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L Z Bito

Publications and source records attributed to L Z Bito.

At least 109 records · Page 6Linked to original sources
PubMed1973

Maintenance of normal corneal thickness in the cold in vivo (hibernation) as opposed to in vitro.

1. Corneal thickness was measured in vivo in normothermic and hibernating (body temperature = 7-10 degrees C) woodchucks and the [Na(+)], [K(+)], [Mg(2+)] and water content of woodchuck and rabbit corneas were determined on freshly isolated tissues.2. Woodchuck eyes from both normothermic and hibernating animals were incubated in moist chambers at 5 or 11 degrees C and the corneal thickness was measured periodically.3. Woodchuck corneas undergo continuous swelling when kept in vitro in a moist chamber at either 5 or 11 degrees C. The rate of this swelling was the same for eyes from active and hibernating animals; it was almost completely reversible upon rewarming at 35 degrees C.4. In the hibernating woodchuck the corneal thickness did not increase measurably, even after several days of hibernation, although the mean corneal temperature was 9.4 degrees C.5. At 7 degrees C, the lactate production of corneas from both hibernating and normothermic woodchucks was reduced to about one fifth its levels measured at 37 degrees C. Oxygen consumption was also greatly reduced in the cold although the endothelial O(2) consumption of corneas from hibernating woodchucks appears to be relatively insensitive to cold.6. It is concluded that removal of the eye and/or the in vitro conditions per se render the cornea more vulnerable to the effects of cold, possibly as a result of the elimination of the influences of orbital tissues and/or secretions or as a result of changes in some intrinsic properties of the cornea due to the elimination of neurohumoural factors or the release of autocoids.7. The finding that normal corneal thickness can be maintained under conditions where the environment is maintained essentially constant for days strongly argues against the validity of the recently proposed nonsteady-state theory of corneal thickness control.

Animals↗
PubMed1972

On the physiological response of the cerebral cortex to acute stress (reversible asphyxia).

1. Rhesus monkey (Macaca mulatta) foetuses were delivered by Caesarean section 3-10 days before term. Aortic blood and cerebrospinal fluid (c.s.f.) samples were taken, the latter from the cortical subarachnoid space and the cisterna magna. The umbilical cord was clamped and foetal breathing prevented for 14-17 min. Blood and c.s.f. were sampled further during this total asphyxiation and for up to 24 hr thereafter.2. The [K(+)] in the cortical subarachnoid fluid started to rise within 2-3 min after the onset of asphyxia and increased up to 7 times the normal level. The [K(+)] of blood plasma and cisternal fluid also increased, but much more moderately. All these effects reversed rapidly upon resuscitation of the foetus.3. A pronounced rise in the cortical subarachnoid fluid [glucose] and a lesser effect on cisternal fluid [glucose] were noted in most cases by the end of, or immediately following, the period of asphyxia. The onset, magnitude and reversal of these effects on [glucose] were less predictable than the observed effects on [K(+)].4. There were no significant changes in the [Mg(2+)], [Ca(2+)] or [Na(+)] of any of these fluids. The calculated total osmolarity of the cortical subarachnoid fluid and, to a much lesser extent, of cisternal fluid and plasma, increased during asphyxia mainly as a result of increased [K(+)].5. The results are interpreted as indicative of a rapid release of K(+) from cortical cells during total asphyxia. The (immature) haematoencephalic K(+) transport system becomes saturated and thus K(+) accumulates in the extracellular fluid (e.c.f.) whence it diffuses into adjacent regions of the c.s.f. system.6. The intracellular fluid of apical dendrites must become even more hypertonic than the e.c.f., since these cellular processes are known to swell during asphyxia at the expense of the e.c.f. space. This apparent increase in intracellular osmolarity could be accounted for by the release of normally bound intracellular cations.7. On the basis of our results and review of the relevant literature, the following sequence of events is proposed: the cortex responds to acute physiological stress (asphyxia, overstimulation, chemical or physical irritation, etc.) by releasing intracellularly bound cations (K(+) and possibly Na(+)). The increased intracellular osmolarity results in the absorption of water from the e.c.f. space. Passage of water across the blood-brain barrier is restricted; thus the e.c.f. space of the cortex does not swell, but becomes hyperosmotic. Under these circumstances, swelling of the cortical cells is limited by the volume of e.c.f. available.8. It is proposed that the release of intracellularly bound cations is a result of their displacement from their binding sites by NH(4) (+) which is released to, and recovered from, these cation binding sites by a glutamate-glutamine interconversion.9. It is concluded that the apparent organized ;shutdown' of the cortical cells in response to acute stress may contribute to the relative insensitivity of this area of the brain to permanent histopathological damage.

Animals↗
PubMed1972

Accumulation and apparent active transport of prostaglandins by some rabbit tissues in vitro.

1. Slices or bits of rabbit tissues, not exceeding 100 mg, were incubated in tissue culture medium containing tritium-labelled prostaglandin ([(3)H]PG). In some experiments, incubation medium also contained saturating concentrations of an unlabelled prostaglandin (PG), or [(14)C]-sucrose for determination of extracellular space. At the end of the incubation period, usually 1 hr, the tissues were removed and weighed, and their (3)H (and (14)C) content were determined along with that of a unit volume of medium.2. Tissues known to play a central role in PG metabolism (lung and liver) and in its excretion (kidney cortex) and tissues which have a known function in blood-brain and blood-ocular barriers (choroid plexuses and ciliary processes) show a large accumulation of (3)H when incubated in a medium containing [(3)H]PGE(1). In addition, tissues of the female reproductive tract, and the aorta of the rabbit show similar (3)H accumulation. When uncorrected for tissue solid content or extracellular water volume, the extent of this accumulation is two- to sixfold. Calculated on the basis that all excess (3)H is present in the free form in the intracellular water, the accumulation ratio for ciliary processes, for example, indicates an over fortysix-fold gradient of PGE(1) across the cell membrane.3. Tissues which accumulate [(3)H]PGE(1) also accumulate [(3)H]PGA(1), [(3)H]PGF(1alpha) and [(3)H]PGF(2alpha). In some tissues specificity is, however, apparent; in the lung accumulation of [(3)H]PGA(1) was significantly greater than that of [(3)H]PGF(1alpha).4. The extent of [(3)H]PGE(1) accumulation was decreased, or in some tissues completely inhibited, by incubation at 2 degrees C, or by addition of large concentrations of unlabelled PG.5. Accumulation of [(3)H]PGE(1) by the foetal liver is not apparent on the 20th day of gestation, but is fully developed by the 30th day of gestation. The foetal lung does not accumulate [(3)H]PGE(1) at any stage of gestation.6. In some tissues, most notably muscle, there appears to be full equilibrium of [(3)H]PGE(1) between tissue water and medium within 1 hr of incubation.7. PGs are partially excluded from the intracellular volume of some other tissues, most notably the spleen and subcutaneous connective tissues. This apparent exclusion cannot be blocked by incubation in the cold, or by the addition of saturating levels of unlabelled PG.8. The simplest explanation for all observed results is that cell membranes are, in general, impermeable to PGs. However, there are specific, carrier-mediated mechanisms across some membranes which facilitate the entry of PGs. In some cells these transport mechanisms are linked to a source of metabolic energy, and/or to the counter-transport of some other substance, thus allowing net accumulation of PGs against a concentration gradient. Alternatively, (3)H accumulation may represent adsorption of [(3)H]PGs or one of their labelled metabolites on to specific adsorption sites.

Animals↗
PubMed1971

Cholinergic sensitivity: normal variability as a function of stimulus background.

The sensitivity of the normally innervated iris sphincter to its neuro-transmitter, acetylchloline, and to relatd agents varies inversely with the preexisting physiological stimulus background, that is, the environmental light intnsity. This normal variability suggests the existence of a negative feedback mechahnism whereby sensitivity of the effector cell is modutlated by a product of neuronal activity.

Acetylcholine↗
PubMed1970

The ontogenesis of haematoencephalic cation transport processes in the rhesus monkey.

1. This investigation was undertaken to determine the time course of development of cation transport processes between blood and the extracellular fluid compartments of the central nervous system (C.N.S.) of the foetal rhesus monkey. The development of concentration gradients within the cerebrospinal fluid (c.s.f.) system was also studied in an attempt to gain information on regional variations in transport activities.2. Cerebrospinal fluid samples were obtained from the lateral ventricle, the cisterna magna, the cortical subarachnoid space and the lumbar region of the spinal subarachnoid space of adult monkeys. Foetal c.s.f. samples were obtained from the cisterna magna and the frontal region of the cortical subarachnoid space. Blood samples were taken within 3-10 min of the c.s.f. samples. The concentration of K, Mg and Ca were determined on appropriately diluted samples by atomic absorption spectrophotometry.3. The concentrations of K, Mg, and Ca in the plasma and c.s.f.s of the adult monkey are similar to those of other mammalian species. The c.s.f./blood concentration gradients of these cations are in the same direction but generally of greater magnitude than those in non-primate mammals. The indicated [Mg] in the extracellular fluid of the adult monkey's cerebral cortex is high (more than 2 m-equiv/kg H(2)O) and the [K] is low (less than 2 m-equiv/kg H(2)O).4. Accumulation of Mg into the c.s.f. system against a concentration gradient is evident in the earliest foetuses studied (50 days of intrauterine life) and by the second half of gestation the concentration gradients of this cation are similar to that of the adult.5. In the second trimester foetus, the [K] in the cisternal fluid is near the plasma ultrafiltrate level. It then decreases gradually throughout the remainder of gestation, approximating the adult value at birth.6. The very low [K] typical of the adult cortical subarachnoid fluid is observed by the sixth month following birth but not during foetal life or within the first few weeks of post-natal life. This indicates that the transport processes at the cortical region of the haematoencephalic interphase do not fully develop until well after birth.7. It is concluded that the various transport processes responsible for the elaboration and maintenance of adult type of K, Ca and Mg concentrations within the extracellular fluid compartments of the monkey C.N.S. do not develop at the same time. This temporal dissociation provides strong evidence against any direct association or coupling between the haematoencephalic K and Mg transport systems.8. Existence of normal cation concentration gradients between c.s.f. and blood may serve as a criterion for the normality of the (foetal) blood-brain barrier.

Age Factors↗