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Biomedical subjects

E Reichart

Publications and source records attributed to E Reichart.

At least 19 recordsLinked to original sources
PubMed1998

Determination of Sn(II) in technetium cold kits by voltammetry at the hanging mercury drop electrode (HMDE) and relevant radiopharmaceutical applications.

A novel approach for the determination of the stannous content in cold kits for labelling with 99mTc is described. The method is based on differential pulse polarography on the hanging mercury drop electrode in a methanol/water/perchloric acid mixture and is easy to perform. Examples for the determination of tin(II) in fractionated technetium cold kits are shown. The stability of tin(II) in solution was mainly dependent on the storage temperature and the kit composition. The low stability of stannous ions under certain conditions was shown to be the main reason for low radiochemical purity. Limits and dangers of fractionating kits are discussed and related to content and instability of tin(II).

Electrochemistry↗
PubMed1996

The trypsin-induced leucostasis which leads to emphysema in the hamster is not due to contaminating endotoxins.

Intravenous injection of trypsin in the rat induces early lung leucostasis and emphysema of delayed onset. This report confirms that this emphysema is not rat-specific and that the leucostasis is not related to the presence of contaminating endotoxin in the trypsin. In hamsters (n = 37), leucostasis did not occur when they were injected with heat-treated trypsin, but numerous granulocytes were sequestered in the vessels of hamsters receiving a fresh solution of trypsin. In these hamsters, the number of granulocytes harvested by lavage increased significantly (1.87 x 10(6) per ml, P < 0.001) compared with hamsters injected with either heat-denatured trypsin (0.89) or saline (0.86), or compared with controls (0.86). Emphysema was inconstantly observed in hamsters 6 or 12 weeks after injection with trypsin for 1 h. It was frequently (17/20) present and always (20/20) well developed (intercept + 180 per cent) in the 2-h perfused hamsters whose lungs were abnormally heterogeneous (index + 100 per cent) relative to the seven controls and to the nine saline-injected hamsters. The efficiency of trypsin in triggering emphysema (percentage of hamsters having abnormal values of intercept) was dependent on the time of perfusion. This form of experimental emphysema is thus considered to be due to an endotoxin-independent leucostasis.

Animals↗
PubMed1996

[Trypsin-induced leukostasis: granulocyte migration in airspaces].

Injection of trypsin triggers the delayed appearance of a lung emphysema. Classically, emphysema is attributed to elastase, more particularly to leucocyte elastase. Indeed the acute phase of this experiment is characterized by a granulocyte sequestration within the lung microvessels in diverse species. We also found granulocytes within the terminal airspaces; this fact implies a granulocyte extravasation and directed migration. In order to evaluate this airspace invading by granulocytes during trypsin induced-vascular leucostasis, we washed the lung in cats since this species develop leucocytosis easily. One lobe only was washed for avoiding to harvest the cells present in the trachea and the main bronchi. This study was designed in several parts: (1) the lungs were washed in normal condition and several months later when trypsin was given; (2) in a kinetic experiment, 3 lavages were made consecutively a day either in normal condition or under trypsin treatment; (3) the lung was washed one day after trypsin administration. The granulocytes, and among them the neutrophils particularly, increased in number or in percentage transiently within the terminal airspaces under trypsin treatment; these granulocytes found within the airspaces are about 20% of the lung granulocytes.

Animals↗
PubMed1992

Parenteral administration of trypsin triggers lung emphysema.

Eight weeks after a single intravenous injection of trypsin, more than half of 26 treated rats showed pulmonary emphysema, as demonstrated by a significant increase of the mean linear intercept (MLI = 107 microns) in comparison with 11 controls (69 +/- 15 microns) (mean +/- SD). As observed 56 days after the injection, the intraperitoneal administration of trypsin (24 rats) also leads to lung emphysema (MLI = 101-106 microns), as does endotracheal instillation of elastase (13 rats), (MLI = 108 microns). The intraperitoneal administration of trypsin in animals constitutes a model close to human pathology with which lung alterations in acute pancreatitis may be studied. Having no elastolytic properties, trypsin cannot directly induce emphysema. The observation of a pulmonary leucostasis in eight rats sacrificed early after the trypsin injection suggested that leucocyte trapping and activation are important for the genesis of this trypsin-triggered emphysema.

Acute Disease↗
PubMed1991

[Quantimetry and lung heterogeneity in hamsters (Mesocricetus auratus) treated with endotracheal or intrapleural infusion of elastase. Individual and contralateral variations].

Intrapleural administration of elastase was found to induce pulmonary emphysema identical to that seen after an endotracheal instillation of elastase in 33% of cats and 14% of rats given the treatment [15]. This experiment was repeated using hamsters, a species extremely sensitive to elastolytic factors reaching the lung via the airways. Linear intercept measurements (Lm) demonstrated no evidence of emphysema or alveolar dilatation four weeks after an intrapleural infusion of elastase, whereas quantified lung heterogeneity reached 40%, i.e., twice the control value; 17% of treated hamsters exhibited a statistically significant increase in heterogeneity of the right or left lung. These findings suggest that occurrence of alveolar dilatation after administration of a protease is dependent on access of the enzyme to the lung; if the enzyme fails to access the lung, abnormal lung heterogeneity may develop: this anomaly reflects a strong statistical likelihood of a disease state with or without concomitant emphysema, as was found in other species under identical conditions.

Administration, Inhalation↗
PubMed1990

Stress adaptation and low-frequency impedance of rat lungs.

At transpulmonary pressures (Ptp) of 7-12 cmH2O, pressure-volume hysteresis of isolated cat lungs has been found to be 20-50% larger than predicted from their amount of stress adaptation (J. Hildebrandt, J. Appl. Physiol. 28: 365-372, 1970). This behavior is inconsistent with linear viscoelasticity and has been interpreted in terms of plastoelasticity. We have reinvestigated this phenomenon in isolated lungs from 12 Wistar rats by measuring 1) the changes in Ptp after 0.5-ml step volume changes (initial Ptp of 5 cmH2O) and 2) their response to sinusoidal pressure forcing from 0.01 to 0.67 Hz (2 cmH2O peak to peak, mean Ptp of 6 cmH2O). Stress adaptation curves were found to fit approximately Hildebrandt's logarithmic model [delta Ptp/delta V = A - B.log(t)] from 0.2 to 100 s, where delta V is the step volume change, A and B are coefficients, and t is time. A and B averaged 1.06 +/- 0.11 and 0.173 +/- 0.019 cmH2O/ml, respectively, with minor differences between stress relaxation and stress recovery curves. The response to sinusoidal forcing was characterized by the effective resistance (Re) and elastance (EL). Re decreased from 2.48 +/- 0.41 cmH2O.ml-1.s at 0.01 Hz to 0.18 +/- 0.03 cmH2O.ml-1.s at 0.5 Hz, and EL increased from 0.99 +/- 0.10 to 1.26 +/- 0.20 cmH2O/ml on the same frequency range. These data were analyzed with the frequency-domain version of the same model, complemented by a Newtonian resistance (R) to account for airway resistance: Re = R + B/ (9.2f) and EL = A + 0.25B + B . log 2 pi f, where f is the frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1990

[Experimental emphysema following intravenous injection of trypsin].

The injection of trypsin provokes a decrease of the circulating antiproteases. Its effect on an elastase-induced emphysema is negligible. Paradoxically, emphysema is quantitatively demonstrated in rats treated with trypsin alone: an influx of polymorphonuclear leucocytes into the lung is observed during the acute phase of experiment.

Animals↗
PubMed1989

[Experimental study in the cat on the alveolar density and heterogeneity in the obstructed lung. Comparison with the emphysematous lung in the aged].

An experimental model of lung obstruction has been achieved in the cat reared in our laboratory. 30 young adults (J) and one adult subject (A) had tracheal stenosis from 8 to 15 weeks and were the object of a study of pulmonary airways and were compared with four young controls and seven older controls. The presence of emphysema was revealed by microscopy. The size of the alveoli was measured by the mean linear intercept (MLI). The study was systematized by an image analyser giving the ratio of airway spaces to pulmonary tissue (% of surface). The mean value S represented the alveolar section in the lung. Alveolar heterogeneity was expressed by the dispersion of the point values S around the mean S. The animals had episodes of ventilatory distress. Cytology of the broncho-alveolar lavage performed when the animals were sacrificed did not distinguish between the obstructive and other subjects. Emphysema was found in 10 out of 22 of the young stenosed animals. No control J were abnormal. 5 adults were emphysematous through ageing (5 years or more). The mean linear intercept of the alveoli was increased in the emphysematous (115%) and even more in the obstructive cases without or with emphysema where MIL attained 173%. The obstructive lung, whether emphysematous or not, is heterogeneous. Emphysema, always focal, corresponded to an alveolar section which was weakened (S less than S controls - 2 standard deviations) for 40% of the older subjects and for 50% of the J obstruction, up to two times more often than in obstruction without emphysema.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Intrapleural injection of elastase: a model for inducing subpleural emphysema?

Subpleural emphysema induction was attempted by injecting elastase intrapleurally into rats and cats. Microscopic evaluation of emphysema (alveolar dilation and septal rupture) was compared with a quantification of alveolar dilation (Fawell-Newman method). The emphysema found in animals treated with an intrapleural injection of porcine pancreatic elastase did not appear to be specifically located in a subpleural zone, and was identical to the focal emphysema induced by an enzyme instillation into the airways. It should be noted that a placebo instillation into the feline airways sometimes induced alveolar dilation without septal disruption presumably by causing bacterial contamination. Cats were seen to be very sensitive to pleural stress since this enzyme injection produced an alveolar dilation (increased mean intercept) as significant as that in cats treated by an intrabronchial instillation of elastase (P less than 0.001).

Administration, Inhalation↗
PubMed1987

[Pulmonary emphysema induced by elastase: influence of the dose and effect of added collagenase].

The endotracheal deposition of pancreatic porcine elastase (EPP) at 40 u X kg-1 body weight provokes a typical pulmonary emphysema (alveoli disruption) in rats. This emphysema is significant (p less than 0.001) when quantitatively compared to a placebo (100% increase of the mean linear intercept, ILM). The EPP-treated lungs are very heterogeneous and the size of the alveoli vary as much as 30% versus 19% in controls. The emphysema is more effective at a 80 u X kg-1 dose and the individual disparities are reduced (dose effect). When bacterial collagenase (200 u X kg-1 body weight) is added to EPP, the pulmonary abnormalities (disruptions, ILM) are in no way increased (no enzymatic synergy, repair by collagenesis?). In contrast, alveolar dilation is slightly reduced 8 weeks after enzyme administration (p less than 0.05): EPP is not altered in vitro by collagenase and despite several hypothesis, the moderating effect of collagenase in vivo still remains unexplained. This result suggests that the joint presence of several proteases is not necessarily an aggravating factor in the etiopathogenesis of emphysema.

Animals↗
PubMed1984

[Tracheal stenosis in the cat: anatomopathologic repercussions on the pulmonary parenchyma].

A calibrated stenosis of the trachea was performed in 6 young cats and 1 old one (TS cats); the animals were observed for 8 or 15 weeks thereafter. The percentage of macrophages in bronchoalveolar lavage fluid was greater in the TS cats than in the controls. An irregular distribution of pulmonary lesions was found. 4 TS cats presented with a real emphysema with tracheobronchial inflammation, a parenchymatous infection which was histologically shown or quantified in lavage fluid (Haemophilus (10(8]. They exhibited episodes of hypoventilation which followed in quick succession. The alveolar section of the TS emphysematous lung was equal or greater (up to 88% of the lung surface observed) than that of both the same-aged controls (81.5%) and of an old emphysematous cat (88 months). The alveoli were more homogeneous (lower deviation). TS lung was characterized by a higher amount of dry tissue protein but hydroxyproline varied individually. A possible synergy between infection and ventilatory obstruction may be a tentative explanation for the etiogeny of this emphysema which appears to be secondary to tracheal stenosis.

Airway Obstruction↗
PubMed1979

Intracellular pH changes during experimental sustained hypercapnia.

During various time periods lasting 3--28 days rats were continuously exposed to FICO2 = 0.08 or 0.16 in normoxic conditions, pHi was measured by the 3H-inulin and 14C-DMO method in the erythrocyte, the gastrocnemius and in the whole body. The erythrocyte acid base disturbances were linked to the extracellular acidosis. The muscle and the mean body pHi developments were the same during 9 or 14 days depending on the FICO2. They diverged after 28 days at FICO2 = 0.08 (Tables and Fig. 2). This could be explained as an acid base reaction of the "non-muscular" part of the whole body intracellular compartment which may be different from the acid base development of the muscular mass. A short term (1 h) acute hypercapnia (FICO2 - 0.20--0.22) was superimposed on the sustained hypercapnia (FICO2 = 0.16). Acid base disturbance was greater when the acute hypercapnia was added at the beginning (3rd day) of the CO2 exposure (Fig.1).

Acid-Base Equilibrium↗