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C Hirth

Publications and source records attributed to C Hirth.

At least 91 records · Page 5Linked to original sources

Comparative study of the ventilatory responsiveness to CO2 in bronchitic and emphysematous patients with chronic respiratory failure.

The comparative ventilatory responsiveness to CO2 was studied in 13 chronic bronchitics and 14 emphysematous patients, all exhibiting respiratory insufficiency and with FEV1 less than 1,500 ml. The gas inhaled was enriched with oxygen (F1O2 =0.6) and contained 6% CO2, and measurements were taken when the patients had reached a stable state. The ratio delta VE/deltaPaCO2, which represents the ventilatory responsiveness to CO2, was higher in the emphysematous patients (1.18+/-0.51 liters-min-1. Torr-1) than in the bronchitics (0.76+/-0.34, p less than 0.025), but the deviation on either side of the mean was large in each group. The ventilatory responsiveness to CO2 was proportional to the initial PaCO2, FEV1, total airways resistance, total pulmonary work and especially to inspiratory mechanical work done on the lung ( r=-0.73, p less than 0.001). The difference in ventilatory responsiveness to CO2 between the bronchitic and emphysematous patients may be explained by the difference in energy expended in breathing. It was not possible to exclude an effect due to a difference in sensitivity within the respiratory centers, since inspiratory mechanical work was not measured during CO2 inhalation. It was thought likely that mechanical factors play a triggering role, in that they cause a fall in ventilatory responsiveness to CO2 and hypercapnia, the latter causing the central hyposensitivity which maintains the retention of CO2.

Aged↗

[Clinical, functional and hemodynamic course in patients with chronic bronchitis at the stage of chronic cor pulmonale].

Twenty seven patients, almost all chronic bronchitic, and with a "chronic cor pulmonale" according to the E. C. G., were followed clinically, radiologically and for E. C. G. and pulmonary functions, and also for the hemodynamics, during a minimum of 3 years, the average length of observation period being about 5 years. Twelve patients died during this observation time. Periods of right heart failure (R. H. F.) were frequent : 3.6 +/- 3.0 in average, slightly more frequent in the deceased patients than in the others. The average delay between the onset R. H. F. and death was of 49.3 +/- 30.8 months ; the survivors on average lived another 54.6 +/- 30.8 months after their first R. H. F. The mean pulmonary arterial pressure (PAP) was quite stable, going from 27.5 +/- 7.0 to 31.2 +/- 9.6 torr (an unsignificicant difference); in only 9 cases did the PAP increase of more than 5 torr during the observation period (acute attacks excepted). The PAP evolution was not significantly different in the deceased and the survivors. PAP worsening by steps after a fit of R. H. F. was observed in only 4 cases. Chronological variations of PAP were well correlated with those of Pao2 during the same period : r = -- 0.68, P less than 0.001. The hemodynamic evolution (PAP), that of the E. C. G. and the volume of the heart were reasonably parallel to the overall clinical evolution ; the E. C. G. evolution had the closest match with the overall clinical evolution (78% of cases). The E. C. G. enables only a late diagnosis of CCP but its evolution is very valuable for prognosis. Hemodynamic tests have a double value initially for diagnosis and later for the evolution.

Adult↗

[Value of pulmonary hemodynamic exploration during muscular exercise in chronic bronchitis?].

The value of pulmonary haemodynamic tests during physical exercise in chronic bronchitis was shown by the comparison of two groups of patients. In the first group (n=24) the PAP during exercise is lower than 30 torr. In the second it was over 30 torr. The PAP at rest was always lower than 20 torr. The load was 40 to 50 watts, i.e. an average O2 consumption of 500-600 ml.mm-1 m-2. The cardiac output doubled on average in exercise. Both groups varied markedly in their PAP at rest: 13.6 +/- 1.7 torr for the first group and 15.8 +/- 2.4 for the second (p less than 0.001). In fact differences in pressure during exercise (I=25.0 +/- 3.4 torr; II=39.6 +/- 7.4 torr, p less than 0.001) could be explained mainly by the differences of pulmonary vascular resistances (I=0.91 +/- 0.37; II=1.47 +/- 0.61, p less than 0.005): they tended to fall during effort in the first group and increased slightly in the second; and by the much higher increase in the pulmonary "capillary" pressure during exercise in the second group (I=12.5 +/- 4.4 torr; II=19.7 +/- 72 torr, p less than 0.001). The cardiac output during rest and exercise was equal in both groups. The haemo-dynamic "recovery delay" was much higher in the second group. The spirographic shortage was on the whole identical in both groups. PaO2 on average was higher in group I (p less than 0.05) where it improved during exercise (p less than 0.01). The PaO2 of the second group did improve during exercise. The haemodynamic differences were concomitant with the differences in gas exchanges during effort, of well known prognostic significance. As the "foretelling" of PAP in effort from the PAP at rest was quite poor, it appeared that haemodynamic test in effort has a real value in contributing efficiently to the differenciation of the degree in severeness. The threshold of 30 torr for PAP in exercise (and for the load mentioned above) seemed a good discriminating factor.

Adult↗

Preparation and properties of an inhibitory extract from frog virus 3 particles.

The structural constituents of the frog virus 3 particle were solubilized by treatment with a nonionic detergent followed by the addition of a high salt concentration. This soluble viral extract (SVE) inhibits host nucleic acid synthesis. Its activity on RNA synthesis was studied in KB cells and found to be dependent on the presence of DEAE dextran. Inactivation of the inhibitory properties of SVE were obtained by trypsin digestion, treatment with urea, or heat denaturation. Neutralization of the activity of SVE was obtained by anti-frog virus 3 serum but not by anti-BHK serum. In vitro a complex may be formed between polynucleotides and the inhibitor indicating a possible mechanism for vivo inhibition.

Animals↗

Synthesis of an acetylcholine receptor-specific toxin derivative regioselectively labeled with an undecagold cluster.

The regioselective modification of a snake curaremimetic toxin is described. Toxin-alpha from Naja nigricollis was derivatized with an electron-dense maleimido undecagold cluster 5. The cluster-bound obtained toxin 8 has a very high affinity for the cholinergic binding site (Ki = 70 pM) of Torpedo marmorata nicotinic receptor. It is harboring a compact heavy atom core of about 8 A which makes it very useful for electron microscopy experiments.

Animals↗

The renal response to acute hypervolemia is caused by atrial natriuretic peptides.

In anesthetized rats, synthetic rat atriopeptin II produced an increase in urinary volume and sodium excretion as well as a decrease in arterial blood pressure. Both the natriuretic and hypotensive effects were blocked by monoclonal antibodies directed against atriopeptin II. The diuresis and natriuresis caused by furosemide was not inhibited by these antibodies. Thus, the monoclonal antibodies provide a specific inhibitor for atriopeptin-mediated responses in vivo and can be used to investigate the role of atriopeptin in volume regulation. Volume expansion with 20 ml/kg i.v. homologous blood induced strong diuresis and natriuresis in the anaesthetized rat. This response was also blocked by the described monoclonal antibodies. A radioimmunoassay for the determination of atriopeptin-like immunoreactivity (ANP-IR) is described. The plasma levels of ANP-IR 8 min after blood injection were 3-4 times higher than in control rats. Thus, the strong diuresis observed after volume expansion is due to an increase in circulating atrial natriuretic peptides that obviously exert a regulative function in fluid volume control.

Animals↗