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Biomedical subjects

S Matalon

Publications and source records attributed to S Matalon.

116 records · Page 7Linked to original sources
PubMed1982

Effects of hyperventilation on pulmonary blood flow and recirculation time of humans.

We used direct invasive techniques to measure the effects of hyperventilation on the pulmonary blood flow (Q) and on recirculation time of helium and of carbon dioxide in humans. The subjects hyperventilated with a tidal volume of 1.5 liters (BTPS) and a frequency of 20 or 30 breaths/min. There was no significant change in Q from control at either level of hyperventilation. Helium first appeared in the pulmonary artery within 12 s from the onset of hyperventilation and increased by approximately 0.7% of its equilibrium arterial value per second at both levels of hyperventilation. In contrast, the PVCO2 remained at base-line level until 43 s from the onset of hyperventilation. We conclude that hyperventilation at 30 or 45 l/min with constant tidal volume does not significantly affect the value of Q and that the amount of recirculation of the two gases does not result in underestimation of Q when this variable is measured by indirect respiratory rebreathing techniques.

Adult↗
PubMed1982

Pulmonary and circulatory changes in conscious sheep exposed to 100% O2 at 1 ATA.

We have measured the effects of normobaric hyperoxia on arterial and mixed venous gas tensions, cardiac output, heart rate, right atrial, pulmonary, and aortic pressures in 12 conscious chronically instrumented sheep. Regional blood flow to brain, heart, kidney, intestines, and respiratory muscles was assessed in five sheep by injecting 15-micrometers microspheres labeled with gamma-emitting isotopes. Survival time ranged from 60 to 120 h (mean = 80 h). All variables except arterial O2 partial pressure (PaO2) and mixed venous O2 partial pressure remained at base-line level during the first 40 h of exposure, after which PaO2 decreased gradually but remained above 200 Torr at death. After this there was a progressive uncompensated respiratory acidosis with terminal arterial CO2 partial pressure values exceeding 90 Torr. There was a considerable rise in the brain blood flow, whereas flow to the other organs either remained unchanged or increased in proportion to cardiac output. Our experiments also showed that systemic hyperoxic vasoconstriction did not occur, and any local changes were not of sufficient magnitude to affect perfusion.

Animals↗
PubMed1981

Effects of 100% O2 breathing on permeability of alveolar epithelium to solute.

We measured the effects of 100% O2 exposure at 1 atm for 48 (n = 5) and 63 h (n = 6) on the solute permeability of the alveolar epithelium of rabbits. We instilled 10-15 ml of saline containing trace amounts of 131I-albumin (r approximately 35 A), 125I-cytochrome c (r approximately 17 A), and [57Co]cyanocobalamin (r approximately 6.5 A) into an atelectatic segment of the right lower lobe. Egress of these tracers was determined from their change in concentration in the alveolar saline and their detection in arterial blood. All tracers left the alveolar space and appeared in the arterial blood on the 63-h O2 group, cytochrome c and cyanocobalamin in the 48-h O2 group, and only cyanocobalamin in the control (air breathing). The O2-exposed animals had PaO2 values higher than 500 Torr, normal PaCO2 and pH, and wet-to-dry lung weight ratios not different from control. We concluded that increasing the length of O2 exposure increases the solute permeability of the alveolar epithelium and this precedes the appearance of pulmonary edema.

Albumins↗
PubMed1981

An ultrastructural study of alveolar permeability to cytochrome C in the rabbit lung: effect of exposure to 100% oxygen at one atmosphere.

Rabbits were exposed to 100% oxygen or to air at one atmosphere. No alterations were observed in the lung of rabbits breathing air for up to 66 hours or 100% oxygen for 24 hours; after 48 hours, inflammatory cells, chiefly neutrophils, were located in the interstitium of the lung. By 66 hours of oxygen, the number of inflammatory cells in the interstitial space was greater than at 48 hours. At 72 hours, alveolar space in focal areas of the lung was filled with edema fluid containing a lightly flocculent material, and more densely staining fibrin. In experiments for the study of alveolar permeability, cytochrome C was instilled through the tracheobronchial tree into alveoli and demonstrated ultracytochemically by its peroxidase activity. No electron-opaque reaction product was observed in control rabbits or in those breathing oxygen for 24 hours, indicating that the tracer did not leave the alveolar space. However, after 48 hours of the breathing of 100% oxygen, electron-opaque reaction product was localized to the basal lamina of alveolar capillaries in focal areas, whereas in other alveolar capillaries there was no reaction product in the basal lamina. Vesicles filled with reaction product were observed in Type 1 pneumocytes and in alveolar capillary endothelial cells within capillary loops having increased electron density in the basal lamina. After 66 hours of the breathing of 100% oxygen, virtually all alveolar capillaries showed electron-opaque reaction product in the basal lamina and in vesicles within Type 1 cells and capillary endothelial cells. Increased permeability of Type 1 pneumocytes appears as an early manifestation of oxygen-induced changes in the lung preceding pulmonary edema. The presence of numerous inflammatory cells in the interstitium and in alveolar capillaries may play some part in the pathogenesis of the oxygen-induced increase in alveolar permeability.

Animals↗
PubMedDate not supplied

The teratogenic effect of carbamazepine: a meta-analysis of 1255 exposures.

Maternal use of antiepileptic drugs during pregnancy has been associated with an increased risk of major congenital abnormalities in the fetus. Carbamazepine (CBZ) is an antiepileptic drug that was developed and marketed mainly for the treatment of epileptic seizures. Some investigators described an increased rate of major congenital anomalies following treatment with CBZ during pregnancy while others found no such increase. In order to quantify better the risks of exposure to CBZ during pregnancy, we pooled data from prospective studies known to us. We found in prospective studies involving 1255 cases of exposure that CBZ therapy increased the rate of congenital anomalies, mainly neural tube defects, cardiovascular and urinary tract anomalies, and cleft palate. CBZ may also induce a pattern of minor congenital anomalies and developmental retardation, but our study did not address these endpoints. CBZ also appears to reduce gestational age at delivery. A combination of CBZ with other antiepileptic drugs is more teratogenic than CBZ monotherapy. Children born to untreated epileptic women do not appear to have an increased rate of major birth defects. In light of these results, we recommend performing a level 2 ultrasound and fetal echocardiography in women treated with CBZ during pregnancy.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Modulation of rat lung Na+,K(+)-ATPase gene expression by hyperoxia.

Rats exposed to 85% O2 for 5-7 days develop tolerance to otherwise lethal hyperoxia (100% O2). The rate of alveolar fluid clearance increases during adaptation to hyperoxia, due in part to increased alveolar epithelial sodium channel activity. In these studies, we have investigated molecular mechanisms leading to increased lung Na+,K(+)-ATPase activity in hyperoxia. We exposed adult rats to 85% O2 (sublethal hyperoxia) for 7 days, followed by 2, 3, or 4 days in 100% O2. Steady-state levels of the Na+,K(+)-ATPase alpha 1 and beta 1 subunit mRNAs increased in whole lung tissue during hyperoxia exposures. Stability of the Na+,K(+)-ATPase alpha 1 and beta 1 subunit mRNA messages in whole lung RNA did not change significantly. Thus, lung Na+,K(+)-ATPase gene expression in sublethal hyperoxia appears to be regulated in part at the transcriptional level. Alveolar epithelial type II (ATII) cell Na+,K(+)-ATPase alpha 1 and beta 1 subunit proteins, measured by quantitative immunofluorescence, increased significantly after sublethal hyperoxia and 100% O2 exposures. Increases in lung fluid clearance after sublethal hyperoxia are associated with increased ATII cell Na+,K(+)-ATPase protein and whole lung Na+,K(+)-ATPase mRNA expression, which correspond to previously described increases in epithelial sodium channel expression under these conditions.

Animals↗
PubMedDate not supplied

A method for the in vitro measurement of tensions of blood gases with a mass spectrometer.

A specially designed cuvette with an in vivo catheter allows the in vitro measurement of gas tensions in heparinized samples of blood with a mass spectrometer. Approximately 1.5 cc of blood is required, half of which is used to clear the dead space of the cuvette. The partial pressures of oxygen (P-o2) and of carbon dioxide (Pco2) of arterial and venous samples obtained from the catheterized femoral arteries and veins of 10 mongrel dogs were measured with the mass spectometer and with a conventional pH/gass analyzer. Good agreement was obtained between the two methods. The range of validation for P-o2 was between 35 and 100 mmHg; for P-co2 it was between 20 and 88 mmHg. Depletion, temperature control, flow dependency, and calibration problems are discussed.

Animals↗