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Biomedical subjects

J Roca

Publications and source records attributed to J Roca.

At least 253 records · Page 14Linked to original sources
PubMed1991

[An elevated prevalence of subclinical pulmonary involvement in systemic lupus erythematosus].

Lung function was prospectively studied in a group of non-selected systemic lupus erythematosus (SLE) female patients who consecutively came to our Lung Function Laboratory. There was no previous history of smoking in any patient nor there was clinical and/or radiographic evidence of lung affectation prior to the diagnosis of SLE. Some respiratory lung function abnormalities were observed in 17 patients (65%). The most frequent functional anomaly was the alteration in carbon monoxide transfer (DLCO), which was present in 10 cases (38%). On the other hand, a restrictive ventilatory failure was observed in 8 patients (31%) and a obstructive ventilatory failure in 6 other (23%). Out of these, 3 patients (12% of the total number of cases) presented bronchial hyperreactivity, which could also be confirmed in a patient presenting a mixed ventilatory failure. Isolated air entrapment could be observed in 2 patients, which could indicate disfunction of small airways in these cases. There was no correlation between functional respiratory failure and clinical activity of SLE, duration of the disease, other organ involvement, treatment and/or serum antibodies. Given that a great number of these functional lung anomalies (42%) exist in the absence of any clinical and radiological anomalies and that an important subgroup of patients are responsive to bronchodilators, we consider that the systemic evaluation of lung function must be obliged in the clinical treatment of SLE patients.

Adolescent↗
PubMed1991

[Respiratory response to chemical stimuli and exercise capacity under conditions of acute hypoxia in elite mountain climbers].

To investigate the factors that modulate exercise performance at extreme altitude, the role of the following variables was analyzed in 16 climbers: 1) ventilatory response to chemical stimuli (hypoxia and hypercapnia); and, 2) maximum exercise performance while breathing room air and during acute hypoxia (F1O2, 0.11). Seven climbers (elite climbers, AE) had previously ascended to 8,000 m or more above sea level, and 9 (A) had never achieved such extreme altitude. Then healthy sedentary subjects (C) of similar age (31.1 +/- 6.0 SD years) were used as control group. Elite climbers showed higher ventilatory responses to both transient hypoxia (-0.49 +/- 0.13 L x min-1 x %-1) (p less than 0.05) and progressive hypoxia (-0.47 +/- 0.13 L x min-1 x %-1) than C (-0.33 +/- 0.14 and -0.30 +/- 0.15 L x min-1 x %-1, respectively). By contrast, no differences were observed between the two groups of climbers. The ventilatory response to hypercapnia was higher in AE (3.04 +/- 1.03 L x min-1 mmHg-1) compared to A (1.85 +/- 0.73 L x min-1 mmHg-1) (p less than 0.05) but similar to that observed in C. Breathing 11% O2, maximum workload and oxyhemoglobin desaturation during maximum exercise were similar in both groups of climbers. Additionally, the ventilatory response to hypoxia did not correlate with maximum workload (F1O2, 0.11), maximal ventilation during exercise (F1O2, 0.11), nor with the altitude score. The present study supports previous reports that inform about the role of the ventilatory response to hypoxia in the exercise performance at high altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1991

Left ventricular dynamics and plasma catecholamines during isometric exercise in patients following cardiac transplantation.

Haemodynamics and plasma catecholamine responses to isometric exercise were evaluated invasively in 11 orthotopic heart transplant recipients and seven control subjects. Differences in haemodynamic responses between the two groups were already apparent after one min of handgrip at 30% of maximal voluntary contraction, and very pronounced at the end of the fourth minute. At this point transplanted patients showed smaller increments in heart rate (4.8 +/- 3.2 vs 20.4 +/- 14.1 beats.min-1, P less than 0.001), mean arterial pressure (13.7 +/- 7.2 vs 31.5 +/- 12.2 mmHg, P less than 0.001) and cardiac index (0.51 +/- 0.22 vs 1.02 +/- 0.53 L.min-1.m-2, P less than 0.01), whereas left ventricular end-diastolic pressure increased to a greater extent (8.8 +/- 4.9 vs 2.2 +/- 1.8 mmHg, P less than 0.01). Stroke volume index increased similarly (3.8 +/- 1.8 vs 2.0 +/- 3.5 ml beat-1.m-2, NS) and systemic vascular resistance remained unchanged in both groups. The slopes of the left ventricular function curves (ratio of change in left ventricular work to change in left ventricular end-diastolic pressure) indicated depressed left ventricular function in the transplanted patients. The two groups showed similar increments in mixed venous plasma norepinephrine and epinephrine indicating normal sympathoadrenal activation in the transplanted patients. In conclusion, transplanted hearts respond to handgrip with attenuated increases in heart rate, cardiac output and arterial pressure and by increasing left ventricular filling pressure, suggesting a poor contractile reserve probably due to denervation. Circulating catecholamines, especially epinephrine, probably contribute to the cardiac responses to isometric exercise.

Adult↗
PubMed1990

Experimental support for the theory of diffusion limitation of maximum oxygen uptake.

The four experiments summarized above demonstrate that there is a strong relationship between both measured muscle venous PO2 and calculated mean muscle capillary PO2 and VO2max. This is true for whole body or exercising muscle VO2max, and is seen both in isolated canine gastrocnemius and intact man. This behavior is exactly what would be expected if the diffusing properties for oxygen in skeletal muscle play a constraining role in setting maximum VO2. These data therefore support the hypothesis we advanced (Wagner, 1988a; Wagner, 1988b), that it is a quantitative integrative relationship between convective and diffusive phenomena that combine to set maximum VO2. A specific prediction of this integrative hypothesis (i.e., the non-uniqueness of VO2max as a function of convective oxygen delivery) was confirmed (Experiment 3). While at this point in time phenomena such as perfusion heterogeneity and muscle shunts cannot be quantitatively taken into account in such analyses, the remarkable concurrence between expectations of the hypothesis and experimental data continue to lend support to the basic idea that maximum VO2 is not limited by any single step of the oxygen transport pathway from atmosphere to mitochondria, but rather by the way in which each and every step combines with every other step to determine oxygen supply.

Animals↗
PubMed1990

The lung in patients with cirrhosis.

To summarize, nowadays it seems clear that in patients with cirrhosis: (a) the pulmonary circulation is usually markedly dilated. (b) This vasodilation is due to a loss of vascular tone and it is characterized by a poor (or even absent) vascular reactivity in front of the hypoxic stimulus. (c) This abnormal behaviour of the pulmonary circulation results in VA/Q mismatching (basically perfusion of low VA/Q units) independently of airway disease, and may lower arterial PO2. (d) In the most severe cases, shunt (and perhaps O2 diffusion limitation) is becoming progressively more important. (e) The high cardiac output and minute ventilation of these patients minimize or prevent the appearance of arterial hypoxemia at rest. (f) The fall in arterial PO2 during exercise is not due to a deterioration of the degree of VA/Q mismatching seen at rest nor to any limitation in the diffusion of oxygen. It is caused by the relative 'normalization' (with respect to the metabolic demands) of the haemodynamic and ventilatory status of the patient. This may not apply to patients with severe resting arterial hypoxemia in whom the mechanisms modulating pulmonary gas exchange during exercise have not yet been addressed. What remains to be elucidated at the present time? (a) Which is (are) the precise biochemical mediator(s) of this low pulmonary vascular tone and, presumably, failure of hypoxic pulmonary vasoconstriction? It might be either a substance(s) that the failing liver fails to produce or detoxify. Thus, the ultimate biochemical basis of these physiological abnormalities must still necessarily remain speculative while awaiting future studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1990

Pulmonary gas exchange in severe chronic asthma. Response to 100% oxygen and salbutamol.

Ventilation-perfusion (VA/Q) inequality has been evaluated using the multiple inert gas technique in nine nonsmoking patients (mean +/- SD, age 56 +/- 10 yr) with stable, severe, chronic asthma (partially reversible airway obstruction; baseline FEV1, 39 +/- 10% predicted) before and during 100% O2 breathing and then 15 min after three puffs (300 micrograms) of inhaled salbutamol. The aim of this study was to investigate whether this type of asthma was associated with a different pattern of VA/Q inequality from that observed in acute episodes and in particular to determine whether the VA/Q pattern was fixed or could be altered by bronchodilator agents or O2 breathing. The predominant pattern of VA/Q distribution was broad and unimodal but without shunt (VA/Q = 0) or low VA/Q areas (VA/Q less than 0.1 to greater than 0.005). The amount of VA/Q inequality as assessed by the dispersion of the distribution of pulmonary bloodflow (log SDQ) was not great (log SDQ, 0.77 +/- 0.09), and no correlation was found with the degree of airway obstruction, PaO2 or AaPO2. During 100% O2 breathing, VA/Q inequality worsened (from log SDQ of 0.77 +/- 0.09 to 1.11 +/- 0.21, p = 0.01) with an increase in the perfusion of low VA/Q units (from 0.43 +/- 0.66% to 6.3 +/- 6.5%, p = 0.02) but still no development of shunt. This suggests the presence of hypoxic pulmonary vasoconstriction breathing air, possibly contributing to the preservation of VA/Q relationships.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1990

Single-breath carbon monoxide diffusing capacity prediction equations from a Mediterranean population.

Because of unanswered questions about prediction equations for the single-breath carbon monoxide diffusing capacity (DLCO) and as part of a larger collaborative project, standardized DLCO measurements were carried out in a selected sample of 361 healthy nonsmoking volunteers (194 men and 167 women) living in the Barcelona metropolitan area (Spain). Except for the test FIO2 (0.18), the study essentially followed the American Thoracic Society (ATS) and European Community for Coal and Steel (ECCS) recommendations for standardizing the methodology of measuring DLCO. Prediction equations for ages 20 through 70 were calculated separately for both sexes. Simple linear equations using age, height, and body weight as independent variables predicted the DLCO indices (DLCO, VA, and DL/VA) as well as more complex equations. In addition, a complete analysis of the residuals (predicted measured values) showed that the assumptions of the multiple regression analysis (independence, homoscedasticity and Gaussian distribution of residuals) were fulfilled using simple linear equations. Correction for the instrumental and anatomic dead spaces decreased the DLCO an average of 4.7%. The standard error of estimates was lower than those reported from other series in the literature. The predicted values from this study were lower than those reported by some investigators and were in reasonable agreement with other studies. A portion but not all of the differences could be explained on the basis of recognized differences in testing methodology. The results of this study may be of value to clinical laboratories seeking predictive equations for DLCO most appropriate for their testing methodology and patient population, and may assist in the resolution of some controversies regarding differences among predictive equations for DLCO.

Adolescent↗
PubMed1990

Lung structure and gas exchange in mild chronic obstructive pulmonary disease.

To investigate the influence of pulmonary emphysema and small airways abnormalities on ventilation-perfusion (VA/Q) mismatching in mild chronic obstructive pulmonary disease (COPD), we studied 23 patients (mean predicted FEV1, 76 +/- 15%) before lung resection because of a localized neoplasm. Respiratory gas exchange and VA/Q distributions were measured while the patients breathed room air and 100% O2. Breathing room air, the AaPO2 was moderately increased (25 +/- 12 mm Hg) as was VA/Q mismatching, indicated by the dispersion (log SD) of both blood flow (Q) and ventilation (V) distributions (log SD Q, 0.78 +/- 0.3; and log SD V, 0.66 +/- 0.28, respectively) (normal range, 0.3-0.6). AaPO2, log SD Q, and log SD V all significantly correlated with the emphysema severity assessed morphologically from the resected lung specimens (r = 0.57, r = 0.62, and r = 0.45, respectively). Log SD V also significantly correlated with the severity of the inflammatory infiltrate of membranous bronchioles (r = 0.62). During 100% O2 breathing there was an increase in VA/Q mismatching (log SD Q rose to 1.12 +/- 0.08, p less than 0.001), suggesting release of hypoxic pulmonary vasoconstriction. This increase in VA/Q inequality was not significantly related to the severity of lung pathologic findings. We conclude that, in mild COPD, both pulmonary emphysema and small airways abnormalities contribute to VA/Q mismatch, the severity of emphysema being the major morphologic correlate of the increase in AaPO2.

Adult↗
PubMed1990

Effects of propranolol on arterial oxygenation and oxygen transport to tissues in patients with cirrhosis.

Patients with cirrhosis may show ventilation-perfusion (VA/Q) inequality in the absence of any intrinsic heart or lung disease. However, the high cardiac output of cirrhosis generally prevents or minimizes the appearance of a severe degree of arterial hypoxemia. Propranolol has been used to reduce cardiac output and portal pressure in these patients. We wondered whether it might alter arterial oxygenation and reduce O2 transport to tissues. We studied eight patients (three women) 54 +/- 3 (SEM) yr of age before and after intravenous propranolol (0.1 mg/kg followed by 2 mg/h). Cardiac output (QT) fell from 7.8 +/- 0.7 to 6.0 +/- 0.7 L/min (p less than 0.05), and portal pressure was reduced (22 +/- 2 to 19 +/- 2 mm Hg, p less than 0.01). Arterial PO2 did not change (88 +/- 4 to 89 +/- 5 mm Hg) because the fall in mixed venous PO2 (43 +/- 1 to 40 +/- 1 mm Hg, p less than 0.01) that followed the lower QT was counterbalanced by a lower intrapulmonary shunt (multiple inert gas technique) (4 +/- 2 to 2 +/- 1%, p less than 0.05) and a shift of the VA/Q distributions toward a higher VA/Q ratio. Paralleling the fall in QT, oxygen transport to tissues (QO2) was reduced (19 +/- 2 to 14 +/- 1 ml/min/kg, p less than 0.01). However, O2 uptake (VO2) remained constant (3.4 +/- 0.2 to 3.6 +/- 0.2 ml/min/kg) because O2 extraction by the tissues increased appropriately (22 +/- 2 to 28 +/- 1%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1990

Hypoxic pulmonary vasoconstriction and gas exchange during exercise in chronic obstructive pulmonary disease.

In patients with chronic obstructive pulmonary disease (COPD) studied at rest, nifedipine releases hypoxic pulmonary vasoconstriction (HPV) and worsens gas exchange. During exercise, this drug lowers pulmonary hypertension, but the effects of this lower pulmonary vascular tone on ventilation-perfusion (VA/Q) relationships are still poorly understood. To analyze them, we determined the VA/Q distributions in eight patients with stable COPD (FEV1, 36 percent of predicted) at rest and during exercise (60 percent VO2 max), before and after nifedipine (20 mg sublingually). Nifedipine shifted to the right the pulmonary pressure-flow relationship (p less than 0.01) and increased the dispersion of the blood flow distribution at rest and during exercise (p less than 0.005). These observations strongly suggest that nifedipine released HPV under both conditions. However, even after releasing HPV by nifedipine, exercise distributed blood flow more homogeneously than at rest (p less than 0.05). Besides, exercise greatly decreased the overall degree of VA/Q mismatching (p less than 0.001) not only before but also after nifedipine. Thus, we postulate that most of the VA/Q improvement that exercise may induce in patients with COPD, as it is shown here, is due to improvement in the ventilation distribution. Interestingly, this VA/Q improvement was not paralleled by a significant decrease of P(A-a)O2. This apparent paradox could be explained by 20 percent of the actual P(A-a)O2 during exercise due to diffusion limitation, as assessed through the inert gas approach. Taken all together, these results help to better understand the mechanisms that govern pulmonary gas exchange during exercise in COPD.

Exercise↗
PubMed1990

Bronchial reactivity in patients with chronic renal failure undergoing haemodialysis.

We hypothesized that patients with chronic renal failure may present nonspecific bronchial hyperreactivity due to subclinical interstitial lung oedema. To assess lung function disturbances and methacholine (MTH) bronchial responsiveness in this condition, we studied 12 patients (9 men and 3 women; 41.8 +/- 13.3 yrs (SD] with chronic renal failure undergoing regular haemodialysis (HD). Before HD, mean results of conventional lung function tests were within the normal range: forced expiratory volume in one second (FEV1), 89 +/- 12.9% predicted; forced mid-expiratory flow (FEF25-75), 81 +/- 36.7% predicted; total lung capacity (TLC), 94 +/- 14.6% predicted, but 3 subjects presented mild reduction in lung volumes and 5 individuals showed mild obstructive ventilatory impairment. After HD, maximal expiratory flow rates increased significantly (FEV1, + 8.2 +/- 5.1% (p less than 0.005); FEF25-75, +26.2 +/- 25.9% (p less than 0.005]. Interestingly, these increases in FEV1 after HD correlated with body weight loss during HD (r = 0.74, p less than 0.01). In contrast, pre-HD bronchial reactivity was within the normal range (mean % change in FEV1 after MTH, -3.7 +/- 4.5%; range, +1- -14%) without significant changes in methacholine bronchial responsiveness after HD. We speculate that interstitial lung oedema may play a significant role in lung function impairment observed in patients with chronic renal failure. This study shows that nonspecific bronchial hyperreactivity is not present in clinically stable patients with this disorder.

Adult↗
PubMed1990

Characteristics of patients with soybean dust-induced acute severe asthma requiring mechanical ventilation.

Patients presenting with acute severe asthma during the Barcelona's outbreaks caused by soybean dust inhalation from August, 1981, through September, 1987, characteristically showed an abrupt severe onset of each attack followed by a rapid relief of symptoms after treatment. To throw further light on clinical findings, pathophysiology and outcome in the most life-threatening episodes, we reviewed records of acute severe asthma patients treated by mechanical ventilation in one of the four main hospitals of the city. Twelve such patients (15 episodes) were compared to 24 non-epidemic asthmatic patients (25 episodes) also treated by mechanical ventilation in the same institution during the same period of time. There was a male predominance during outbreaks (p less than 0.03) and epidemic patients were ventilated fewer hours (12 +/- 8 h) (mean +/- SD), admitted fewer days to intensive care (1.6 +/- 0.7 days), and hospitalized fewer days (7.1 +/- 4.4 days) than non-epidemic patients (65 +/- 84 h, 4.6 +/- 3.8 days (p less than 0.001, each), and 16.0 +/- 13.2 days (p less than 0.004), respectively). These differences together with both the fulminant presentation of the episodes of epidemic asthma and the point-source origin of the asthma outbreaks previously shown are consistent with the unusual nature of the aetiologic agent, soybean dust.

Acute Disease↗
PubMed1989

DNA topoisomerase II activity in nonreplicating, transcriptionally inactive, chicken late spermatids.

To study a possible differential involvement of type I and type II DNA topoisomerases in the functional and structural changes that chromatin undergoes during spermatogenesis, we have determined both enzymatic activities in chicken testis cell nuclei at successive stages of differentiation. Whereas DNA topoisomerase I varies in parallel with transcriptional activity, DNA topoisomerase II was present in both replicating, transcriptionally active chicken testis cells and nonreplicating, transcriptionally inactive late spermatids. The presence of DNA topoisomerase II activity in late spermatids and, in addition, the relative increment of drug-induced topo-II-mediated DNA cleavage detected in these cells, suggest that DNA topoisomerase II might modulate the topology of DNA during the marked changes that chromatin structure undergoes in the nucleohistone-nucleoprotamine transition at the end of the spermiogenesis and could be involved in the final organization of DNA within the nucleus of the male gamete.

Animals↗
PubMed1989

New design for fixation of surgically obtained lung specimens.

A new design for lung fixation at a constant transpulmonary pressure is described. The head pressure of the apparatus can easily be set in a range from 15 to 95 cm H2O and maintained at a constant level through the recirculation of the fixative fluid. Moreover, the dimensions of the device are smaller than those previously reported. To analyze the efficiency of the equipment the estimated total post-fixing lung volume (TLV) in 12 surgically obtained lung specimens was calculated and compared with helium single-breath total lung capacity measurements (TLCsb). The TLV/TLCsb ratio was 102 +/- 5%. In addition, TLV was related to predicted TLC values (TLCpred) from different reference equations. The TLV/TLCpred ratios ranged from 89 to 99%. Estimated volumes of formalin fixed lungs did not show significant differences to those obtained by TLCsb measurements (p = 0.49). Consequently, it can be concluded that the fixation procedure performed with this device does not produce changes in air space dimensions of surgically obtained lung specimens. Moreover, the variability in TLV/TLC ratios depends upon either the technique of TLC measurement or the set of predicted values used.

Adult↗
PubMed1989

Ventilation-perfusion mismatching in acute severe asthma: effects of salbutamol and 100% oxygen.

Ventilation-perfusion (VA/Q) relationships and gas exchange were studied by the multiple inert gas technique in 19 patients admitted to hospital with acute severe asthma (FEV1 41% predicted) before and during the administration of intravenous salbutamol, inhaled salbutamol, or 100% oxygen. Eight patients received a continuous intravenous infusion of salbutamol (4 micrograms/min, total dose 360 micrograms) and were studied before treatment, after 60 and 90 minutes of treatment, and one hour after treatment had been discontinued. Six patients had measurements before and 15 minutes after inhaling 300 micrograms salbutamol from a metered dose inhaler on two occasions (total dose 600 micrograms) and one hour after the last dose. Measurements were also made in five patients before and while they breathed 100% oxygen for 20 minutes. At baseline (fractional inspired oxygen (FiO2) 21%) all patients showed a broad unimodal (n = 10) or bimodal (n = 9) distribution of blood flow with respect to VA/Q. A mean of 10.5% of the blood flow was associated with low VA/Q units without any appreciable shunt. One of the best descriptors of VA/Q inequality, the second moment of the perfusion distribution on a log scale (log SD Q), was moderately high with a mean of 1.18 (SEM 0.08) (normal less than 0.6). Measures of VA/Q inequality correlated poorly with spirometric findings. After salbutamol the increase in airflow rates was similar regardless of the route of administration. Intravenous salbutamol, however, caused a significant increase in heart rate, cardiac output, and oxygen consumption (VO2); in addition, both perfusion to low VA/Q areas and log SD Q increased significantly. Inhaled salbutamol caused only minor changes in heart rate, cardiac output, VO2, and VA/Q inequality. Arterial oxygen tension (PaO2) remained unchanged during salbutamol administration, irrespective of the route of administration. During 100% oxygen breathing there was a significant increase in log SD Q (from 1.11 to 1.44). It is concluded that patients with acute severe asthma show considerable VA/Q inequality with a high level of pulmonary vascular reactivity. Despite similar bronchodilator effects from inhaled and intravenous salbutamol, VA/Q relationships worsened only during intravenous infusion. PaO2 remained unchanged, however, because the change in VA/Q relationships was associated with an increase in metabolic rate and cardiac output.

Acute Disease↗