Search PubMed⌕ Search

Biomedical subjects

G Greisen

Publications and source records attributed to G Greisen.

115 records · Page 7Linked to original sources
PubMed1977

Drug absorption and hepatic drug metabolism in patients with different types of intestinal shunt operation for obesity. A study with phenazone.

Seventeen patients with intestinal shunt for obesity and 11 control patients were given 15 mg phenazone per kg perorally to estimate the rate of absorption and hepatic metabolism of phenazone. The rate of absorption and the plasma clearance of phenazone as well as the 4-hydroxyphenazone excretion in the urine did not differ in the patients with intestinal shunt after the weight had stabilized. Thus, drug absorption and hepatic drug metabolizing capacity appear to be unaffected 12--57 months after intestinal shunting.

Adult↗
PubMed1976

Pharmacokinetics of diazepam in disordered liver function.

The plasma elimination curves of diazepam following intravenous administration of 10 mg were studied in nine patients with cirrhosis of the liver and four patients without liver disease. The data were analyzed according to a two compartment model. The mean biological half-life (T/2) of diazepam was increased five-fold in patients with cirrhosis compared to the controls (164 hours vs. 32.1 hours). The plasma clearance of diazepam could be correlated neither with a quantitative measure of liver function, as estimated by galactose elimination capacity, nor to semiquantitative measures of liver function, such as serum albumin and prothrombin. It is suggested that the plasma clearance of diazepam is an inaccurate index of its rate of hepatic metabolism due to the complex kinetics of the drug.

Adult↗
PubMed1976

Phenazone metabolism in patients with liver disease.

Phenazone metabolism was studied in 14 patients with liver disease and six normal volunteers. The plasma and renal clearance of phenazone and the 4-hydrozyphenazone excretion in urine was significantly decreased in the patients with liver disease. The urinary excretion of 4-hydroxyphenazone was significantly correlated to the plasma clearance of phenazone (r= + 0.95, P less than 0.001), to quantitative liver function as measured by the galactose elimination capacity (r= + 0.95, P less than 0.001), and to the prothrombin values (r= + 0.82, P less than 0.001). The determination of the 4-hydroxyphenazone excretion in urine may be used as an easy and non-invasive test of quantitative liver function.

Adult↗
PubMedDate not supplied

Visual evoked potentials in preterm infants during the first hours of life.

Flash evoked cortical potentials (VEPs) were studied in 33 preterm infants with gestational ages from 27 to 33 weeks. During the first 12 h after birth a visual response was evoked in all infants. Better estimates of the VEP latency and amplitude were obtained by using the values of 3 VEPs recorded at 30 sec intervals. The VEP latency decreased during the first hours of life, which was accounted for by an increase in core temperature; the latency decreased 6 msec/degrees C increase. Changes in amplitude were less influenced by changes in temperature. Both VEP latency and amplitude were inversely related to gestational age, but there was no association between head circumference and latency. The flash intensity could be reduced from 155 cd to 39 cd without any effect on VEP latency or amplitude. Similarly, a variation of background illumination below 200 lux did not cause VEP changes. The VEP was not affected by development of minor subependymal haemorrhages but it was severely attenuated during a short episode of hypoxia. It is suggested that when taking core temperature into account the VEP can be used to determine changes in the cerebral function in preterm infants.

Cerebral Hemorrhage↗
PubMedDate not supplied

Preservation of single-flash visual evoked potentials at very low cerebral oxygen delivery in preterm infants.

Single-flash visual evoked potentials (VEPs) were recorded in 32 preterm infants (mean gestational age: 29 weeks) during extreme physiologic conditions within the first day of life. The VEP configuration was normal in all patients at the onset of the investigation. Hypoxic episodes (PaO2 less than 3 kPa) caused rapid and consistent attenuation of the VEP mostly with an instantaneous recovery after normalization of PaO2. In contrast, VEP amplitude and latency were unaffected during episodes with low cerebral blood flow (4.5 ml/100 gm/min) and correspondingly low oxygen delivery to the brain (1 ml/100 gm/min), severe hypocapnia (PaCO2 1.6 kPa), and severe arterial hypotension (MABP 10 mm Hg), provided that the arterial oxygen tension was greater than 5 kPa. Absence of N1 was observed soon after the development of severe intracranial hemorrhage; however, this abnormality was short in duration. We conclude that the neurons generating VEPs are supported sufficiently during extreme physiologic episodes, except during severe hypoxia. The recovery time may be proportional to the cerebral insult.

Carbon Dioxide↗