Minor vascular anatomy of the abdomen and pelvis: a CT atlas.

With the early generations of computed tomographic (CT) scanners, interpretation of abdominal and pelvic scans focused on the solid organs, hollow viscera, and retroperitoneum. Attention to blood vessels generally was given only to the aorta and inferior vena cava and their larger branches. The newer generations of scanners allow rapid acquisition of high-resolution images during the vascular phase of mechanical bolus injection of intravenous contrast material. Visualization of second-order vascular branches has thus become routine. Recent improvements in software allow real-time reconstruction of data in multiple planes, which enables demonstration of long segments of vessels within a single image. Approximately 7,000 abdominal and pelvic CT scans were reviewed with attention to vascular detail. Cases are presented that illustrate peripancreatic, perigastric, parietal, and hypogastric vessels; fetal remnants and structures that may be mistaken for vessels; and collateral pathways of both arterial and venous flow. With increasing use of helical CT scanning, smaller vessels can be identified with greater confidence. Knowledge of normal CT vascular anatomy facilitates understanding of collateral pathways when vessel engorgement is perceived.

Labor and infection. II. Bacterial endotoxin in amniotic fluid and its relationship to the onset of preterm labor.

We have previously reported the detection of endotoxin in the amniotic fluid of patients with gram-negative intraamniotic infection. Endotoxin or lipopolysaccharide is a potent biologic product capable of inducing prostaglandin release from several cell types and, therefore, may be involved in the onset of human parturition in the presence of intraamniotic infection. This article describes a technique for the quantification of endotoxin in amniotic fluid. The method uses a computer-assisted quantification of the turbidimetric reaction between the Limulus amebocyte lysate and endotoxin. Serial dilutions of Escherichia coli endotoxin in culture-negative amniotic fluid were prepared, and the samples were run in the assay. Amniotic fluid was found to enhance the reaction, and a dilution of 1:20 was required for this biologic fluid to behave similarly to pyrogen-free water. The sensitivity of this kinetic turbidimetric technique in the detection of endotoxin in amniotic fluid was 40 pg/ml. This method was applied to the quantification of endotoxin concentration in amniotic fluid in 26 patients with intraamniotic infection and premature rupture of membranes. Patients in active labor had higher concentrations of endotoxin (median = 47,514 pg/ml) than nonlaboring patients (median = 635 pg/ml) (p less than 0.025). Therefore, women with preterm labor had a higher median concentration of endotoxin in amniotic fluid than patients who were not in labor.

Cholinergic modulation of human limbic evoked potentials.

Limbic evoked potentials (LEPs) were recorded from the hippocampi of three epilepsy surgery patients with unilateral medial temporal lobe seizure onset. In each patient, stable large amplitude LEPs which displayed polarity inversion across successive levels of hippocampus were present unilaterally, but were absent or rudimentary in the hippocampus corresponding to the electrographically proven seizure onset. After administration of scopolamine, LEPs in the "normal" hippocampi were markedly altered with slowing of the individual components and increased trial to trial variability. In addition, two patients developed reliable, high amplitude, polarity inverting LEPs on the side of seizure onset which had either absent or rudimentary LEPs in the baseline state. The results suggest that LEPs are under cholinergic modulation.

Limbic evoked potentials predict site of epileptic focus.

Limbic evoked potentials (LEPs) were recorded from intracerebral electrodes in the hippocampi of seven preoperative epilepsy surgery patients. LEPs were evaluated using amplitude, form, and asymmetry by raters blinded as to the side of electrographically proven seizure onset. Raters correctly predicted the side of focus in all four patients with proven unilateral temporal lobe seizure onset. Further, LEP amplitudes in two patients with bilateral independent temporal lobe seizure onset were markedly diminished compared with one patient with a nontemporal lobe seizure onset. LEP recordings may assist in determination of the site of epileptogenic pathology.

Modulation by small hydrophobic molecules of valinomycin-mediated potassium transport across phospholipid vesicle membranes.

The effects of small hydrophobic molecules on valinomycin-mediated K+ transport in small unilamellar soybean phospholipid vesicles have been studied by using a vesicle-entrapped pH-sensitive hydrophilic fluorescence probe to monitor counterion-limited, passive H+ diffusion into vesicles after an abrupt decrease in external pH [Clement, N. R., & Gould, J. M. (1981) Biochemistry (preceding paper in this issue)]. Under conditions where, even in the absence of valinomycin, transmembrane KL+ movement represented the primary and limiting counterion flux, less than 1 valinomycin molecule/vesicle was sufficient to accelerate the rate of H+ entry into all of the vesicles. Incorporation of the bulkily substituted molecules butylated hydroxytoluene (BHT), butylated hydroxyanisole (BHA), and p-di-tert-butylbenzene into soybean lipid bilayers had no effect upon K+ diffusion in the absence of valinomycin. However, the presence of these hydrophobic molecules increased the apparent efficacy for K+ transport of a given valinomycin concentration by as much as 4-6 fold. The less bulky membrane perturbants tert-butyl alcohol, phenol, and heptane showed very much less dramatic effects. While the rate of valinomycin-mediated K+ transport (in the presence or absence of BHT) was very sensitive to temperature-induced changes in membrane fluidity, the degree of synergistic interaction between valinomycin and BHT was independent of temperature. Furthermore, BHT, BHA, and p-di-tert-butylbenzene, at levels which alter valinomycin-mediated K+ transport, did not by themselves induce changes in membrane fluidity. It is postulated that changes in phospholipid head-group packing and/or surface charge density brought about by the presence of bulky perturber molecules leads to changes in partitioning of valinomycin or the valinomycin-K+ complex between the aqueous and membrane phases.