Biomedical subjects
Publications and source records attributed to I Alter.
The cerebral origin of a directional bias in visual perception has proved difficult to ascertain. By means of a brief and reliable visuographic task, from which is derived an index of directionality (D), distributions of directional bias are shown to be related to handedness, as well as to other variables usually associated with cerebral lateralization. Familial sinistrality, gender, and age also influence the direction of bias.
We have shown that a directional bias (D), previously thought to be unrelated to cerebral lateralization, is, in fact, intimately associated with it. In a group of fully consistent dextrals without familial sinistrality, the direction of lateral asymmetries depended upon the direction of D. Left-directed dextrals manifested the usual visual field advantages for linguistic and spatial material, while right-directed dextrals did not. D is therefore recommended as moderator variable for future studies of laterality.
The Fourier descriptor (FD) method of shape representation provides a convenient description for the outlines of shapes. It can also be used to generate orthogonal patterns (FD stimuli) which are uniquely characterized by their frequency, amplitude, and phase. Psychophysical studies were conducted to assess threshold tuning properties and frequency specificity during adaptation to FD stimuli. The results suggest the operation of filters which are characterized by the parameter 'curvature frequency'.
A simple technique has been devised to catheterize the pulmonary artery in rats for measurement of pulmonary artery pressure. A no. 3 1/2 French umbilical vessel catheter (Argyle), angled to 90 degrees over the distal 1 cm, was introduced into the right external jugular vein of the anesthetized (50 mg/kg pentobarbital sodium, ip) rat (male Wistar, 250-350 g). With the angle directed anteriorly, the catheter was inserted 2.5 cm proximally, which placed the catheter in the right atrium. The catheter was rotated 90 degrees counterclockwise and inserted 1.0 cm further, which placed the catheter in the right ventricle. Advancement of the catheter an additional 1.5 cm allowed placement in the pulmonary artery. Placement at each stage was confirmed by the respective pressure contours. This technique is easily and rapidly performed and has many potential applications in measuring parameters of the pulmonary circulation in a variety of small laboratory animals.
Arachidonic acid (AA) produces characteristic hemodynamic changes in the canine circulation. These responses are blocked by prostaglandin (PG) synthetase inhibitors, indicating that AA and its nonprostanoic metabolites are not vasoactive. The hemodynamic effects of the cyclic endoperoxides, thromboxanes, and PGD2, PG2, and PGF2a differ from those produced by AA. PGI2, a newly identified product of AA, is reported to relax arterial strips. However, its cardiac and systemic effects are unknown. In 12 open-chest, anesthetized dogs, PGI2 (0.25-5.0 microgram/kg) produced a dose-related decrease in systemic arterial pressure (BP) and myocardial contractile force (MCF). In five left ventricular bypass preparations, PGI2 produced only a slight decrease in MCF at all doses, whereas the BP decreases were parallel to those in the intact preparation. AA, PGD2, PGE2, and PGI2 were administered in random order by bolus intravenous injections in approximately equidepressor doses to intact dogs. BP fell with each agent (AA, 300 microgram/kg, -25 percent; PGD2, 5 microgram/kg, -26 percent; PGE2, 5 microgram/kg, -26 percent PGI2, 0.5 microgram/kg, -26 percent). The vasodepressor action of PGI2 was approximately 10 times greater than that of PGD2 and PGE2. Pulmonary arterial pressure (PAP) rose significantly with PGD2 and PGE2 (AA, -1 percent; PGD2 +66 percent; PGE2, +20 percent; PGI2, -1 percent). Only PGE2 had a significant effect on MCF (AA, +7 percent; PGD2, +5 percent, PGE2, +20 percent; PGI2, -0.3). At this dose, PGI2 resembles AA in that it has little effect on either PAP or MCF. Of all known AA metabolites the response to PGI2 most closely resembles that of exogenous AA in the dog.
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Arachidonic acid (AA) (100 and 200 microgram/kg) and prostacyclin (PGI2) (0.25, 0.5, 1,2 and 3 microgram/kg) were administered by bolus injection into the inferior vena cava (i.v.) and left ventricle (i.a.) in spontaneously breathing anesthesized dogs (25). PGI2 like its precursor AA, decreased arterial diastolic pressure in a dose-dependent manner. The depressor responses after i.a. administration of a given dose of either AA or PGI2 did not differ significantly when the same dose was given i.v.; the i.v./i.a. ratio was 1. In comparison, the vasodepressor response to PGE2 (1, 2 and 3 microgram/kg i.v.) was reduced 12- to 40-fold by passage through the dog lung. The vasopressor response to PGF2alpha (1, 2, 3 and 5 microgram/kg i.v.) was diminished 5- to 8-fold by lung transit. Similarly, the pressor response to norepinephrine was also reduced by pulmonary transit. These studies support the view that (1) the lung plays a minor role in the systemic depressor response to AA and PGI2 and (2) the lack of an i.v./i.a. difference for AA and PGI2 indicates that the depressor response to AA may be due to generation of PGI2 by the vessel wall.
Efforts to develop an in vivo prostaglandin (PG) antagonist have met with limited success. In this study, N-dimethylamino analogs of PGF2alpha which have proven to be effective in vitro prostaglandin antagonists, were tested for antagonism to the PGF2alpha and arachidonic acid (AA) responses in the canine lung lobe preparation. PGF2alpha (1 microgram/kg) and AA (100 microgram/kg) increased lobar arterial pressure by 54 and 83%, respectively. Infusion of analogs did not change lobar arterial pressure. N-dimethylamine PGF2alpha (0.8-3.2 microgram/ml) antagonized the PGF2alpha response by 66 to 79%. N-dimethylamide PGF2alpha (1.6-8.0 microgram/ml) produced a dose-dependent antagonism (24-75%) with an IC50 value of 3.8 microgram/ml. Neither analog significantly attenuated the pulmonary response to AA. Thus, these N-dimethylamino analogs of PGF2alpha exhibit a potency which is superior to previous in vivo prostaglandin antagonists. In addition, they have effectively differentiated the pulmonary vascular responses of AA and PGF2alpha.
1. Intravenous administration of both the 9alpha,11alpha-(epoxymethano) and 11alpha,9alpha-(epoxymethano) analogues of prostaglandin H2 (0.25 microgram/kg) produced a prominent rise in pulmonary arterial pressure and a moderate increase in systemic arterial pressure. 2. Direct administration of the endoperoxide analogues (1.25 microgram/kg) into the bypass reservoir produced a greater rise in systemic arterial pressure and less prominent rise in pulmonary arterial pressure. 3. An intravenous dose of prostaglandin F2alpha that was 20 times larger was needed to produce a comparable rise in pulmonary arterial pressure. 4. The pulmonary and systemic pressor responses produced by the endoperoxide analogues were due to a direct increase in the vascular resistance.
A combination of several automatically-extracted quantitative features of evoked potentials (EPs) can discriminate between globally good and poor outcomes following severe head injury. Further, a single EP feature, its peak-to-peak variance, can select for the severely disabled survivor from among other poor outcomes, a potentially important distinction for the management of patients suffering severe head trauma.