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Biomedical subjects

J Lonsdorfer

Publications and source records attributed to J Lonsdorfer.

At least 19 recordsLinked to original sources
PubMed1999

Lung membrane diffusing capacity, heart failure, and heart transplantation.

The pulmonary diffusing capacity for carbon monoxide (DLCO) is reduced in chronic heart failure and remains decreased after heart transplantation. This decrease in DLCO may depend on a permanent alteration after transplantation of one or the other of its components: diffusion of the alveolar capillary membrane or the pulmonary capillary blood volume (Vc). Therefore, we measured DLCO, the membrane conductance, and Vc before and after heart transplantation. At the time of hemodynamic measurements, the Roughton and Forster method of measuring DLCO at varying alveolar oxygen concentrations was used to determine the membrane conductance, Vc, DLCO/alveolar volume (VA), the membrane conductance/VA and thetaVc/VA (theta = carbon monoxide conductance of blood, VA = alveolar volume) in 21 patients with class III to IV heart failure before and after transplantation, and in 21 healthy controls. Transplantation normalized pulmonary capillary pressure and increased cardiac index. DLCO was decreased before transplantation (7.11 vs 10.0 mmol/min/kPa in controls), but DLCO/VA was normal (1.67+/-0.44 vs 1.71+/-0.26 mmol/min/kPa/L in controls). DLCO/VA remained unchanged after transplantation, because the decrease in Vc (82+/-30 vs 65+/-18 ml before and after transplantation) and thetaVc/VA was not compensated by the changes in membrane conductance (11+/-4 vs 12+/-5 mmol/min/kPa before and after transplantation, respectively) and membrane conductance/VA. We conclude that the decrease in DLCO in patients with chronic heart failure is due to a restrictive ventilatory pattern because their DLCO/VA remains normal; the decrease in the membrane conductance is compensated by the increase in Vc. After transplantation, the decrease in Vc due to normalization of pulmonary hemodynamics is not completely compensated for by an increase in membrane conductance. Because the membrane conductances, measured before and after transplantation, are negatively correlated with duration of heart failure, its abnormal pulmonary hemodynamics may have irreversibly altered the alveolar capillary membrane.

Adult↗
PubMed1999

Circulating adrenomedullin is increased after heart transplantation.

OBJECTIVE: Adrenomedullin (ADM), secreted by the failing human heart, is a newly discovered potent endogenous vasorelaxing and natriuretic peptide that may play a role in cardiorenal regulation. No data are available on ADM in heart-transplant recipients (Htx) and the aim of this study was to determine the short- and long-term responses of ADM after heart transplantation. METHODS: Circulating ADM and its relationship with parameters of cardiovascular hemodynamics, humoral factors and renal function were determined in normal subjects and Htx early (1, 2, 4, 8, 15 and 30 days) and late (32 +/- 16 months) after transplantation. Additionally, ADM was obtained in matched hypertensive and renal-transplant patients (n = 9 in each group). RESULTS: Plasma ADM, elevated in heart failure patients, further increased transiently at day 1 after transplantation (from 37.9 +/- 15.9 to 125.8 +/- 15.3 pmol/l, P < 0.01) and, although decreasing thereafter, remained elevated until the 30th day after transplantation (52.1 +/- 25.2 pmol/l). Late after transplantation. ADM concentrations were still increased compared to normal values (31.3 +/- 5.3 vs. 19.4 +/- 2.7 pmol/l, P < 0.001). ADM positively correlated with endothelin, atrial natriuretic peptide (ANP) and cyclosporine. ADM was also correlated with increased diastolic (r = 0.68, P < 0.04) and systolic (r = 0.66, P < 0.05) blood pressure in late Htx. No relationship was observed between ADM and left ventricular mass index, aldosterone and creatinine. ADM elevation was similar in hypertensive, renal-transplant patients and in Htx. CONCLUSIONS: Circulating ADM is increased after heart transplantation, in relation to hypertension, endothelin, cyclosporine and ANP. In view of ADM's biological properties, these results might suggest a compensatory role for ADM against further development of vasoconstriction and fluid retention states after heart transplantation.

Adrenomedullin↗
PubMed1999

Enhanced natriuretic response to neutral endopeptidase inhibition in heart-transplant recipients.

Heart-transplant recipients (Htx) generally present with body fluid and sodium handling abnormalities and hypertension. To investigate whether neutral endopeptidase inhibition (NEP-I) increases endogenous atrial natriuretic peptide (ANP) and enhances natriuresis and diuresis after heart transplantation, ecadotril was given orally to 8 control subjects and 8 matched Htx, and levels of volume-regulating hormones and renal water, electrolyte, and cyclic guanosine monophosphate (cGMP) excretions were monitored for 210 minutes. Baseline plasma ANP, brain natriuretic peptide (BNP), and cGMP were elevated in Htx, but renin and aldosterone, like urinary parameters, did not differ between groups. NEP-I increased plasma ANP (Htx, 20.6+/-2.3 to 33.2+/-5.9 pmol/L, P<0.01; controls, 7.7+/-1. 2 to 10.6+/-2.6 pmol/L) and cGMP, but not BNP. Renin decreased similarly in both groups, whereas aldosterone decreased significantly only in Htx. Enhanced urinary sodium (1650+/-370% versus 450+/-150%, P=0.01), cGMP, and water excretions were observed in Htx and urinary cGMP positively correlated with natriuresis in 6 of the Htx subjects. Consistent with a normal circadian rhythm of blood pressure, without excluding a possible effect of NEP-I, mean systemic blood pressure increased similarly in both groups at the end of the study (6.9+/-2.0% versus 7.4+/-2.8% in controls and Htx). Thus, systemic hypertension, mild renal impairment, and raised plasma ANP levels are possible contributory factors in the enhanced natriuresis and diuresis with NEP-I in Htx. These results support a physiological role for the cardiac hormone after heart transplantation and suggest that long-term studies may be useful to determine the potential of NEP-I in the treatment of sodium retention and water retention after heart transplantation.

Adult↗
PubMed1998

Skeletal muscle response to short endurance training in heart transplant recipients.

OBJECTIVES: We sought to examine the effects of endurance training on the ultrastructural characteristics of skeletal muscle in heart transplant recipients (HTRs) and age-matched control subjects (C). BACKGROUND: Deconditioning is one of the factors involved in the peripheral limitation of exercise capacity of HTRs, and training has proven to be beneficial. METHODS: Biopsies of the vastus lateralis muscle, analyzed by ultrastructural morphometry, and quadriceps muscle cross-sectional area, assessed by computed tomography (CT), were performed in 12 HTRs and 7 age-matched C before and 6 weeks after an endurance training program. Maximal oxygen uptake (peak VO2) was determined by an incremental exercise test. Additionally muscle biopsies were performed before and after a 6-week control period in four HTRs to check for spontaneous improvement. RESULTS: Training resulted in similar increases in peak VO2 (11% in HTRs, 8.5% in C), ventilatory threshold (23% in HTRs, 32% in C) and total endurance work (54% in HTRs, 31% in C). Volume density of total mitochondria increased significantly (26% in HTRs, 33% in C) with a predominant increase of subsarcolemmal mitochondrial volume density (74% in HTRs, 70% in C). The capillary/fiber ratio increased by 19% in C only. In the nontrained group, none of the structural markers was spontaneously modified. CONCLUSIONS: Six weeks of endurance training in HTRs and C led to similar improvements of aerobic work capacity. However, the decreased muscular capillary network in HTRs remained unchanged with training. Immunosuppressive therapy might be responsible for the discrepancy between the normal mitochondrial content and the reduced capillary supply of these patients.

Adult↗
PubMed1998

Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients.

We investigated the atrial (ANP) and brain natriuretic peptides (BNP), catecholamines, heart rate, and blood pressure responses to graded upright maximal cycling exercise of eight matched healthy subjects and cardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP (15.2 +/- 3.7 vs. 4.4 +/- 0.8 pmol/l; P < 0.01) and BNP (14.3 +/- 2. 6 vs. 7.4 +/- 0.6 pmol/l; P < 0.01), were elevated in HTR, but catecholamine levels were similar in both groups. Peak exercise O2 uptake and heart rate were lower in HTR. Exercise-induced maximal ANP increase was similar in both groups (167 +/- 34 vs. 216 +/- 47%). Enhanced BNP increase was significant only in HTR (37 +/- 8 vs. 16 +/- 8%; P < 0.05). Similar norepinephrine but lower peak epinephrine levels were observed in HTR. ANP and heart rate changes from rest to 75% peak exercise were negatively correlated (r = -0.76, P < 0.05), and BNP increase was correlated with left ventricular mass index (r = 0.83, P < 0.01) after heart transplantation. Although ANP increase was not exaggerated, these data support the idea that the chronotropic limitation secondary to sinus node denervation might stimulate ANP release during early exercise in HTR. Furthermore, the BNP response to maximal exercise, which is related to the left ventricular mass index of HTR, is enhanced after heart transplantation.

Adult↗
PubMed1998

Effect of lung volume reduction surgery on gas exchange and pulmonary hemodynamics at rest and during exercise.

Lung volume reduction surgery (LVRS) has become an extended surgery for emphysema in order to improve the dyspnea of severely affected patients. Because resection of lung areas may reduce the vascular bed, which is an important factor of pulmonary hypertension in emphysematous patients, especially during exercise, the aim of our study was to assess the outcome of pulmonary hemodynamics and gas exchange at rest and during exercise after LVRS. Nine patients had right heart catheterization before and 3 to 12 mo (mean, 4.5 mo) after LVRS. FEV1 increased from 705 to 1,005 ml (p < 0.05) after LVRS. PaO2, PaCO2 and mean pulmonary artery pressure (Ppa) did not change after LVRS, either at rest or during exercise. However, a significant overall decrease of the respiratory swings of the pulmonary artery diastolic pressure (DeltaPd) at rest (median value, from 12 to 8 mm Hg, p < 0.01) and during exercise (from 20 to 15 mm Hg, p < 0.05) was observed. There was a significant correlation between the change in resting Ppa (Ppa before minus Ppa after LVRS) and the change in resting DeltaPd (r = 0.73, p < 0.03), and also between the change in exercising Ppa and the change in resting DeltaPd (r = 0.80, p < 0.02). Significant correlations were also found between the change in exercising Ppa and the change in exercising PaO2 (r = -0.70, p < 0.05), and between the change in exercising Ppa and the change in exercising PaCO2 (r = 0.76, p < 0. 03). We conclude that pulmonary hemodynamics in most cases are not impaired by LVRS either at rest or during exercise. The possible mechanisms influencing hemodynamics after a lung volume reduction procedure are discussed.

Adult↗
PubMed1997

Moderate endurance training has no effect on the parathyroid function of heart transplant patients.

The benefit of retraining for heart transplant recipients (HTR) is now well established. The rehabilitation of these patients can be compromised by osteopenia and bone fractures. The resting levels of parathyroid hormone (PTH) and exercise-induced increases are higher in HTR than in healthy controls. To evaluate the effect of a moderate endurance training programme on parathyroid activity, six HTR, an average of 18 months after transplant, and seven healthy sedentary controls have been studied. None of the subjects had a history of bone disease. Two exercise tests (square wave endurance exercise tests, SWEET) with identical work rates were performed before and after training. Intact PTH, ionized calcium (Ca2+), phosphorus (Pi) and pH were measured at rest, during exercise and in the recovery periods. Training consisted of a 45-min SWEET three times a week for 6 weeks. Levels of Ca2+, Pi and PTH showed a significant increase during the exercise session in both groups. Ca2+ and Pi levels decreased rapidly after the cessation of exercise whereas PTH reached a peak at the 10th min of the recovery in both groups. This increase in PTH was significantly higher in HTR than in controls. However, despite a significant improvement of total endurance work (+ 28% in HTR, +29% in controls) this endurance training had no effect on resting levels of PTH, plasma Ca2+ or Pi, nor on their exercise-induced variations. The exercise-induced decrease in pH was less pronounced after training which is evidence of training. We conclude that a short endurance training programme does not alter the moderate hyperparathyroidism of HTR. The effect of such a training programme on bone mass and bone mineral density needs now to be evaluated.

Acid-Base Equilibrium↗
PubMed1996

Effect of short-term endurance training on exercise capacity, haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients.

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ.kg-1 (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats.min-1 (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol.l-1 (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg.ml-1. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg.ml-1 vs 116.0 (SEM 13.5) pg.ml-1 and 200.0 (SEM 23.0) pg.ml-1 vs 206.5 (SEM 25.9) pg.ml-1, respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.

Adult↗
PubMed1996

The concept of Raynaud's phenomenon of the lung revisited.

PURPOSE: Having observed that a cold pressor test (CPT) induces a decrease in carbon monoxide single breath diffusing capacity (DLco) in normal subjects contrary to the findings of Fahey et al (Am J Med. 1984; 76:263-269), we compared the response to CPT for the two types of Raynaud's phenomenon. PATIENTS: Two groups of 8 patients suffering from primary or secondary Raynaud's phenomenon were examined. METHODS: Single breath diffusing capacity, mean pulmonary artery pressure (PAP), cardiac output (CO), pulmonary capillary wedge pressure (PwP), and pulmonary vascular resistance (PVR) were measured before and 30 minutes after CPT, which consisted of immersing both hands in a water bath at 12 degrees C for 2 minutes. RESULTS: Cold pressor testing induced no change in DLco or cardiovascular parameters in patients with secondary Raynaud's phenomenon. Conversely, in patients with the primary form, it induced a significant decrease in DLco (16%), PAP (20%), and PVR (27%), whereas CO and PwP remained unaltered. CONCLUSIONS: The concept of pulmonary Raynaud's phenomenon had to be reconsidered, as it is also observed in normal subjects, and is due to a vasodilatation and not to a vasoconstriction of the pulmonary artery (Frans et al, J Appl Physiol. 1994; 76:750-755). In patients with primary Raynaud's phenomenon, the decrease in DLco is not only a physiological response, but a pathological response to a CPT, as it is significantly more marked in patients than in control subjects (16% versus 10% for controls, same reference). The contribution by Fahey et al remains important, however, in that it allows assessing whether a patient with Raynaud's phenomenon suffers from the primary or secondary form of the disease.

Adult↗
PubMed1996

Structure of skeletal muscle in heart transplant recipients.

OBJECTIVES: This study sought to define the ultrastructural characteristics of skeletal muscle in heart transplant recipients (HTRs) in relation to exercise capacity compared with that in age-matched control subjects. BACKGROUND: Muscle structural features seem to play an important role in the limitation of exercise capacity of HTRs long after transplantation. METHODS: The structure of the vastus lateralis muscle was analyzed by ultrastructural morphometry in 16 HTRs and 20 healthy control subjects. Maximal oxygen consumption (peak Vo2) was determined by an incremental exercise test. RESULTS: Peak Vo2 was significantly lower (by 35%) in HTRs. Fiber size, volume density of mitochondria and intramyocellular lipid deposits were not significantly different between HTRs and control subjects. In contrast, the capillary density and the capillary/fiber ratio were both significantly reduced in HTRs (by 24% and 27%, respectively). CONCLUSIONS: A normal volume density of mitochondria and a reduced capillary network are the main characteristics of muscle ultrastructure in HTRs by 10 months after transplantation. The muscle structural abnormalities and reduced exercise capacity might be related to immunosuppressive therapy with cyclosporine and corticosteroids as well as deconditioning.

Adult↗
PubMed1996

Persistent exercise intolerance following cardiac transplantation despite normal oxygen transport.

UNLABELLED: To define the respective roles of the periphery and central oxygen transport in the exercise limitation of heart transplanted patients (HTR), we compared 11 HTR (15.1 +/- 10.8 months after transplantation) to six age and weight matched normal controls (C), during an incremental exercise test (30 W/3 min steps; supine position), up to peak exercise level. The C stopped between 120 and 240 W (mean = 180 +/- 39 W), whereas the HTR all reached 90 W, with a significantly lower oxygen uptake (VO2), cardiac index (CI) and arterio-venous oxygen difference (AVO2D) values (respectively VO2: 16.6 +/- 2.6 vs 30.0 +/- 9.3 ml.min-1.kig-1 STPD; CI: 6.84 +/- 1.10 vs 10.55 +/- 2.86l.min-1.m-2; AVO2D: 94 +/- 13 vs 109 +/- 9 ml.l-1; all p < 0.05) but with similar lactate (LA) values (respectively 7.25 +/- 1.98 vs 7.71 +/- 1.55 mmol.l-1; p = NS). At the 90 W step which corresponds to the peak level that all the HTR reached, the C were close to their anaerobic threshold and showed similar parameters of oxygen transport (VO2: 17.4 +/- 2.0; CI: 7.50 +/- 0.41; AVO2D:90 +/- 10) but a lower lactate level (LA: 2.93 +/- 4.76; p < 0.002). At the same intermediate exercise levels VO2, CI and AVO2D were similar in both groups, while the closely matched LA and ventilation increased faster in HTR, reaching significantly higher levels as soon at the 30 W step. This evidence for an increased anaerobic exercise energy generation in HTR suggests that the periphery participates significantly in their exercise limitation, a phenomenon that might be improvable by retraining. VALUES: means+/-standard deviation.

Cardiac Output↗
PubMed1996

Short endurance training improves lactate removal ability in patients with heart transplants.

Eight male patients with heart transplants at least a year after the operation were submitted to a 6-wk endurance training program and explored for their blood lactate kinetics before and after exercise. The tests consisted of a bicycle exercise upgraded by 20 W every 2 min until volitional fatigue. Training induced a significant (P < 0.025) decrease in lactate concentrations from the 40-W to the 120-W exercise step and a significant increase (P < 0.025) in the time into exercise (9.87 +/- 0.87 min vs 7.17 +/- 0.90 min) at which a lactate concentration of 2 mmol.l-1 was reached. Lactate recovery curves were significantly lower (P < 0.036) after training than before training, except at minutes 1, 2, 8, and 60. The fits of a biexponential mathematical model to the lactate recovery curves reveal a significant (P < 0.036) training-induced increase (+71%) in the slow-velocity constant gamma 2v of the model. In view of the functional meaning given to this parameter, namely the ability to remove lactate, it is concluded that training lowers blood lactate concentrations during exercise and recovery in patients with heart transplants at least in part by raising the efficiency with which lactate is removed, and that the ability to remove lactate can be a valuable criterion to evaluate physical fitness.

Adult↗