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Biomedical subjects

H Leinberger

Publications and source records attributed to H Leinberger.

At least 19 recordsLinked to original sources
PubMed1992

Baroreceptor-mediated release of vasopressin in patients with chronic congestive heart failure and defective sympathetic responsiveness.

In patients with congestive heart failure (CHF), overactivity of the sympathetic nervous system may be accompanied by an impairment of the baroreflex control mechanism. To evaluate the reflex responses of the sympathetic nervous system, the renin-angiotensin system and vasopressin release to baroreceptor unloading, 38 patients with left ventricular dysfunction were studied. Hemodynamic data, and plasma norepinephrine, renin activity and vasopressin concentrations were measured before and 60 minutes after administration of high-dose hydralazine (0.4 mg/kg intravenously). On the basis of blood pressure response to vasodilator administration, patients were divided arbitrarily into those with a decrease in mean arterial blood pressure greater than or equal to 15 mm Hg (group A; n = 12) and those with a decrease less than 15 mm Hg (group B; n = 26) compared with control values. In response to hydralazine, heart rate decreased in group A from 100 to 92 beats/min (p less than 0.001) and increased in group B from 90 to 96 beats/min (p less than 0.05). In group A, hemodynamic changes induced by hydralazine were accompanied by a decrease in plasma norepinephrine from 822 to 518 pg/ml (p less than 0.01) and an increase in plasma vasopressin from 8.4 to 45.2 pg/ml (p less than 0.001). In group B, plasma norepinephrine and vasopressin did not change significantly (407 vs 447, and 8.4 vs 8.3 pg/ml, respectively). Plasma renin activity remained unchanged in group A and increased in group B (p less than 0.001). The data show that baroreceptor-mediated release of vasopressin is not impaired in patients with CHF and a defective sympathetic reflex control mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Acute and chronic effects of low dose almitrine bismesylate in the treatment of chronic bronchitis and emphysema.

OBJECTIVES: Study of the acute and chronic effects of low-dose almitrine therapy in stable hypoxaemic patients with chronic bronchitis and emphysema. METHODS: A low daily dose of 75 mg almitrine bismesylate was administered for six months in 23 patients with chronic bronchitis and emphysema. Nine patients (group 1) were placed on oral almitrine bismesylate 25 mg t.i.d. after they had received a single intravenous dose of 60 mg almitrine three months earlier. Fourteen additional patients, seven receiving almitrine (group 2) and seven placebo (group 3) were randomized for a 6 month double-blind evaluation of both acute and chronic effects of 75 mg almitrine on pulmonary gas exchange and on pulmonary haemodynamics. All patients were followed-up with regular measurements of blood gases, body plethysmography and with evaluation of peripheral nerve function. RESULTS: Acute effects of almitrine were a significant increase in arterial oxygen tension by 14 mmHg after intravenous (p < 0.001) and by 15 mmHg after oral administration (p < 0.001), amelioration of hypercapnia, a slight transient increase in mean pulmonary artery pressure from 26 +/- 7 to 29 +/- 6 mmHg (NS) and a decrease of shunt due to improvement in ventilation/perfusion mismatching. In contrast, no acute changes in blood gases and pulmonary pressures were seen in the placebo group. A combination of almitrine with oxygen (8-10 L/min) was most effective in amelioration of hypoxaemia and shunt. With chronic almitrine therapy, the improvements in gas exchange persisted without elevation of pulmonary artery pressure (26 +/- 8 mmHg), whereas a negative trend in change of blood gases and pulmonary artery pressure occurred in the placebo treated group (NS). No significant changes in external ventilation, other spirometric parameters or adverse effects concerning peripheral nerve function were seen after almitrine or placebo treatment. The elimination of almitrine was fitted to a three compartment model and the terminal half-life in the patient population was found to be 32 +/- 29 days after intravenous dosing. CONCLUSION: Acute and six-month almitrine bismesylate therapy at a low daily dose of 75 mg is found to be safe, even in severely compromised patients, with regard to pulmonary haemodynamics and peripheral nerve function. The agent is beneficial to pulmonary gas exchange, with reduction of hypercapnia, of intrapulmonary shunt and also with regard to sustained elevation of arterial oxygen tension. A combination with inhaled oxygen seems especially efficacious.

Aged↗
PubMed1988

[Steroid-refractory amiodarone-induced pulmonary fibrosis. Clinical features and morphology after an amiodarone-free interval of 3 months].

Amiodarone-induced bilateral diffuse pulmonary fibrosis developed in a 47-year-old woman with idiopathic hypertrophic subvalvular aortic stenosis who had been treated with amiodarone (Cordarex), 300 mg daily for about 18 months. Although the drug was discontinued and cortisone treatment begun, the pulmonary fibrosis did not regress. When gentamicin (Refobacin) and cefotaxime (Claforan) were administered for suspected fibrosis-induced right-sided bronchopneumonia, gentamicin-induced acute tubular renal damage occurred, requiring dialysis. The patient died soon after of myocardial electro-mechanical dissociation. At necropsy there was, in addition to the idiopathic hypertrophic subvalvular cardiomyopathy, extensive bilateral pulmonary fibrosis, lamellar bodies in foam-cell intraalveolar macrophages, in hepatocytes and in the epithelium of the proximal and distal tubules. Although amiodarone had been discontinued three months previously, high concentrations of the drug were still present, especially in both lungs, fat tissue and the liver.

Adipose Tissue↗
PubMed1988

Isometric exercise for the evaluation of vasodilatory therapy in severe congestive heart failure.

There are few data available about the hemodynamic effects of isometric handgrip in severe congestive heart failure and its role in the evaluation of vasodilatory therapy. Therefore, we studied 20 patients with dilated cardiomyopathy at rest, during isometric handgrip, and during supine bicycle exercise before and after a single 25-mg dose of captopril. During handgrip, heart rate (p less than 0.001); systemic vascular resistance (p less than 0.01); systolic, mean, and diastolic pulmonary artery pressure (p less than 0.01) increased significantly; stroke volume index fell (p less than 0.05); whereas mean arterial pressure showed only a small increase, and cardiac index did not change. In contrast, mean arterial pressure and cardiac index increased during dynamic exercise (p less than 0.001), and peripheral resistance decreased (p less than 001). During both handgrip and bicycle exercise, captopril induced a decrease of arterial pressure (p less than 0.01 and p less than 0.001; respectively), peripheral resistance (p less than 0.001 and p less than 0.01; respectively), and systolic (p less than 0.01 and p less than 0.001, respectively) mean (p less than 0.001), and diastolic pulmonary artery pressure (p less than 0.001). Captopril induced and increase in stroke volume index (p less than 0.01) and cardiac index (p less than 0.001 and p less than 0.01 respectively) during both types of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Life-threatening flecainide toxicity. A pharmacodynamic approach.

Ventricular tachyarrhythmias and severe bradycardia, flecainide acetate's most serious side effects, occur in patients with chronic heart disease or in healthy persons after frank overdose. Toxic effects appear to correlate closely with drug levels in plasma. The surface electrocardiogram can indicate toxicity by demonstrating this drug's electrophysiologic potency to depress all major cardiac conduction pathways with marked prolongation of the PR and QRS intervals. We report the clinical course of a young, healthy person who developed polymorphous ventricular tachycardia after taking a 3800-mg dose of flecainide acetate. Sinus rhythm was restored without pacing or cardioversion after infusion of a beta-sympathomimetic agent, physostigmine, and a sodium load. The initial flecainide serum levels were five times greater than the usual upper therapeutic level. Electrocardiography showed that the lengthened electrocardiographic time intervals decreased in correlation with falling drug levels. Flecainide-associated life-threatening arrhythmias and available therapeutic interventions are discussed.

Adult↗
PubMed1986

Pulmonary pressure-flow relation after trauma and hemorrhagic shock.

The significance of pulmonary pressure-flow relation and its correlation to alveolar dead space and histological lesions of the lung were evaluated in ten mongrel dogs, which were subjected to standardized bone trauma and hemorrhagic hypotension at 40 mm Hg for 3h. These results were compared with those of 5 control dogs without trauma and shock. Two different pressure-flow curves were obtained by consecutive measurements of cardiac output and mean pulmonary artery pressure during stepwise arterial hemorrhage and reinfusion. In each experiment, the difference between the two curves at CO of 100 ml/kg min was obtained and represents an increase in pulmonary artery pressure (delta MPP). This increase in pulmonary artery pressure is flow-independent and, therefore, can be used as a quantitative indicator of pulmonary vasoconstriction or vascular obstruction. Severity of shock (uptake) as well as grade of early histological lesions of the lung (microthrombi, edema, hemorrhage) and increased alveolar dead space after reinfusion were associated with a more pronounced shift of the pulmonary pressure-flow curve. In severe experimental shock, therefore, a consistent pattern of pulmonary hemodynamics, lung histology, and respiratory function was demonstrated by the pulmonary pressure-flow relation. This approach permits estimation of the effects of therapeutic interventions and may be suitable for assessing postshock pulmonary impairment.

Animals↗
PubMed1984

[Left ventricular function and activity of vasoconstrictor systems in patients with chronic heart insufficiency].

An increased activity of vasoconstrictor mechanisms may play an important role in circulatory adjustments to heart failure. Thus, hemodynamic data and the plasma hormones epinephrine (E), norepinephrine (NE) and arginin vasopressin (AVP) as well as the plasma renin activity (PRA) were assessed in 50 patients undergoing coronary angiography and right heart catheterization. Patients were classified into three groups according to severity of left ventricular (LV) dysfunction as assessed by ejection fraction (LVEF): those with normal left ventricular function (group 1 (n = 12): LVEF greater than or equal to 55%, mean 70 +/- 3%) and those with moderate (group 2 (n = 16): LVEF 54-35%, mean 43 +/- 2%) or severe LV dysfunction (group 3 (n = 22): LVEF less than 35%, mean 22 +/- 1%). At rest plasma NE concentrations in patients with heart failure (group 2: 187 +/- 17 pg/ml; group 3: 299 +/- 27 pg/ml) did not differ significantly from control values (199 +/- 26 pg/ml). During exercise, NE concentrations increased in all patients (p less than 0.001). This increase in plasma NE was more pronounced in group 3 (753 +/- 71 pg/ml) than in group 1 (262 +/- 37) and group 2 (388 +/- 64). A significant inverse correlation was found between plasma NE and stroke index at rest (r = -0.592, p less than 0.001) as well as during exercise (r = -0.659, p less than 0.001). PRA was elevated at rest and during exercise in patients of group 3 but not of group 2 as compared with control patients (p less than 0.05). Plasma E and AVP were similar in all groups. Patients of group 3 were subdivided according to exercise capacity into patients who tolerated a maximum work load of 50 watts or more (group 3A) and those who did not tolerate a work load exceeding 25 watts (group 3B). At rest and during exercise, patients of group 3A had a higher stroke index than patients of group 3B. In contrast, there was no significant difference in LVEF between group 3A and 3B (22 +/- 2 vs 20 +/- 1%). During exercise patients with low exercise capacity (group 3B) had higher NE levels than patients with less impaired exercise capacity (group 3A) (948 +/- 86 vs 590 +/- 65 pg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1982

Dose-dependent haemodynamic response to prenalterol in patients with congestive heart failure.

The effect of three doses of prenalterol, 12.5, 25 and 50 micrograms, on cardiac index (CI), pulmonary artery pressure (PAP), heart rate (HR), and stroke volume index (SVI) was investigated in 18 patients with congestive heart failure (CHF). Twelve patients received only prenalterol, while 6 patients received prenalterol 1 hour after an oral dose of hydralazine and isosorbid dinitrate. In 7 out of 12 patients a dose-dependent increase in HR was observed. The response of HR was inversely correlated to resting catecholamine levels; patients with high resting catecholamines--these are patients with severe CHF--did not show any increase in HR. CI increased in 8 out of 12 patients (average 1 . 1/min m) and SVI in 5 out of 12 patients. This inconsistent response was not dependent on left ventricular ejection fraction or plasma catecholamines at rest. Pretreatment with vasodilators did not improve the haemodynamic response to prenalterol. Four out of 17 patients demonstrated an increase in severity of arrhythmias suggestive of arrhythmogenic properties of prenalterol.

Administration, Oral↗
PubMed1982

[Pretreatment with heparin in experimental trauma and haemorrhagic shock].

A severe shock is produced in 18 mongrel dogs by standardized bone trauma and haemorrhagic shock. Impairment of microcirculation is demonstrated by acidosis, reduced oxygen uptake and disseminated intravascular coagulation (DIC). Further, a specific increase in pulmonary vascular resistance--independent of the reduction in blood flow--is evoked, concomitantly with the occurrence of microthrombi, oedema and haemorrhage in lung tissue. Pretreatment with heparin inhibits disseminated intravascular coagulation and reduces impairment of microcirculation and the consecutive damage of intestinal organs. However increase of pulmonary vascular resistance is unchanged and pulmonary haemorrhage is pronounced. Therefore heparin pretreatment enhances pulmonary histologic impairment after trauma and haemorrhagic shock.

Acidosis↗
PubMed1979

Microcirculation of the epimyocardial layer of the rat heart: no recruitment after hypoxia.

1. In vivo microscopic studies of the microcirculation of the beating mammalian heart are accomplished by use of small needles connected to the operation table, restricting excessive movement of the cardiac surface. 2. Fluorescence microscopic techniques combined with a highly sensitive TV tape system, enable to determine microvascular diameters, intercapillary distances, as well as directions and velocities of capillary flow in the epimyocardial layer of the mammalian heart. 3. During acute hypoxia, no recruitment of previously resting capillaries could be observed. 4. The capillary flow pattern of the epimyocardial layer reveals a mixed countercurrent system.

Animals↗
PubMed1976

[Pulmonary hemodynamics, coagulation and morphological changes in the lung after thrombocyte aggregation inhibition and intravasal coagulation in experimental trauma and hemorrhagic shock].

26 mongrel dogs are subjected to a standardized bone trauma followed by a hypotonic hemorrhagic shock. Compared with a control and heparin group prophylactic treatment with Dipyridamol and Acetylsalicylic Acid decreases pulmonary vascular resistance significantly. After an initial period of hyperocagulability secondary fibrinolysis develops. The decrease of the fibrinogen level and the fall of total platelet count after trauma and hemorrhage can partly be prevented by the application of heparin, likewise the development of pulmonary microthrombosis. Histological examination shows a markedly diminished pulmonary microthrombosis.

Airway Resistance↗
PubMed1975

[Significance of intravascular coagulation and acidosis on increase of pulmonary vascular resistance following trauma and hemorrhagic shock].

24 anesthetized mongrel dogs are subjected to a standardized trauma followed by a hypotonic hemorrhagic shock. Compared with the control group (n equals 8) prophylactic treatment with heparin in the second group (n equals 8) reduces the rise of pulmonary vascular resistance only insignificantly. The correction of the metabolic acidosis with Tris does not prevent a rise of PVR in third group (n equals 8).

Acidosis↗