Biomedical subjects

R Barroso-Moguel

Publications and source records attributed to R Barroso-Moguel.

35 records · Page 2Linked to original sources

PubMedDate not supplied

Experimental neuromyopathy induced by thallium in rats.

A histopathological study, with a light microscope, of experimental neuromyopathy produced by thallotoxicosis was undertaken in 40 newborn Wistar rats. Treatment consisted of a single i.p. injection of an aqueous solution of 16 mg kg-1 thallium(I) acetate 1 day after birth. Groups of ten animals were euthanized at either 8 or 50 days of age. Sural nerves, as well as peroneus muscle, were fixed in 10% formaldehyde solution for 15 days and then prepared for histopathological observation. At 8 days of age sural nerves of thallium-treated animals showed a moderate reduction in the large- and medium-sized fibres and several of the myelin sheaths had initial degeneration along the course of the axon. Interstitial oedema was found in both neural and muscular tissues. Distinct features of focal necrosis as well as small haemorrhages were seen in peroneus muscle. At 50 days of age, the lesions were more diffuse. Large and small myelinated fibres were found to be sinuous, fragmented and scanty. Alterations in the large- and medium-sized axons were seen and the myelin sheaths were altered along the course of the axon, suggesting a progressive distal axonopathy. Additionally, muscle fibres had myopathic changes with abnormal central nucleoli and the striated transverse fibres had disappeared in many areas of the sample. Several interstitial foci of muscular necrosis accompanied by phagocytosis and fibrosis were also present.

Animals↗

PubMedDate not supplied

Testicular lesions by chronic administration of cocaine in rats.

Although cocaine is a common drug of abuse, its effects on the testicular structure have not been studied in depth. We report here the testicular lesions produced by chronic cocaine administration to rats. Twenty-eight male Wistar rats weighing 225-250 g were used throughout. Fourteen of them (controls) were injected i.p. with saline solution and the remaining 14 received 30 mg kg-1 day-1 i.p. of aqueous cocaine hydrochloride solution. Animals from both groups were sacrificed at variable times: 7, 15, 30, 45, 60, 75 and 90 days of treatment. Histopathological examination of the testes showed initial alterations at day 15: capillary dilatation; interstitial oedema with lipoid drops due to incipient necrosis of interstitial cells; and necrosis of the cells of the seminiferous tubules. Lesions progressed until 90 days of treatment, showing atrophic and necrotic cells and terminal tubule fibrosis. At this time, the testes were found to be diminished in size. The seminiferous tubules were shrunken, of small diameter and contained necrotic spermatogenic cells and fibrosis. These lesions may produce testosterone diminution and thus sterility due to the disappearance of spermatogenesis.

Animals↗

PubMedDate not supplied

Retinal lesions in rat fetuses prenatally exposed to cocaine.

The increased use of cocaine in the United States and worldwide has created great concern about its effects on fetuses and neonates of pregnant cocaine abusers. The effects on neonates are varied: fetal growth delay, microcephaly, abnormal neurological functions, microphthalmia, and maternal obstetric complications. In this study, the effect of prenatal cocaine administration was studied microscopically in the retina of rat fetuses. Twenty-five pregnant Wistar rats were injected i.p. with an aqueous cocaine solution using a 30 mg/kg daily dose for 45 days. Control group rats (15 pregnant animals) received saline solution for the same period. Day 0 of gestation was the day after mating. Dosing began on this day. The rats were killed on gestation day 21 and fetuses were obtained for examination. The histopathological light and electron microscope studies of the retinas showed interstitial oedema, areas depleted of cells, necrosis, and hyperchromatic ganglion cells. There also was a significantly lower number of retinal cells compared to control fetuses. In four cases, teratogenic lesions of the retina were observed whereas no changes were present in control fetuses. Results indicate that development of retina in fetuses prenatally exposed to cocaine was altered by cocaine exposure.

Animals↗

PubMedDate not supplied

Medical causes and effects of cocaine abuse.

Historical data concerning the use of cocaine, its epidemiology, chemistry and pharmacology, as well as its medical complications and treatment, in both acute intoxication and chronic addiction is reported. Its repercussion and damage upon the nervous system with neurologic and psychiatric alterations is also reported. The frequency of cerebral hemorrhages and myocardial, and other visceral infarctions due to vascular lesions are discussed. Various pulmonary lesions produced by the different routes used and the multiple obstetric problems during pregnancy, such as abnormal labour with products showing cerebral damage and teratogenic lesions due to the use of cocaine are presented. Finally, the present prophylactic campaigns against the use of cocaine and other drugs are mentioned.

Adolescent↗

PubMedDate not supplied

[Teratologic cranio-encephalic effects of chronic thinner inhalation in progenitors, in rats and humans].

Inhalation of thinner by youngsters and adolescents is an increasing drug abuse problem in Mexico. It presents serious repercussions upon socio-economic, cultural, legal and health (neurologic and psychiatric) problems. We report a comparative study in humans and rats which demonstrate the embryotoxic and craneo encephalic teratologic effects in the children and brood of progenitors who have chronically inhaled thinner (in the case of pregnant women, before, at the beginning and throughout pregnancy). Inhaled thinner passes directly to the blood stream and crosses the placentary barrier freely reaching the embryo. It may cause craneal bone and partial or total encephalon agenesia, added to macro and microscopic lesions secondary to direct aggression to the neuroepithelial germ cells. Abortions and premature labor with weight and size underdeveloped products and placentary hemorrhages occur. Usually these die, but if they survive they show trascendental mental retardation, as well as neurologic and psychiatric sequels.

Abnormalities, Drug-Induced↗

PubMedDate not supplied

[Causes and medical effects of cocaine abuse].

Historical data concerning the use of cocaine, its epidemiology, chemistry and pharmacology, as well as its medical complications and treatment, in both acute intoxication and chronic addiction is reported. Its repercussion and damage upon the nervous system with neurologic and psychiatric alterations is also reported. The frequency of cerebral hemorrhages and myocardial, and other visceral, infarctions due to vascular lesions are discussed. Various pulmonary lesions produced by the different routes used and the multiple obstetric problems during pregnancy, such as abnormal labour with products showing cerebral damage and teratogenic lesions due to the use of cocaine are presented. Lastly, the present prophylactic campaigns against the use of cocaine and other drugs is mentioned.

Adolescent↗

PubMedDate not supplied

Neurotoxicity of thallium: biochemical and morphological study of organic lesions.

A biochemical study of experimental thallium intoxication in newborn rats and its morphological consequences upon the brain of developing animals was undertaken. The thallium content was analyzed in the following encephalic regions: hippocampus, hypothalamus, mesencephalon, cerebellum, and cortex. One day after application of the toxic substance, a homogeneous distribution of the metal in the brain was found. Thallium concentrations in the mentioned regions were twice as high as those found in an adult rat, at the same dosage, 20 newborn Wistar rats were used for the histopathological study. 5 remained as witnesses, the rest received a single injection of thallium of .07 ml. of a solution with a concentration of .32 mg/Kg. 3 rats were sacrificed at 24, 48 and 72 hours; 3 at 7 days and 3 at 51 days. The brain , sciatic and crural nerves were fixated in 10% formaldehyde for 15 days. Cuts in paraffin and frozen sections measuring between 5 and 7 microns were taken from the fragments of different areas. These were stained with aniline methods (Masson, Gallego and H-E) and silver-gold impregnation as modified by Río-Hortega.

Animals↗

PubMedDate not supplied

Experimental neuropathy produced in rats with industrial solvents (thinner).

Thinner is a very potent neurotoxic compound which damages both the central and peripheric nervous system, as well as the rest of the organism, when it is used or inhaled spontaneously chronically. 20 Wistar rats were used. They inhaled 1.5 ml of thinner per day and were sacrificed by pairs upon days 7, 15, 30, 45, 60, 75, and 90. Four of them were sacrificed after suspending the inhalation 15, 30, 60 and 90 days later so as to study the process of recuperation. The hind legs were fixated in 10% formaldehyde for 15 days. Fragments of sciatic and crural nerves were included in paraffin and histological cuts were performed both in transversal and longitudinal sections of 5 to 7 micra. Techniques for myelin and argento-auric ones were performed. Incipient lesions are described as well as intermediate and terminal ones produced after having inhaled 45 ml of thinner for 30 days. The myelin sheath shows edema, ballooning and destruction due to lysis after inhaling 135 ml in 90 days. In a parallel manner the nerve fibers show edema, irregular thickening and after inhaling 135 ml in 90 days there is atrophy or disintegration. A partial regeneration is produced if inhalation is suspended after 30 days and 30 more days are allowed for recuperation, when some Schwann cells are still active. We believe that the lesions which begin to appear on the myelin sheath occur because thinner is a fat solvent, fats being important elements in their structure and the nerve fiber injury may be secondary to the demyelinization, or due to destruction of the central neuron from which they originate.

Animals↗

PubMedDate not supplied