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C Melot

Publications and source records attributed to C Melot.

At least 37 records · Page 2Linked to original sources
PubMed1990

Enhancement of hypoxic pulmonary vasoconstriction by metabolic acidosis in dogs.

The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in hyperoxia (fraction of inspired O2 [FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 5 l.min-1.m-2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2 exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCl (2 mmol.kg-1.h-1) decreased arterial pH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in hyperoxia and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol.kg-1.h-1) together with a 7% sodium bicarbonate infusion (adjusted to maintain arterial pH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetylsalicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol.kg-1.h-1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.

Acidosis↗
PubMed1990

Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs.

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.

Acidosis↗
PubMed1990

Inhibition of hypoxic pulmonary vasoconstriction by increased left atrial pressure in dogs.

To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.

Animals↗
PubMed1989

Absence of parasympathetic control of pulmonary vascular pressure-flow plots in hyperoxic and hypoxic dogs.

Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV). This has been explained by a reflex vagal (Chapleau et al., 1988) or sympathetic (Naeije et al., 1989) pulmonary vasodilation. We therefore investigated the effects of bilateral cervical vagotomy and of muscarinic block (atropine sulfate 0.1 mg.kg-1 i.v.) on multipoint pulmonary arterial pressure (Ppa)-cardiac index (Q) plots in 16 sodium pentobarbital-anesthetized dogs ventilated alternately in hyperoxia (fraction of inspired O2, FIO2, 0.4) and in hypoxia (FIO2 0.1). Over the range of Q studied, 2 to 5 L.min-1.m-2, hypoxia increased Ppa and did not change pulmonary capillary wedge pressure (Ppw). After bilateral cervical vagotomy or after atropine, Ppa and Ppw at all levels of Q were not modified either during hyperoxia or during hypoxia. These results show that the parasympathetic system does not affect the global hypoxia-induced pulmonary vasopressor response and thus suggest that the depressor effect of chemoreceptor stimulation on HPV is not vagally mediated.

Animals↗
PubMed1989

Systemic and regional hemodynamic effects of isosorbide dinitrate in patients with liver cirrhosis and portal hypertension.

In a group of 17 cirrhotic patients with portal hypertension, we have investigated the effects of 5 mg sublingual administration of isosorbide dinitrate (IDN) on central hemodynamics, on regional (hepatic and renal) hemodynamics and on blood gases. Fifteen min after drug administration, we observed a decrease in the right atrial mean pressure from 4 +/- 1 to 3 +/- 1 mmHg (mean +/- S.E.M., P less than 0.02) and of pulmonary arterial wedge pressure from 7 +/- 1 to 4 +/- 1 mmHg (P less than 0.001) with decreases of the cardiac index from 4.2 +/- 0.2 to 3.7 +/- 0.2 l/min/m2 (P less than 0.001) and the mean arterial pressure from 89 +/- 4 to 72 +/- 3 mmHg (P less than 0.001) and an increase in heart rate from 86 +/- 4 to 94 +/- 5 beats/min (P less than 0.001). Arterial PO2 decreased from 73 +/- 2 to 66 +/- 2 mmHg (P less than 0.001). As a consequence of both cardiac index and arterial PO2 reductions, O2 transport to the tissues was reduced from 602 +/- 32 to 518 +/- 26 ml/min.m2 (P less than 0.001). The hepatic venous pressure gradient decreased from 17 +/- 1 to 14 +/- 1 mmHg (P less than 0.001) and hepatic vein PO2 did not change. The hepatic blood flow (HBF) determined in 7 patients remained unchanged. Renal blood flow (RBF) determined in 5 patients decreased from 0.76 +/- 0.11 to 0.68 +/- 0.11 l/min (P less than 0.001). In conclusion, isosorbide dinitrate reduces portal hypertension in patients with liver cirrhosis without compromising hepatic perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of propofol on pulmonary and systemic arterial pressure-flow relationships in hyperoxic and hypoxic dogs.

We have investigated the effects of a continuous infusion (18 mg kg-1 h-1) of the aqueous emulsion formulation of propofol on mean pulmonary arterial (PAP)/cardiac output (O) and mean systemic arterial pressure (SAP)/Q relationships in 15 intact pentobarbitone-anaesthetized dogs subjected to hyperoxia (F/O2 0.4) and hypoxia (F/O2 0.1). Five-point PAP/Q and SAP/Q plots were obtained by opening an arterio-venous femoral fistula or by stepwise inflations of an inferior vena cava balloon. Over the range of Q studied (2-5 litre min-1), hypoxia increased PAP in eight dogs ("responders") and did not affect PAP in seven others ("non-responders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in non-responders by the administration of acetylsalicylic acid (ASA) 1 g i.v. Hypoxia did not affect SAP over the range of Q studied in the responders or in the non-responders treated with ASA. Propofol had no effect on hyperoxic or on hypoxic PAP at all values of Q either in responders or in non-responders with HPV restored by ASA. Propofol did not change Q at uncontrolled flow, but decreased SAP at the lowest Q (2 and 3 litre min-1) during hyperoxia and at all values of Q during hypoxia. The systemic vascular effects were the same in animals of both groups, treated with ASA or not. We conclude that propofol does not influence pulmonary vascular tone and does not inhibit HPV, but reduces systemic vascular tone when venous return or oxygenation is decreased. The haemodynamic response to propofol was not affected by cyclo-oxygenase inhibition.

Anesthetics↗
PubMed1989

Pulmonary vascular responses to surgical chemodenervation and chemical sympathectomy in dogs.

We investigated the effects of surgical peripheral chemoreceptor denervation, chemical sympathectomy with 6-hydroxydopamine (6-OHDA), and the peripheral chemoreceptor stimulant almitrine on multipoint pulmonary arterial pressure-cardiac index (PAP/Q) plots in 30 pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia [fraction of inspired O2, (FIO2) = 0.4] and hypoxia (FIO2 = 0.1). A hypoxic pulmonary vasoconstriction (HPV), i.e., a hypoxia-induced increase in PAP over the entire range of Q studied, from 2 to 5 l.min-1.m-2, was elicited in all the animals. Surgical denervation of the carotid and aortic chemoreceptors in a first group of nine dogs increased PAP at the lowest Q of 2 and 3 l.min-1.min-2 in hyperoxia and increased PAP at all levels of Q in hypoxia, so that HPV was enhanced. Chemical sympathectomy in a second group of eight dogs increased PAP at all levels of Q to a comparable extent in hyperoxia and hypoxia so that HPV remained unchanged. Almitrine (8 micrograms.kg-1.min-1 iv) in a third group of eight dogs increased PAP at all levels of Q in hyperoxia but had no effect on PAP/Q plots in hypoxia, so that HPV was inhibited. Almitrine had these same pulmonary vascular effects when administered to the chemodenervated and the sympathectomized dogs. Sham operation and a 2-h delay in a final group of five dogs had no effect on hyperoxic or hypoxic PAP/Q plots. We conclude that in intact dogs 1) the sympathetic nervous system reduces both hyperoxic and hypoxic pulmonary vascular tone, 2) stimulation of the peripheral chemoreceptors inhibits HPV, and 3) almitrine has direct pulmonary vasoconstricting effects in hyperoxia but not hypoxia.

Almitrine↗
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

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

Discrepancy between thermodilution and radionuclide right ventricular ejection fraction measurements: the importance of tricuspid regurgitation.

Measurement of right ventricular ejection fraction (RVEF) by the thermodilution technique has become routinely available at the bedside of the critically ill. We describe 2 patients with tricuspid regurgitation in whom RVEF values were considerably lower by thermodilution than by radionuclide techniques. Discrepancies could be due to the regurgitation of the thermodilution signal and possibly to the different nature of the two measurements (forward stroke volume with the thermodilution technique and total stroke volume with the radionuclide technique). We suggest that lower RVEF measurement by the thermodilution technique could be related to unrecognized tricuspid regurgitation. Measurement of an unexpectedly low RVEF by the thermodilution technique should suggest the presence of tricuspid regurgitation.

Heart↗
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

Hemodynamic effects of dobutamine in patients below and over 65 years, with left heart failure secondary to an acute myocardial infarction.

The cardiac response to sympathomimetic agents has been reported to be reduced in the elderly. We studied the hemodynamic effects of dobutamine in two groups of patients with acute myocardial infarction (AMI) and left heart failure: group A included 10 patients aged 65 years or less and group B 10 others older than 65. After a 1-hour infusion the increase in cardiac index was highly significant in both groups (27%, p less than 0.001 and 25%, p less than 0.001), and the decrease in pulmonary wedge pressure was greater in group A (42%, p less than 0.001 and 17%, p less than 0.02). The increase in double product was similar in both groups (14%, p less than 0.001 and 18%, p less than 0.005); nevertheless the 4 patients developing angina pectoris during dobutamine infusion were over 65 years. We conclude that dobutamine remains effective in the elderly with AMI and left heart failure but is less well tolerated.

Age Factors↗
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↗