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Biomedical subjects

E Becker

Publications and source records attributed to E Becker.

At least 109 records · Page 6Linked to original sources
PubMed1978

Gastrointestinal hemorrhage in long-lasting traumatic coma.

Sixteen cases, aged 19 to 61 years and suffering from traumatic coma were studied for periods varying from 7 to 20 months. Obvious or occult gastrointestinal hemorrhage appeared in every case, the earliest presentation being after a few weeks and the latest at 20 months. Gastric acidity was normal in 15 cases. Five patients had duodenal ulceration in repeated roentgenological examination. Concomitant clinical findings included clubbing and paraarticular new bone formation in 9 patients. In addition, hypoxia with repeated values between 63 and 88 mm was observed in 13 of the 16 patients. The latter observation strongly suggests that hypoxia of gastrointestinal mucosa may, indeed, play a pathogenetic role in gastrointestinal hemorrhage of patients with C.C.I.

Adult↗
PubMed1978

Recovery of communicative functions after prolonged traumatic coma.

Fifteen patients with prolonged coma after craniocerebral injury were observed for a year or more, and their communicative functions were evaluated. Nine of them showed a considerable degree of recovery, while 6 remained in a vegative state. Of the 9 with recovery, 6 showed complete recovery of semantic functions, while 3 remained with aphasic deficits. Eight out of these 9 remained dysarthric. Communicative recovery began as late as 5.7 months after injury, and it roughly paralleled recovery in locomotion and A.D.L. Restlessness and sweating were favorable prognostic factors. Excessive salivation, snout reflex, corneomandibular reflex, retractory nystagmus and stereotypic movements were unfavorable. The 8 patients who remained dysarthric showed marked diminution of their expiratory and inspiratory reserves, and of their forced vital capacity.

Adult↗
PubMed1978

Pulmonary functions and responses to exercise of patients following cranio cerebral injury.

To assess the causes of excessive fatigue among patients who have recovered from cranio-cerebral injury (CCI) nineteen patients and fourteen healthy controls underwent pulmonary function testing at rest and cardiopulmonary evaluation during two submaximal exercise work-loads. Total lung capacity, vital capacity and forced expired volume were reduced by 25--40% among the patients. Functional residual capacity was normal. No improvement was elicited by inhalation of Ventolin and bronchoconstriction could thus be excluded. The above pattern may result from either decreased compliance of the chest wall or from weak (or non-coordinated) respiratory musculature. Exercise heart rate, minute ventilation and ventilatory equivalent were higher, and O2 pulse lower, among the CCI patients compared with the controls. This indicates lower circulatory and ventilatory efficiency during exercise among the patients, possibly due to habitual hypoactivity and detraining.

Adult↗
PubMed1977

Contractile and biochemical responses of cardiac and skeletal muscle to isoproterenol covalently linked to glass beads.

The effects of (-)-isoproterenol covalently linked to glass beads on inotropic state, cyclic AMP concentration, and phosphorylase b to a conversion was studied in cat and guinea pig papillary muscles. Biochemical responses also were measured in mouse diaphragm sections. In cat papillary muscles under normal conditions and in guinea pig muscles partly depolarized with 22 mM K+ an increased inotropic state and phosphorylase activation could be dissociated from the formation of cyclic AMP. This contrasts with close correlation reported between isometric tension and cyclic AMP concentration in guinea pig papillary muscles exposed to varying concentrations of isoproterenol dissolved in the bath medium. The cyclic nucleotide did increase in guinea pig papillary muscles exposed to a freshly prepared batch of isoproterenol beads and in the mouse diaphragms. The type and age of the bead preparation had marked effects on all responses that were measured and on the rate of leakage of biologically active products from the beads. Nevertheless, experimental conditions could be obtained under which the initiation of the contractile and biochemical responses was probably limited to intense stimulation of receptors at or near the points of contact between beads and muscle and not due to gross leakage into the bath. The results indicate that cyclic AMP is probably involved in the initiation but not the propagation of the inotropic response of papillary muscles exposed to isoproterenol glass beads.

Animals↗
PubMed1977

Electrophysiological responses of cardiac muscle to isoproterenol covalently linked to glass beads.

We investigated the effects of isoproterenol aryl glass beads on the electrical properties of cardiac muscle and related these to our previous results concerning biochemical and contractile effects (Ingebretsen et al., Circ, Rs., 40: 474-484, 1977). Beads (10-15) were placed near one end to guinea pig papillary muscles mounted horizontally in a bath perfused with Krebs-Henseleit solution at 30 degrees C and stimulated at 0.2 Hz. The beads produced increased tension and elevation and slight lengthening of the plateau potential when [k+]o = 3.8 mM. After depolarization to a resting potential of -49 mV with [K+]o = 22 mM, isoproterenol beads restored contraction to a comparable extent as occurred with 10(-8) M soluble drug. During field stimulation, action potentials were initiated at the site of bead application and spread decrementally. When beads were placed distal to the site of point stimulation, virtually no excitation could be obtained from cells in the vicinity of the beads. When they were placed close to the stimulating electrode, the beads increased excitability and typical slow action potentials spread to the other end of the muscle. These potentials had the characteristics associated with the slow inward Ca2+ current. The slow channel blocker, D-600, blocked responses to isoproterenol beads. Tetrodotoxin caused responses similar to those obtained with K+ depolarization. The beads probably act by stimulating only a small fraction of the papillary muscle catecholamine receptors. Spread of action potentials from these sites and propagated tension depend on Ca2+ influx, but the nature of an intermediate messenger involved in the propagation of contractions is unknown.

Action Potentials↗
PubMedDate not supplied

Growth stimulation of primary rat hepatocytes by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The modulation of liver growth control by the tumor promoter, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was investigated in primary hepatocytes of adult rats. Under defined conditions in serum-free cultures, the interaction of TCDD with growth-related hormones was studied. TCDD-treatment of the cultured hepatocytes for two days caused a transient stimulation of both DNA synthesis and mitotic activity. This effect was maximal at the very low nontoxic concentration of 10(-12) M TCDD, i.e., two orders of magnitude below the optimal concentrations for induction of drug metabolizing enzymes. Growth stimulation by TCDD was dependent on the presence of growth-related hormones; in primary rat hepatocytes, TCDD acted synergistically with insulin and epidermal growth factor (EGF) and antagonized the growth inhibition by dexamethasone. Under culture conditions allowing high rates of DNA synthesis, e.g., at low concentrations of dexamethasone, in the presence of EGF plus alpha 1-adrenergic agonists or rat serum, no significant effect of TCDD on cellular growth was observed. Furthermore, TCDD failed to stimulate DNA synthesis in a rat hepatoma cell line, H4IIE, which is less sensitive to growth controlling factors than normal hepatocytes. Therefore, the results suggest that the growth modulation of primary rat hepatocytes by TCDD is the most sensitive parameter of the agent thus far observed. This effect may involve both a release from the growth inhibition caused, for instance, by glucocorticoids, as well as a direct growth-stimulating effect, synergistic to the one induced by insulin.

Adrenergic alpha-Agonists↗