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Biomedical subjects

L Z Bito

Publications and source records attributed to L Z Bito.

At least 73 records · Page 4Linked to original sources

Prostaglandin E1-induced latent epileptogenic foci.

Suprafusion of 125 microliter 6% KCl solution over the visual cortex of rabbits 2-24 h after they suffered a prostaglandin (PG) E1-induced epileptic seizure was found to cause a recurrence of seizure activity. The initial seizure was induced by the cortical suprafusion of PGE1 over the left visual cortex of PG transport inhibitor-pretreated rabbits. Control animals that were not pretreated with PG transport inhibitors (bromcresol green or probenecid), or received suprafusion of saline or PGF2 alpha rather than PGE1, did not show initial seizure activity. In these animals, and in animals that had PG-induced seizures 72 h before KCl administration, the KCl solution caused only inhibition of the visually evoked response but no seizure activity. The results are interpreted to indicate that under appropriate conditions PGE1 can create a latent epileptogenic focus which can be reactivated by KCl. It is suggested that since PGE1 is produced by the brain normally, and in increased amounts as the result of overstimulation, irritation or trauma, this potent autacoid may play a role in the spontaneous development of latent epileptogenic foci or the recurrence of epileptic seizures.

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Intraocular pressure of rhesus monkey (Macaca mulatta). I. An initial survey of two free-breeding colonies.

As part of an ophthalmic and anthropometric survey of two free-breeding rhesus monkey (Macaca mulatta) populations, intraocular pressure (IOP) of 114 animals was measured under ketamine catalepsia with the use of a floating-tip pneumatonometer. The mean IOP of the 102 animals included in the main analyses was 14.9 +/- 2.1 (S.D.) mm Hg. The age distribution of animals in this sample ranged from 7 months to 21 years and reflected reasonably well the estimated age distribution in the total population (approximately 1600 macaques). Since ketamine does not have a barbiturate-like effect on IOP, this value can be regarded as a good estimate of the normal IOP of rhesus monkeys. No significant differences were found between left and right eyes nor between males and females. However, the mean IOP of infants and juveniles (7 months to 3 years) was significantly higher (15.7 +/- 2.0 mm Hg; n = 33) than that of young adult and adult rhesus monkeys (14.5 +/- 2.0; n = 69). The IOP of young animals (less than or equal to 6 years) showed a decline between 9 A.M. and 2 P.M., whereas the IOPs of older animals showed only small fluctuations between 8 A.M. and 5 P.M. This study shows that the normal IOP of macaques is remarkably similar to that of humans and demonstrates the fesibility of surveying IOP in free-ranging primates.

Aging↗

The insensitivity of the chicken eye to the inflammatory effects of x-rays in contrast to its sensitivity to other inflammatory agents.

The effects of x-rays and three chemical agents, known to cause intraocular inflammation in mammalian eyes, were studied on the chicken eye because this species was reported to be insensitive to the cataractogenic effects of x-rays. Intravitreal injection of Shigella endotoxin and topical and/or intravitreal administration of PGE2, PGF2alpha, or arachidonic acid caused a breakdown of the blood-aqueous barrier, as indicated by flare and increased protein concentration in the aqueous humor. Following endotoxin injection, there was also a large accumulation of cells in the anterior chamber. The ocular inflammatory effects of endotoxin and arachidonic acid were inhibited by indomethacin. Thus the chicken eye reacts to these inflammatory agents in a manner similar to that previously described for the rabbit. In contrast, the inflammatory response which was reported to occur in the rabbit eye 3 to 4 hr after exposure to 500 or 1000 rads of x-rays was not observed in the chicken eye even after expsoure to 10,000 rads. Minimal flare and a small cellular infiltration were observed in some eyes only after extensive swelling of the surrounding tissues had developed. It is concluded that the insensitivity of the chicken eye to x-rays is due to some unique difference in the chain of events which mediates, or prevents, the effects of ionizing radiation rather than to a general insensivity to inflammatory agents.

Animals↗

The effects of intravitreally injected prostaglandin E1 on retinal function and their enhancement by a prostaglandin-transporter inhibitor.

The effects of intravitreally injected prostaglandins (PG's) E1 and F2alpha were studied on conscious, bromcresol green (BrCG)-pretreated and control rabbits. The electroretinogram (ERG) of both the PG-injected and the contralateral control eyes was recorded with contact lens electrodes; and electrocorticogram and the visually evoked response (VER) were recorded from both hemispheres with previously implanted supradural electrodes. In normal rabbits, intravitreal injection of 0.70 mg of PGE1 resulted in a small reduction in the amplitude of the ERG b-wave and of the slow negative wave (SNW) of the contralateral VER. In BrCG-pretreated rabbits, intravitreal injection of 0.70 mg of PGE1 caused a statistically significant decrease in the amplitude of the ERG b-wave and the SNW. Intravitreal injection of 0.7 mg of PGE1 also caused a significantly prolonged inhibition of the ERG in BrCG-pretreated, but not in normal rabbits, following exposure of the eye to a bright light flash. A smaller dose of PGE1 (0.35 mg/eye) caused more moderate effects on some of these parameters. These effects could not be explained by the PG-induced miosis. PGF2alpha (0.7 mg/eye) caused no significant changes in any of the parameters studied. These results indicate that exogenous PG's can have adverse effects on retinal function and that these effects are enhanced by BrCG, a PG-transport inhibitor. Presumably, this inhibitor blocks the PG-removal mechanisms across the blood-retinal barriers and hence allows the accumulation of PG's in the extracellular fluids of the retina.

Animals↗

Inflammatory effects of endotoxin-like contaminants in commonly used protein preparations.

Protein preparations from commercial suppliers are contaminated with bacterial endotoxins. The continued use of these preparations indicates that many researchers are unaware of this, and they may attribute all observed effects to the proteins themselves. Intravitreous injection of bovine serum albumin has an initial inflammatory effect on the rabbit eye which occurs before an immune reaction to the antigen itself can develop. This direct inflammatory effect can be fully accounted for by endotoxin-like contaminants which are present in protein preparations obtained from commercial suppliers. A pharmaceutical (U.S. Pharmacopeia) serum albumin preparation contains no detectable endotoxin, and has no initial inflammatory effect on the eye. Since endotoxins, even in minute amounts, have a variety of effects, the use of such contaminated protein preparations in biological research can lead to erroneous conclusions and should, therefore, be avoided.

Animals↗

Dependence of pulmonary prostaglandin metabolism on carrier-mediated transport processes.

Inhibitors of prostaglandin (PG) transport (probenecid, indomethacin, or bromcresol green) were found to eliminate the difference between the pulmonary transit time of 3H and 14C when [3H]PGF2alpha and E114C]sucrose were injected as a single intra-arterial bolus into the isolated perfused rat lung. Similar results were obtained with PGE1. The transit time of [3H]PGA1 was not significantly different from that of [14C]sucrose even in the absence of an inhibitor. These inhibitors increased the amount of [3H]PGF2alpha or [3H]PGE1 and decreased the amount of [3H]PG metabolites found in the venous effluent: these agents also inhibited the pulmonary metabolism of continously infused, nonradioactive PGF2alpha. One of the three inhibitors, bromcresol green, was shown not to be an effective inhibitor of PG metabolism in cell-free preparations of rat lung homogenates. These results indicated that under normal conditions, PG's are rapidly transported into intracellular compartment(s) where they are metabolized. Inhibition of this transport process prevents rapid access of PG's to the cytoplasmic enzymes and therefore inhibits pulmonary PG metabolism. This implies that inhibitors of PG transport, including anti-inflammatory organic acids, and some PG antagonists, metabolites, and analogues, can be expected to inhibit the pulmonary metabolism of PG's and thus could potentiate the systemic effects endogenous or exogenous PG's.

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