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Biomedical subjects

R Naeije

Publications and source records attributed to R Naeije.

At least 145 records · Page 8Linked to original sources
PubMed1983

Treatment of portal hypertension with isosorbide dinitrate alone and in combination with vasopressin.

Experimental animal studies have suggested that certain vasodilators could minimize the adverse cardiovascular effects of vasopressin. We investigated the hemodynamic effects of isosorbide dinitrate, alone and in combination with vasopressin, in patients with liver cirrhosis. In 10 patients, isosorbide dinitrate, 5 mg sublingually, reduced portal pressure by 21% as assessed by the gradient between wedged and free hepatic venous pressure, but also decreased mean arterial pressure (MAP) by 20%, pulmonary artery wedge pressure (WP) by 50%, and oxygen delivery (DO2) by 13%. In 6 other patients, isosorbide dinitrate, 5 mg sublingually, combined with vasopressin, 0.4 U/min iv, reduced portal pressure by 37%, increased MAP by 13%, and mean pulmonary artery pressure (MPAP) by 70%, and decreased DO2 by 32%. Thus, isosorbide dinitrate reduces effectively portal hypertension in patients with liver cirrhosis, but also decreases DO2 to the tissues as a consequence of a fall in cardiac output due to decreased preload. At the dosage used in this study, isosorbide dinitrate does not prevent the adverse hemodynamic effects of vasopressin.

Adult↗
PubMed1983

Effects of nifedipine on ventilation/perfusion matching in primary pulmonary hypertension.

The effects of nifedipine on hemodynamics and pulmonary gas exchange were investigated in two patients with primary pulmonary hypertension. After 20 mg of the drug taken sublingually, pulmonary and systemic vascular resistances decreased, cardiac output increased, and blood oxygenation was improved. As assessed by the multiple inert gas elimination technique, nifedipine induced a deterioration in ventilation/perfusion (VA/Q) relationships consisting in an increased perfusion of units with low VA/Q. In spite of this negative effect on gas exchange, arterial PO2 increased as a consequence of increased mixed venous PO2 in relation to an augmented cardiac output, and in one patient there was a decrease in the secondary atrial shunt. Both patients were clinically improved by the nifedipine as a long-term treatment.

Female↗
PubMed1983

Improvement in ventilation-perfusion matching by almitrine in COPD.

Almitrine, a peripheral chemoreceptor stimulating drug, was given 100 mg orally to six patients with advanced chronic obstructive pulmonary disease (COPD), and its effects on hemodynamics, blood gases, lung mechanics, and the distribution of ventilation/perfusion ratios (VA/Q), determined by the inert gas elimination technique, were investigated. Arterial Po2 increased from 52 +/- 4 to 59 +/- 3 mm Hg, mean +/- SEM, p less than 0.01, arterial Pco2 decreased from 46 +/- 3 to 43 +/- 3 mm Hg, p less than 0.05, and venous admixture from 30 +/- 6 to 19 +/- 3 percent, p less than 0.02. No change occurred in ventilation, variables of lung mechanics, systemic and pulmonary hemodynamics, except an increase in pulmonary vascular resistance (from 364 +/- 103 to 438 +/- 99 dyne.s.cm-5, p less than 0.05). A reduction in VA/Q inequality could be demonstrated with a redistribution of blood flow into the lungs by a diversion of 15 percent of total blood flow from units with low VA/Q (between 0.08 and 0.4) to units with normal VA/Q (between 0.5 and 1.8). These changes might be explained by an enhancement of hypoxic pulmonary vasoconstriction. Pharmacologic peripheral chemoreceptor stimulation, at an infra-ventilatory analeptic dosage, might be of therapeutic interest to patients with respiratory insufficiency due to VA/Q inequality.

Administration, Oral↗
PubMed1983

Beneficial effects of almitrine bismesylate on pulmonary gas exchange in COPD.

Almitrine bismesylate 100 mg orally was given to eight patients with severe chronic obstructive pulmonary disease (COPD). In five patients, gasometric, haemodynamic and lung mechanics parameters, and almitrine plasma levels were measured at baseline and every hour up to five hours after almitrine bismesylate intake. Maximal almitrine plasma levels were reached after 2 hours (89 +/- 41 ng/ml, mean +/- SEM) and persisted up to the fifth hour (68 +/- 25 ng/ml). Pulmonary vascular resistance increased significantly from baseline 433 +/- 120 dynes.s.cm-5 to 503 +/- 124, p less than 0.05 at the second hour and to 509 +/- 119, p less than 0.05 at the fifth hour. Arterial oxygen saturation increased significantly from baseline 81.7 +/- 4.9% to 84.5 +/- 5.0, p less than 0.05 at the second hour and to 84.5 +/- 4.6, p less than 0.05 at the fifth hour. Venous admixture decreased significantly from baseline 35 +/- 9% to 30 +/- 9, p less than 0.05 at the second hour and to 28 +/- 9, p less than 0.01 at the fifth hour. Pulmonary artery mean pressure, cardiac output and minute ventilation did not change. The continuous distributions of ventilation-perfusion ratios (VA/Q), using the multiple inert gas elimination technique, were determined in six patients, at baseline and two hours after almitrine bismesylate intake. An improvement in VA/Q matching was observed after almitrine with a diversion of an average of 15 per cent of total blood flow from hypoxic units (VA/Q between 0.08 and 0.4) to normoxic units (VA/Q between 0.5 and 1.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1982

Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis.

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.

Adult↗
PubMed1982

Reduction in pulmonary hypertension by prostaglandin E1 in decompensated chronic obstructive pulmonary disease.

Prostaglandin E1 (PgE1) was administered intravenously to 26 patients with decompensated chronic obstructive pulmonary disease (COPD) in order to investigate the effects on hemodynamics and blood gases of a reduction in pulmonary hypertension in this condition. In the first 10 patients, PgE1 at 0.02 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 20 and 7%, increased cardiac index (CI) and oxygen delivery to the tissues (TO2), and did not affect blood gases. In the next 9 patients, PgE1 at 0.04 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 24 and 14%, increased CI and TO2, slightly decreased arterial oxygenation, and did not affect mixed venous blood gases. Side effects, consisting in facial flush, headache, and malaise occurred in 4 of these patients. In the last 7 patients who were artificially ventilated, PgE1 at 0.02 microgram/kg/min increased CI and TO2 but had no effect on vascular pressures and blood gases. Prostaglandin E1 was also given intravenously to 7 healthy subjects breathing 12.5% O2 in N2 for 10 min. Hypoxic pulmonary vasoconstriction was not inhibited by PgE1, even at the highest dosage of 0.04 microgram/kg/min, which caused a flush of the skin, headache, and malaise in all the subjects. Infusion of PgE1 reduces the pulmonary hypertension secondary to decompensated COPD. At adequate dosage, this effect can be obtained with minimal systemic vasodilation and no alteration in the gas exchange function of the lungs, which may be due to preservation of pulmonary vascular tone adaptation to hypoxia. The vasodilating activity fo PgE1 appears to be blunted during artificial ventilation.

Aged↗
PubMed1982

Effects of vasodilators on hypoxic pulmonary vasoconstriction in normal man.

A reduction of arterial PO2 is generally observed when vasodilators are given to patients with cardiac or pulmonary disease. This has been attributed to a release of preexisting hypoxic pulmonary vasoconstriction (HPV). We investigated the effects of hemodynamics and blood gases of IV nitroglycerin, IV nitroprusside and sublingual nifedipine, at dosages currently used in clinical practice, in 23 healthy volunteers at normoxic conditions (fraction of inspired O2, FIO2 0.21) and at acute inspiratory hypoxia (FIO2 0.125 during 10 min). Breathing FIO2 0.125 elicited pulmonary vasoconstriction in all the subjects. At FIO2 0.21, nitroglycerin reduced preload, nifedipine reduced afterload, nitroprusside had balanced effects, but none of the drugs induced pulmonary vasodilation and only nitroglycerin deteriorated arterial oxygenation. At FIO2 0.125, nitroglycerin did not at all affect the pulmonary pressor response, while both nitroprusside and nifedipine decreased it. An inhibition of HPV was obtained with certainty in only one subject who received nitroprusside. In all the subjects in whom HPV was partially inhibited by vasodilator administration, the alveolar-arterial PO2 gradients remained significantly lowered, suggesting that the pulmonary vascular tone adaptation to alveolar hypoxia still was effective in improving ventilation/perfusion relationships. The role of impaired HPV in the reduction of arterial PO2 in patients under vasodilator therapy may have to be reevaluated.

Adult↗
PubMed1981

Oxygen delivery in acute exacerbation of chronic obstructive pulmonary disease. Effects of controlled oxygen therapy.

The hemodynamic response to controlled oxygen administration was investigated in 35 patients who presented with acute decompensation of chronic obstructive pulmonary disease. Gasometric and hemodynamic data were successively measured under inspiratory fractions in oxygen of 0.21 (room air) and 0.28. Response to oxygen therapy was characterized by a decrease in cardiac output and an increase in oxygen delivery because of a sharp increase in arterial oxygen content. The coefficient of oxygen delivery (oxygen delivery/oxygen consumption) increased in each patient. All these changes were highly significant (p les than 0.001). Somewhat unexpectedly, there was no change in pulmonary artery pressures, so that pulmonary arteriolar resistance even increased (p less than 0.05). Further analysis individualized 2 types of hemodynamic response to oxygen therapy. In 15 patients who presented with severe hypoxemia, oxygen therapy resulted in a significant increase in oxygen delivery without change in cardiac output. By contrast, in 20 patients with moderate hypoxemia, oxygen therapy induced a significant decrease in cardiac output (p less than 0.001) without change in oxygen delivery. Patients in whom cardiac output was unaffected by oxygen administration presented with a lower mixed venous oxygen tension (less than 35 mmHg) and a lower coefficient of oxygen delivery (less than 3.5). This study demonstrated that oxygen therapy does not always increase oxygen delivery in acute decompensation of chronic obstructive pulmonary disease.

Adult↗
PubMed1981

Hypoxic pulmonary vasoconstriction in liver cirrhosis.

Impairment of hypoxic pulmonary vasoconstriction (HPV) is frequently cited as an explanation for the hypoxemia of liver cirrhosis. We investigated the pulmonary and systemic hemodynamic responses to acute inspiratory hypoxia, 12.5 percent oxygen in nitrogen during 10 minutes, in 24 patients with mildly to moderately decompensated liver cirrhosis and arterial hypoxemia. A mean increase of 50 percent in pulmonary vascular resistance (PVR) was observed, which is comparable to reported responses of normal subjects to a similar degree of hypoxia. Seven of the 24 patients showed an increase in PVR of less than 20 percent. Compared with the other patients, no difference could be found between both groups in baseline blood gas and hemodynamic determinations, physical examination, liver function tests, and laboratory tests that may be disturbed by circulating endotoxin. Five of the 24 patients had a hyperkinetic circulatory state, but only one of them failed to increase PVR in response to hypoxia. Considering the whole group of 24 patients, there was no correlation between PaO2, PVR, and PVR response to hypoxia. Impairment of HPV is probably not the right explanation for most cirrhotic patients with arterial hypoxemia.

Adult↗
PubMed1980

Acute pulmonary edema following carbon monoxide poisoning.

This report describes a patient who presented with coma and acute pulmonary edema after severe carbon monoxide poisoning. Hemodynamic evaluation revealed elevated systemic and pulmonary arterial, pulmonary wedge and right atrial pressures, together with an increased cardiac output. These findings are compatible with the hypothesis that a neurogenic mechanism plays a role in the pulmonary edema of carbon monoxide poisoning.

Adult↗
PubMed1980

Chronic alcoholism: a predisposing factor for hypocalcemia in acute pancreatitis.

The serum levels of calcium, corrected for serum albumin, were investigated in 65 consecutive patients with acute pancreatitis. Hypocalcemia was present in 55% of 38 patients in whom chronic alcoholism was the associated etiology, and in 26% of 27 other patients (p less than 0.02). In the alcoholic patients, the mean duration of hypocalcemia was significantly longer than in the non-alcoholic patients (5 vs. 1--2 days; p less than 0.001). The severity of pancreatitis seemed to be comparable in both groups of patients. This suggests that chronic alcoholism may be a predisposing factor for hypocalcemia in acute pancreatitis.

Acute Disease↗
PubMed1979

[Defibrination syndrome during acute pancreatitis: 6 cases. Prospective studies of coagulation in 41 patients (author's transl)].

Studies of coagulation were performed prospectively in 41 patients with mild to moderately severe acute pancreatitis. Six patients (15%) presented with coagulation data suggestive of defibrination; two of them had clinical signs of bleeding. No other cause than pancreatitis was found in these 6 patients to account for coagulation abnormalities. Comparing the patients who presented defibrination to those who did not, no difference was observed in clinical course and admission values of serum amylase, fibrinogen, urea, calcium, glucose, transaminase levels, white blood cell count and arterial partial pressure of oxygen. Platelets counts and serum creatinine levels were respectively lower and higher in the first group of patients.

Acute Disease↗
PubMed1979

Prolactin response to TRH in diabetic ketoacidosis.

The prolactin response to 200 microgram thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis.

Adult↗