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Biomedical subjects

P Mols

Publications and source records attributed to P Mols.

At least 37 records · Page 2Linked to original sources
PubMed1985

High-dose intravenous thrombolytic therapy in acute myocardial infarction: efficiency, tolerance, complications and influence on left ventricular performance.

Ten patients with acute myocardial infarction (AMI) underwent coronarographic studies before, immediately after and ten days after an intravenous infusion of 1 500 000 I.U. streptokinase (STK). Mean time between onset of symptoms to initiation of STK infusion was 03 hours 34 minutes. Occlusion of the infarct-related vessel was present in all of them and successful thrombolysis was obtained in 8 of the patients. Systemic fibrinolytic activity was present in 9 patients, one of whom required a transfusion of blood because of severe bleeding. At ventriculography, the global left ventricular ejection fraction and the regional ventricular ejection fraction, whatever the area involved, showed no significant improvement 10 days after the procedure. This suggests that high-dose intravenous STK in AMI, although causing an effective thrombolysis, does not seem to improve early myocardial function.

Adult↗
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

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

Right atrial thrombus leading to pulmonary embolism.

Cross sectional and M mode echocardiography detected a large right atrial mass in a 70 year old man five days after admission. Three weeks later he developed acute respiratory failure due to a pulmonary embolism. Necropsy showed that the atrial mass was a thrombus. Thus echocardiography should be performed in patients with pulmonary emboli to examine the right cardiac cavities. The need for emergency surgery could then be assessed.

Aged↗
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↗
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

The effective plasma concentrations of sulmazol (AR-L 115 BS) on haemodynamics in chronic heart failure.

Sulmazol (AR-L 115 BS) is a new inotropic drug which has arterial and venous vasodilating properties. We used it in seven patients with severe refractory heart failure to determine the effective plasma concentration levels and the most effective bolus dose on haemodynamics. The haemodynamic monitoring included a Swan-Ganz catheter in the pulmonary artery and a radial catheter. Haemodynamic measurements and plasma concentration determinations were performed before sulmazol injection and at 5, 10 and 30 min after a bolus 0.25, 0.50, 0.75 mg/kg. We observed a gradual increase in cardiac index and decrease in pulmonary wedge pressure when plasma concentration levels rose but the beneficial effects were mainly observed for sulmazol plasma concentrations above 1 microgram/ml. A bolus injection of 0.75 mg/kg was effective in all cases: a significant increase of cardiac index (1.9 to 2.5 1 min-1 m-2; P less than 0.001) and a significant decrease in pulmonary wedge pressure (30 to 25 mm Hg; P less than 0.005) and right atrial pressure (13 to 10 mm Hg, P less than 0.01) were observed. In these patients sulmazol improved the severely deteriorated left ventricular function without affecting heart rate and blood pressure.

Aged↗
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↗
PubMed1982

High uric acid and urea clearance in cirrhosis secondary to increased "effective vascular volume".

Since urea and uric acid clearance are affected by the effective intravascular volume, we measured the fractional urea and uric acid excretion in cirrhosis. High urea and uric acid clearances were observed in 30 and 55 percent, respectively, of 20 consecutive cirrhotic patients with normal renal function. In seven patients with a high fractional uric acid excretion, 5 mg of isosorbide dinitrate every four hours for 24 hours induced a significant increase in the serum uric acid level (from 3.7 +/- 0.8 mg/dl to 4.4 +/- 0.8 mg/dl; less than 0.001) with a concomitant decrease in the fractional uric acid excretion (from 14.0 +/- 3.2 percent to 8.8 +/- 3.1 percent; less than 0.02). During the same test, the blood urea level increased from 3.3 +/- 1.1 mmol/liter to 4.1 +/- 1.2 mmol/liter (p less than 0.005) with a decrease in fractional excretion from 51 +/- 4.5 percent to 39 +/- 5 percent (p less than 0.001). The oral intake of sulfinpyrazone in six of these patients induced a normal uricosuric response. In two cirrhotic patients with ascites, 40 mg of furosemide associated with a 24-hour severe water restriction was also shown to normalize the high fractional excretion of both urea and uric acid. In nine patients with ascites, we observed a significant increase in blood urea and uric acid concentration despite the absence of change in creatinine clearance once ascites was removed by diuretics. On the basis of these findings, we believe that the high fractional excretion of both urea and uric acid frequently observed in cirrhosis is related to an increase in the effective vascular volume.

Blood Volume↗
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↗