Open retromuscular versus laparoscopic ventral hernia repair for medium-sized defects: where is the value?

PURPOSE: There is increasing emphasis on value in health care, defined as quality over cost required to deliver care. We analyzed outcomes and costs of repairing medium-sized ventral hernias to identify whether an open retromuscular or laparoscopic intraperitoneal onlay approach would provide superior value to the patient and healthcare system. METHODS: A retrospective analysis of prospectively collected data from the Americas Hernia Society Quality Collaborative was performed for patients undergoing clean, elective repair of ventral hernias between 4 and 8 cm in width at our institution between 4/2013 and 12/2016 for whom at least 1-year follow-up was available. Recurrence rates, wound complications, length of stay, patient-reported outcomes, and perioperative costs were compared. RESULTS: One hundred and eighty-six patients met criteria (105 open, 81 laparoscopic) with 93.5% having ≥ 2-year follow-up. Patients undergoing laparoscopic repair had higher BMI, lower ASA classification, slightly lower prevalence of recurrent hernias and less prior mesh utilization, and slightly smaller hernias. Length of stay was shorter in the laparoscopic group (median 1 vs. 3 days, p < 0.001), without increased readmissions. Recurrence rates, wound complications, and patient-reported outcomes were similar. Laparoscopic repair had higher up-front surgical costs, yet equivalent total perioperative costs. CONCLUSION: Both laparoscopic and open approaches for elective repair of medium-sized ventral hernias offer similar clinical outcomes, patient-reported outcomes, and total perioperative costs. Laparoscopic repair appears to offer superior value based on a significantly reduced postoperative length of stay.

Potential of saprophage Diptera to acquire culturable livestock-associated antibiotic-resistant bacteria.

The increasing prevalence of antibiotic resistance among bacteria is one of the most intractable challenges in 21st-century public health. Dipterans that associate with livestock, livestock waste products and cadavers have the potential to acquire livestock-associated antibiotic-resistant bacteria (LA-ARB) and transmit them to humans. In this study, piglet cadavers were used to attract saprophage dipterans from the environment and those dipterans were sampled for the presence of LA-ARB. In the first trial, culturable microbes resistant to both aminoglycoside and ß-lactam antibiotics were found in all cadavers and masses of dipteran larvae, and in three-quarters of adult dipterans. In the second trial, over 130 culturable bacterial colonies resistant to ß-lactams were isolated from the cadavers, larval and adult dipterans. Over 100 of those colonies were coliform or metabolically similar bacteria. Adult dipterans carried ß-lactam resistant staphylococci, whereas those bacterial types were absent from larval dipterans and cadavers, suggesting they were picked up from elsewhere in the environment. This research indicates that LA-ARB are ubiquitous in pig farms, and dipterans have the potential to carry medically important microbes. Further research is encouraged to determine the extent to which dipterans acquire microbes from animal agriculture relative to other environments.

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.

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.

Oxidative capacity of skeletal muscle in heart failure patients versus sedentary or active control subjects.

OBJECTIVES: We investigated the in situ properties of muscle mitochondria using the skinned fiber technique in patients with chronic heart failure (CHF) and sedentary (SED) and more active (ACT) controls to determine: 1) whether respiration of muscle tissue in the SED and ACT groups correlates with peak oxygen consumption (pVO(2)), 2) whether it is altered in CHF, and 3) whether this results from deconditioning or CHF-specific myopathy. BACKGROUND: Skeletal muscle oxidative capacity is thought to partly determine the exercise capacity in humans and its decrease to participate in exercise limitation in CHF. METHODS: M. Vastus lateralis biopsies were obtained from 11 SED group members, 10 ACT group members and 15 patients with CHF at the time of transplantation, saponine-skinned and placed in an oxygraphic chamber to measure basal and maximal adenosine diphosphate (ADP)-stimulated (V(max)) respiration rates and to assess mitochondrial regulation by ADP. All patients received angiotensin-converting enzyme (ACE) inhibitors. RESULTS: The pVO(2) differed in the order CHF < SED < ACT. Compared with SED, muscle alterations in CHF appeared as decreased citrate synthase, creatine kinase and lactate dehydrogenase, whereas the myosin heavy chain profile remained unchanged. However, muscle oxidative capacity (V(max), CHF: 3.53 +/- 0.38; SED: 3.17 +/- 0.48; ACT: 7.47 +/- 0.73, micromol O(2).min(-1).g(-1)dw, p < 0.001 vs. CHF and SED) and regulation were identical in patients in the CHF and SED groups, differing in the ACT group only. In patients with CHF, the correlation between pVO(2) and muscle oxidative capacity observed in controls was displaced toward lower pVO(2) values. CONCLUSIONS: In these patients, the disease-specific muscle metabolic impairments derive mostly from extramitochondrial mechanisms that disrupt the normal symmorphosis relations. The possible roles of ACE inhibitors and level of activity are discussed.

Color vision impairment in multiple sclerosis points to retinal ganglion cell damage.

Multiple Sclerosis (MS) results in color vision impairment regardless of optic neuritis (ON). The exact location of injury remains undefined. The objective of this study is to identify the region leading to dyschromatopsia in MS patients' NON-eyes. We evaluated Spearman correlations between color vision and measures of different regions in the afferent visual pathway in 106 MS patients. Regions with significant correlations were included in logistic regression models to assess their independent role in dyschromatopsia. We evaluated color vision with Hardy-Rand-Rittler plates and retinal damage using Optical Coherence Tomography. We ran SIENAX to measure Normalized Brain Parenchymal Volume (NBPV), FIRST for thalamus volume and Freesurfer for visual cortex areas. We found moderate, significant correlations between color vision and macular retinal nerve fiber layer (rho = 0.289, p = 0.003), ganglion cell complex (GCC = GCIP) (rho = 0.353, p < 0.001), thalamus (rho = 0.361, p < 0.001), and lesion volume within the optic radiations (rho = -0.230, p = 0.030). Only GCC thickness remained significant (p = 0.023) in the logistic regression model. In the final model including lesion load and NBPV as markers of diffuse neuroaxonal damage, GCC remained associated with dyschromatopsia [OR = 0.88 95 % CI (0.80-0.97) p = 0.016]. This association remained significant when we also added sex, age, and disease duration as covariates in the regression model. Dyschromatopsia in NON-eyes is due to damage of retinal ganglion cells (RGC) in MS. Color vision can serve as a marker of RGC damage in MS.

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.

Selective changes in mitochondria respiratory properties in oxidative or glycolytic muscle fibers isolated from G93AhumanSOD1 transgenic mice.

Cases of familial amyotrophic lateral sclerosis (FALS) are associated with mutations in cytosolic copper, zinc superoxide dismutase (SOD1). Total SOD activity and functional mitochondrial properties were studied in muscles and nervous tissues of control and transgenic mice mimicking the disease. It was found that total SOD activity was lower in nervous tissues than in muscles in both transgenic and control mice. In addition SOD activity increased during progression of disease in muscle but not in nervous tissue of transgenic mice. Maximal oxygen consumption and apparent Km for ADP were decreased in mitochondria from transgenic soleus (an oxidative muscle). However there was no difference between control and transgenic mice in respiratory parameters of mitochondria in the EDL muscle (a glycolytic muscle). These findings indicate that oxidative stress due to SOD1 mutations could alter energy metabolism in FALS mice, thereby affecting primarily oxidative muscle of the limbs, independently of motoneuron loss.

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.

Effect of cyclosporin A and its vehicle on cardiac and skeletal muscle mitochondria: relationship to efficacy of the respiratory chain.

Although cyclosporin (CsA) is considered to be the best immunosuppressive molecule in transplantation, it has been suspected to alter mitochondrial respiration of various tissues. We evaluated the acute effect of CsA and its vehicle on maximal oxidative capacity (V(max)) of cardiac, soleus and gastrocnemius muscles of rats by an oxygraphic method in saponin skinned muscle fibres. The effects of Sandimmun (a formulation of CsA), vehicle of Sandimmun (cremophor and ethanol (EtOH)), CsA in EtOH and EtOH alone were tested. Increasing concentrations (5 - 20 - 50 - 100 microM) of CsA (or vehicles) were used. Sandimmun profoundly altered the V(max) of all muscles. For example, at 20 microM, inhibition reached 18+/-3, 23+/-5, 45+/-5%, for heart, soleus and gastrocnemius respectively. There were only minor effects of CsA diluted in EtOH and EtOH alone on V(max) of cardiac muscle. Because the effects of vehicle on V(max) were similar or higher than those of Sandimmun, the inhibition of oxidative capacity could be entirely attributed to the vehicle for all muscles. Next, we investigated the potential sites of action of the vehicle on the different complexes of the mitochondrial respiratory chain by using specific substrates and inhibitors. The vehicle affected mitochondrial respiration mainly at the level of complex I ( approximately -85% in skeletal muscles, and -32% in heart), but also at complex IV ( approximately -26% for all muscles). The mechanism of action of the vehicle on the mitochondrial membrane and the implications for the clinical use of immunosuppressive drugs are discussed.

Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients.

To define the parameters of respiratory insufficiency in OSA, 114 consecutive patients (108 men, six women) were prospectively studied. In addition to standard polysomnography, they underwent pulmonary function tests, right heart catheterization, and ventilatory response tests to hypercapnia. Nineteen patients (19 percent) had a resting PAP greater than or equal to 20 mm Hg. Multiple regression analysis showed that FEV1 and PaO2 (both with a negative coefficient) and PaCO2 (with a positive coefficient) significantly contributed to PAP. Thirteen patients (12 percent) had a PaCO2 greater than or equal to 45 mm Hg. A multiple regression analysis showed that FEV1 and the minute ventilation at PETCO2 = 60 mm Hg (both with a negative coefficient) and the cumulative apnea duration (with a positive coefficient) significantly contributed to PaCO2. Thirty-seven patients (33 percent) had a PaO2 less than or equal to 65 mm Hg. A multiple regression analysis showed that FEV1 (with a positive coefficient) and the hypopnea + apnea index (with a negative coefficient) significantly contributed to PaO2. These data confirm that impaired daytime pulmonary function (diffuse airway obstruction) contributes to the development of daytime pulmonary hypertension, hypoxemia, and hypercapnia in OSA patients. They show that the amount of sleep-related breathing disorders also plays a significant role.

Lack of acute cyclosporine nephrotoxicity in late heart-transplant recipients.

BACKGROUND: Cyclosporine induces daily renal hypoperfusion in subjects with normal atrial natriuretic peptide (ANP) levels, but its acute effects in heart transplant patients with increased ANP remain to be determined. METHODS: Cyclosporinemia and creatinine clearance were monitored during 7 hours following cyclosporine administration in 6 heart transplant patients. CONCLUSIONS: No acute cyclosporine-induced decrease in creatinine clearance was observed after heart transplantation. These data suggest that maintenance cyclosporine dose may be less nephrotoxic than suspected and that increased ANP might protect the renal function late after heart transplantation.

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.

Work rate-dependent lactate kinetics after exercise in humans.

Arterial blood lactate concentrations were measured on 19 subjects before, during, and after a 3-min bicycle exercise at several work rates, and the concentrations during the recovery phases were fitted to a biexponential time function consisting of a rapidly increasing and a slowly decreasing component. Highly significant correlations with the work rate of the exercise preceding the recovery were found for all the parameters of the fitted equation. The two velocity constants show inverse linear relationships, whereas the other parameters vary according to a definite power function. A functional meaning has been given to the two velocity constants, namely the ability of the tissues to exchange and to remove lactate. For the group of subjects studied, after exercises at work rates below about 3.5 W/kg, the tissue's ability to utilize, and possibly to exchange lactate, increases over values generally reported for resting conditions, whereas after exercises at higher work rates the inverse occurs. Lactate kinetics during recovery appear to be the result of two underlying processes, one enhancing the ability of the tissues to exchange and remove lactate and the other restraining it.

Effect of cold pressor test on single-breath DLCO in normal subjects.

We hypothesized that the decrease in single-breath diffusing capacity of CO (DLCO) as observed in patients with Raynaud's phenomenon (P.J. Fahey et al. Am. J. Med. 76:263-269, 1984) may be present in normal subjects. Therefore, we examined 31 healthy subjects in two different laboratories. Two series of experiments were performed. In the first series DLCO was measured in 22 volunteers before (twice) and 5, 10, and 30 min after a cold pressor test (CPT), which consisted of immersing both hands in a 12 degrees C water bath for 2 min. In the second series right heart catheterization was performed in nine healthy seated subjects. Cardiac output, mean pulmonary arterial pressure, heart rate, and pulmonary wedge pressure were measured before, during, and 10, 20, and 30 min after the CPT. In every volunteer the CPT induced a decrease in DLCO that was still present 30 min after the test. In the nine catheterized subjects DLCO increased above control values during the CPT and then decreased below control values for 30 min. The CPT had no effect on cardiac output, heart rate, or pulmonary wedge pressure. In contrast, pulmonary arterial pressure and pulmonary vascular resistance increased during the CPT and then became lower than the control values for at least 30 min. In summary, the CPT induced a biphasic evolution of DLCO in normal subjects, being increased during the CPT and decreased after it. Our data are best explained by the West model of the lung. Our data suggest that the pulmonary Raynaud's phenomenon is not specific to patients with primary Raynaud's phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)

VO(2) kinetics reveal a central limitation at the onset of subthreshold exercise in heart transplant recipients.

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O(2) uptake (VO(2)) kinetics at the onset of subthreshold exercise are slowed because of an impaired early "cardiodynamic" phase 1, rather than an abnormal subsequent "metabolic" phase 2. Thus we compared the VO(2) kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 +/- 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 +/- 14 W; C67W group). Time-averaged heart rate, breath-by-breath VO(2), and O(2) pulse (O(2)p) data yielded monoexponential time constants of the VO(2) (s) and O(2)p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 VO(2) time constant (). The VO(2) time constant was higher in HTR (38.4 +/- 7.5) than in C40W (22.9 +/- 9.6; P < or = 0. 002) or C67W (30.8 +/- 8.2; P < or = 0.05), as was the O(2)p time constant, resulting from a lower phase 1 VO(2) increase (287 +/- 59 vs. 349 +/- 66 ml/min; P < or = 0.05), O(2)p increase (2.8 +/- 0.6 vs. 3.6 +/- 1.0 ml/beat; P < or = 0.0001), and a longer phase 1 duration (36.7 +/- 12.3 vs. 26.8 +/- 6.0 s; P < or = 0.05), whereas the was similar in HTR and C (31.4 +/- 9.6 vs. 29.9 +/- 5.6 s; P = 0.85). Thus the HTR have slower subthreshold VO(2) kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.

Interrupter technique versus plethysmography for measurement of respiratory resistance in children with asthma or cystic fibrosis.

The purpose of the present study was to compare measurements of respiratory system resistance by the interrupter method (Rrsint) with those of airway resistance by plethysmography (Raw) in nonobstructed children with asthma or cystic fibrosis (ratio of forced expiratory volume in 1 sec to vital capacity, FEV(1)/VC >/=80% with a forced expiratory flow rate between 25-75% of forced vital capacity, FEF(25-75) >/=75% of normal values) and in obstructed children with the same diseases (FEV(1)/VC <80% and/or FEF(25-75) <75% of normal values). Eighty-one children (47 asthmatics and 34 suffering from cystic fibrosis) aged 5-18 years (mean 11.2 +/- SD 3.4 years) were included in the study. For the overall group, we observed generally lower values for Raw (4.7 +/- 2. 8 cmH(2)O.L(-).s) than for Rrsint20 (extrapolation of the mouth pressure during occlusion to 40 ms after interruption) (5.6 +/- 1.7 cmH(2)O.L(-1).s) (P < 0.02), or for Rrsint40 (extrapolation of the mouth pressure during occlusion to 60 ms after interruption) (6.6 +/- 2.2 cmH(2)O.L(-1).s) (P < 0.001), but there was no difference between Rrsint20 and Raw in the obstructed subgroup. Moreover, we observed a correlation between the difference (Rrsint20 - Raw) expressed in percentage of predicted values and the degree of obstruction estimated by FEV(1)/VC (r = 0.56, P < 0.001). The differences between the specific resistances (sRrsint20 - sRaw, sRrsint40 - sRaw) were also correlated with the severity of the obstruction (r = 0.65, P < 0.001 and r = 0.57, P < 0.001, respectively). We observed also that the tendency to underestimate resistance by Rrsint in obstructed children was not the same in children with asthma and cystic fibrosis. We conclude that the tendency of Rrsint, as measured with our method, to underestimate airway obstruction appears to increase in proportion to the severity of the airway obstruction.

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.

Exercise training with a heart device: a hemodynamic, metabolic, and hormonal study.

PURPOSE: The mechanisms of the training-induced improvements in left ventricular assist (LVAD) patients are unknown. METHODS: We measured the hemodynamic, gas exchange, and metabolic and hormonal effects of 6-wk exercise training in a cardiogenic shock patient who was assisted by an LVAD. RESULTS: After training, the peak power and VO2 increased by 166% and 56%, respectively (80 W and 16.1 mL x min(-1) x kg(-1)), whereas the ventilatory drive decreased. Although the LVAD output increased little with exercise, the systemic cardiac output rose (adequately for the VO2) from 5.91 and 4.90 L x min(-1) at rest to 9.75 and 9.47 L x min(-1) at peak work rate, before and after training, respectively. Thus, the left ventricle ejected again through the aortic valve. Unloading and/or retraining resulted in a left ventricular filling pressure decrease. Although the right ventricular ejection fraction increased with exercise, it decreased again at the maximal load after training. For a given work rate the arterial lactate, the norepinephrine (NE) and epinephrine (E) concentrations fell after training, but the enhanced maximal work rate elicited higher NE and E concentrations (4396 and 1848 pg x mL(-1), respectively). The lack of right ventricular unloading might have kept the atrial natriuretic peptide higher after training, but the blood cyclic GMP and endothelin were lower after training. CONCLUSION: In an LVAD patient, retraining returns the exercise capacity to the class III level by peripheral and left ventricular hemodynamic improvements, but the safety of maximal exercise remains to be proven in terms of right ventricular function and orthosympathetic drive.

[Criteria and validity of continuous measurement of pO2 and pCO2 in man]. / Critères et validité de la mesure en continu de la PaO2 et de la PaCO2 chez l'homme

After description of a method of continuous measurement of partial pressure of blood gases, the authors describe the technical difficulties : behaviour of the electrodes, problems associated with continuous measurement, and emphasise the influence of the method on the results, e.g. heparinisation, blood flow rate, quantity of blood consumed. The results obtained under suitable physiological conditions show the difficulty of interpretation of continuous measurement of gaseous parameters and show interest in short but significant function tests.