FIO2 0.4 and 0.125. Hypoxia-induced increases in PVRI were unaffected by dopamine. Dobutamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased CI, with an increase in PAP without change in PVRI at FIO2 0.4, and at FIO2 0.125 there was no change in PAP and a decrease in PVRI. Hypoxia-induced increases in PVRI were inhibited by dobutamine, partially at 5 and 10 micrograms X kg-1 X min-1, and completely at 20 micrograms X kg-1 X min-1. In two additional groups of seven dogs the effects of reducing FIO2 from 0.4 to 0.1 without and with dopamine or dobutamine either at 10 micrograms X kg-1 X min-1 (n = 7) or at 20 micrograms X kg-1 X min-1 (n = 7) were studied at an unchanged CI obtained by stepwise inflations of a balloon placed in the inferior vena cava. At constant flow both amines increased PVRI at FIO2 0.4 and did not significantly affect hypoxia-induced increases in PVRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Inhibition of angiotensin-converting enzyme by perindopril diacid in canine oleic acid pulmonary edema.

To test the hypothesis that angiotensin II could be a mediator of acute lung injury, we studied the effects of perindopril diacid, a new angiotensin-converting enzyme inhibitor, on hemodynamics, blood gases, lung mechanics, and extravascular lung water (EVLW). Twenty-four dogs were anesthetized, paralyzed and ventilated with a fraction of inspired oxygen of 0.4 in which pulmonary edema was induced by 0.1 ml/kg iv oleic acid. Perindopril diacid (1 mg/kg) was administered iv either before (eight dogs) or 100 min after (eight dogs) oleic acid injection. In the control group (eight dogs) not treated with perindopril diacid, 150 min after oleic acid injection, PaO2 changed from 193 +/- 7 (mean +/- SEM) to 55 +/- 4 torr, venous admixture from 3 +/- 1% to 52 +/- 5%, cardiac index from 4.1 +/- 0.3 to 3.1 +/- 0.3 L/min X m2, mean pulmonary artery pressure from 13 +/- 1 to 17 +/- 1 mm Hg, dynamic compliance from 90 +/- 8 to 46 +/- 7 ml/cm H2O, and EVLW from 165 +/- 25 to 750 +/- 92 ml/m2. Administration of perindopril diacid reduced systemic BP by 20% but did not affect other hemodynamic variables, blood gases, or dynamic compliance. Maximum increases in EVLW were from 169 +/- 16 to 615 +/- 54 ml/m2 in the pretreated group and from 188 +/- 23 to 675 +/- 56 ml/m2 in the treated group (no significant difference from the control group). However, pretreatment with perindopril diacid significantly (p less than .05) slowed the rise in EVLW, which was lower 60 and 90 min after oleic acid injection compared to untreated dogs. Plasma renin activity and angiotensin I concentration increased after oleic acid injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Pulmonary arterial pressure-flow plots in dogs: effects of isoflurane and nitroprusside.

We investigated the effects of nitroprusside and isoflurane on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FIO2, 0.4) and hypoxia (FIO2 0.1). Over the entire range of Q studied, 2-5 l.min-1.m-2, hypoxia increased PAP in 16 dogs ("responders") and did not affect PAP in 16 other dogs ("nonresponders"). A hypoxic pulmonary vasoconstriction (HPV) was restored in the nonresponders by intravenous administration of 1 g of acetylsalicylic acid (ASA). Nitroprusside (5 micrograms.kg-1.min-1) inhibited HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). End-tidal 1.41% isoflurane (a minimal alveolar concentration equal to one for dogs) did not affect HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). In the latter group isoflurane increased PAP at the highest Q studied (3-5 l.min-1.m-2) in hyperoxia and hypoxia. In a final group of eight dogs with Q kept constant, PAP remained unchanged during two consecutive sequences of alternated 30-min periods (maximum time to generate a PAP/Q plot) successively at FIO2 0.4 and 0.1, and the hypoxia-induced increase in PAP was reproducible. Thus the present experimental model appeared suitable for the study of the effects of hypoxia and drugs on pulmonary vascular tone of intact dogs. At the given doses HPV was inhibited by nitroprusside and not affected by isoflurane. Products of arachidonic acid metabolism possibly could be implicated in the pulmonary vascular effects of isoflurane.

Animals↗
PubMed1987

Effects of dopamine and dobutamine on hyperoxic and hypoxic pulmonary vascular tone in dogs.

The pulmonary vascular effects of dopamine and of dobutamine have been reported variably in the literature. We investigated the effects of dopamine and of dobutamine, at doses of 10 and 20 micrograms/kg/min, on the relationships of overall mean pulmonary arterial pressure (Ppa) to cardiac index (Cl) in 14 dogs ventilated alternatively in hyperoxic (FIO2, 0.4) and in hypoxic (FIO2, 0.1) conditions. Five-point Ppa/Cl plots were constructed by opening an arteriovenous femoral fistula or by stepwise inflations of a balloon in the inferior vena cava. These Ppa/Cl plots were rectilinear in all experimental conditions. Hypoxia was associated with an increase in Ppa over the entire range of Cl studied (2 to 5 L/min/m2). A deterioration in arterial oxygenation and an increase in O2 consumption constantly occurred after dopamine as well as after dobutamine administration. At 10 micrograms/kg/min (n = 6 dogs) neither drug affected Ppa over the entire range of Cl at both 0.4 and 0.1 FIO2. At 20 micrograms/kg/min (n = 8 dogs), dopamine and dobutamine increased Ppa at the lowest Cl (2 to 4 and 2 to 3 L/min/m2, respectively) at 0.4 FIO2, and attenuated hypoxia-induced increases in Ppa over the entire range of Cl. Two repetitions of alternated 0.4 and 0.1 FIO2 exposures had no effect on Ppa/Cl plots in 6 additional dogs given no drug. We concluded that at dosages as great as 20 micrograms/kg/min, as generally given in clinical practice, dopamine and dobutamine exerted similar effects upon the pulmonary circulation of intact dogs; either no change or an increase in hyperoxic pulmonary vascular tone and either no change or an attenuation of hypoxic pulmonary vasoconstriction.

Animals↗
PubMed1987

Pulmonary vascular tone improves pulmonary gas exchange in the adult respiratory distress syndrome.

Hemodynamics, blood gases, lung mechanics, and the distributions of ventilation-perfusion ratios (VA/Q) were studied before and after iv diltiazem, 0.5 mg/kg over 30 min, in 6 patients with pulmonary hypertension secondary to the adult respiratory distress syndrome (ARDS) ventilated with 7 to 20 cm H2O positive end-expiratory pressure (PEEP). Diltiazem decreased systemic and pulmonary arterial pressures without changes in cardiac output and in filling pressures of the heart, and with a slowing of heart rate. Pulmonary vascular resistances decreased from 401 +/- 59 to 329 +/- 58 dyne.s.cm-5.m2 (mean +/- SEM), p less than 0.01. Arterial Po2 decreased from 87 +/- 10 to 80 +/- 11 mm Hg (p less than 0.02) without changes in arterial PCO2, mixed venous PO2, and O2 consumption. Lung compliance and airway resistances did not change. Diltiazem increased true shunt from 23 +/- 5 to 30 +/- 7% of total blood flow (p less than 0.02) without other modification in the pattern of VA/Q distribution as measured by the multiple inert gas elimination technique. These results suggest that pulmonary vascular tone contributes to the maintenance of VA/Q matching in patients with ARDS.

Adult↗
PubMed1987

Reduction in pulmonary hypertension and in airway resistances by enoximone (MDL 17,043) in decompensated COPD.

Hemodynamics, blood gas values, and lung mechanics were investigated in 19 patients with decompensated COPD before and 30 and 60 minutes after a slow (15 minute) intravenous administration of 3 mg/kg enoximone (MDL 17,043). In the first 11 patients who were spontaneously breathing, enoximone significantly decreased pulmonary arterial wedge pressure, right atrial pressure, mean systemic arterial pressure, and mean pulmonary arterial pressure. Cardiac output remained unchanged, while heart rate increased slightly. Lung resistance decreased and dynamic lung compliance increased. Blood gas values remained unchanged. Similar effects were observed in the next eight patients who were artificially ventilated, except for an increase in cardiac output. These results show that enoximone has bronchodilating and pulmonary vasodilating properties.

Aged↗
PubMed1986

Acute central and renal haemodynamic responses to tertatolol and propranolol in patients with arterial hypertension following head injury.

We compared the central and renal haemodynamic effects of tertatolol, a new non-cardioselective beta-adrenergic blocking drug without partial agonist activity, with those of an equipotent dosage of propranolol in two groups of 10 patients each with acute cerebral injury who had developed systemic hypertension. After tertatolol, 5 mg orally, mean arterial pressure was unchanged, heart rate decreased by 22% (P less than 0.01) and cardiac index by 24% (P less than 0.01), while renal blood flow remained unchanged (-5%, NS). After 160 mg propranolol orally, mean arterial pressure was unchanged, heart rate decreased by 12% (P less than 0.01), cardiac index by 16% (P less than 0.01) and renal blood flow by 17% (P less than 0.01). There was a moderate rise in norepinephrine levels after tertatolol only. Thus in this particular model of acute hypertension, tertatolol acted as a potent beta-blocking agent but differed from propranolol by preserving renal perfusion.

Adolescent↗
PubMed1986

Cardiovascular and blood gas responses to inhaled anaesthetics in normoxic and hypoxic dogs.

Changes in haemodynamics and blood gases were investigated before and after administration of 0.5, 1 and 1.5 MAC of halothane, enflurane and isoflurane in respectively 7, 7 and 9 dogs ventilated alternatively with a fraction of inspired O2 in N2 (FiO2) of 0.4 and with brief periods (10 min) of FiO2 of 0.1. Anaesthesia was induced with pentobarbital and the animals were paralysed with pancuronium. Acute hypoxic challenges with FiO2 of 0.1 consistently decreased arterial PO2 to 3.5-4.5 kPa and increased pulmonary vascular resistances by 60-100%. At identical inspired concentrations, as expressed in MAC units, all three inhaled anaesthetics induced a broadly comparable dose-related decrease in systemic blood pressures, due to a depression in cardiac performance as well as a reduction in systemic vascular resistances. Enflurane was the most potent myocardial depressor and isoflurane the most potent vasodilator, halothane being intermediate. Oxygen deprivation was associated with some enhancement of the cardiovascular depressant effects of the inhaled anaesthetics but, in spite of this, matching of O2 transport to tissue O2 demand appeared to be improved, probably in relation to a concomitant reduction in metabolic rate. Only isoflurane inhibited the hypoxic pulmonary pressor response, and this was associated with a slight deterioration in arterial oxygenation in both normoxic and hypoxic conditions.

Adaptation, Physiological↗
PubMed1986

Tertatolol preserves renal perfusion in patients with arterial hypertension after head injury.

Tertatolol is a noncardioselective beta-adrenergic blocking agent without partial agonist activity. Its central and renal hemodynamic effects were compared to those of an equipotent dosage of propranolol in two groups of 10 patients each who developed arterial hypertension and a hyperdynamic circulatory state after head injury. After tertatolol, 5 mg orally, mean arterial blood pressure was unaffected, heart rate decreased by 22% (p less than 0.01) and cardiac index by 24% (p less than 0.01) while renal blood flow remained unchanged (-5%; not significant) so that the renal fraction of cardiac index was increased by 22% (p less than 0.05). After propranolol, 160 mg orally, mean arterial blood pressure was not modified, heart rate decreased by 12% (p less than 0.01), cardiac index by 16% (p less than 0.01) and renal blood flow by 17% (p less than 0.01) so that the renal fraction of cardiac index remained unchanged (-3%; not significant). Tertatolol is a potent beta-blocking agent comparable to propranolol apart from the fact that it preserves renal perfusion; this peculiar effect is related to a redistribution of the reduced cardiac output to the benefit of the kidney.

Adolescent↗
PubMed1986

Hypoxic pulmonary vasoconstriction and high altitude pulmonary edema.

The pulmonary hemodynamic response to an acute normobaric inspiratory hypoxia, a fraction of inspired O2 of 0.125 and the balance nitrogen for 10 min, was investigated in a 51-year-old man 11 months before and again 3 wk after he experienced an episode of pulmonary edema while mountaineering near the summit of the Chimborazo (Ecuador) at an altitude of about 5,700 m. Pulmonary vascular resistance increased by 72 and 70 dyne . s . cm-5 . m2 in the presence of decreased arterial PO2 to 40 and 43 mmHg, respectively, which is in the average of previously reported changes in normal volunteers in identical experimental conditions. These results suggest that susceptibility to high altitude pulmonary edema cannot be reliably detected by pulmonary vasoreactivity testing to hypoxia at sea level.

Altitude↗
PubMed1984

Hypouricemia in cirrhosis reflects hemodynamic alterations.

In a population of 27 consecutive patients with liver cirrhosis, systemic hemodynamics were investigated and correlated to uric acid concentrations, fractional uric acid excretion, and creatinine clearances. Mean serum uric acid concentration was lower than in normal controls, and this was related to abnormally high uric acid clearances. Uric acid concentrations correlated positively to total peripheral resistances and negatively to cardiac output. Fractional uric acid excretions correlated negatively to total peripheral resistances and positively to cardiac output. There was no correlation between creatinine clearances and any variable of systemic hemodynamics. Serum uric acid concentration and fractional uric acid excretion are dependent of the hemodynamic state in cirrhosis.

Bilirubin↗
PubMed1984

[Low-capillary-pressure pulmonary edema occurring in the acute phase of myocardial infarction].

A 44-year old man presented a postanoxic coma and acute pulmonary oedema after cardiopulmonary resuscitation in the acute phase of myocardial infarction. Early haemodynamic measurements revealed low right and left ventricular filling pressures and a low cardiac output. Haemodynamic and clinical improvement was obtained after volume expansion. The cause of low-pressure pulmonary oedema occasionally seen in patients with acute myocardial infarction is sometimes unclear. In the present case, a neurogenic mechanism may be involved. The early diagnosis of this oedema has important therapeutic implications.

Adult↗
PubMed1984

Hemodynamic effects of vasopressin, alone and in combination with nitroprusside, in patients with liver cirrhosis and portal hypertension.

We have investigated the effects on systemic, pulmonary, hepatic, and renal hemodynamics, and on blood gases of vasopressin, 0.4 U/min I.V. first alone, then in combination with nitroprusside 1-5 micrograms/kg/min I.V., in 12 patients with liver cirrhosis and portal hypertension. Portal pressures were estimated by the gradient between occluded and free hepatic vein pressures, hepatic blood flow was measured by indocyanine green infusion, renal blood flow by an isotopic method, and cardiac output by thermodilution. Vasopressin alone reduced cardiac output (-23%) and O2 delivery to the tissues (-25%), increased mean arterial pressure (+20%) and filling pressures of the heart (+136%), reduced portal pressures (-36%) (from 19 +/- 1 to 12 +/- 1 mmHg, mean +/- SEM), hepatic blood flow (-35%) (1.33 +/- 0.2 to 0.87 +/- 0.1 l/min), and renal blood flow (-16%) (0.77 +/- 0.07 to 0.65 +/- 0.05 l/min). Adding nitroprusside restored cardiac output, preload and afterload, and renal blood flow to pretreatment values. Oxygen delivery remained depressed (-12%) because of a negative effect on pulmonary gas exchange (physiologic shunt increased from 16 +/- 2 to 28 +/- 4%). Portal pressures remained reduced by 31% and hepatic blood flow by 25%. These results suggest that small doses of I.V. nitroprusside minimize the deleterious hemodynamic effects of vasopressin while maintaining the therapeutic benefit of portal pressure reduction in cirrhotic patients.

Adult↗
PubMed1984

Acute hemodynamic effects of controlled oxygen therapy in decompensated chronic obstructive pulmonary disease.

The acute effects of controlled O2 therapy on hemodynamics and blood gases were investigated in 22 patients with decompensated chronic obstructive pulmonary disease (COPD). An inspired O2 fraction (FIO2) of 0.24 and 0.28 given to the first 12 patients markedly improved arterial and mixed-venous blood oxygenation with no (FIO2 0.24) or slight (FIO2 0.28) aggravation of hypercapnia, but did not change O2 delivery to the tissues. Higher FIO2 values of 0.35 and 0.40 in the next ten patients improved blood oxygenation even more, together with an increase in O2 delivery to the tissues and a significant aggravation of hypercapnia. All four FIO2 values reduced cardiac output without changing pulmonary vascular resistance. These results suggest that in patients with decompensated COPD, low-flow O2 improves oxygenation by diffusion rather than convection. On the other hand, controlled O2 therapy does not appear to be an immediately effective pulmonary vasodilating treatment in these patients.

Adult↗
PubMed1984

Deleterious effect of nifedipine on pulmonary gas exchange in chronic obstructive pulmonary disease.

Nifedipine was given, 20 mg sublingually, to 6 patients with pulmonary hypertension secondary to advanced chronic obstructive pulmonary disease, and its effects on hemodynamics, blood gases, lung mechanics, and the distribution of ventilation-perfusion ratios (VA/Q) were investigated. Systemic vasodilation was obtained, with a reduction in mean systemic arterial pressure and in systemic vascular resistance by 16 and 36%, respectively. Cardiac index increased by 29%. Pulmonary vascular resistance decreased by 28%, without changes in pulmonary arterial mean pressure. Arterial PO2 decreased from 52 +/- 4 to 47 +/- 3 mmHg (p less than 0.001). A deterioration in VA/Q matching could be demonstrated, with a redistribution of blood flow into the lungs by a diversion of 20% of total blood flow from units with normal VA/Q, between 0.23 to 3.0, to hypoxic units with low VA/Q between 0.19 to 0.009. These changes might be explained by a partial inhibition of hypoxic pulmonary vasoconstriction.

Aged↗