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J Tejada

Publications and source records attributed to J Tejada.

At least 37 records · Page 2Linked to original sources

Cooling to heat of fusion (HOF), followed by rapid rewarming, does not reduce the integrity of microvascular corrosion casts.

This study utilized microvascular corrosion casting techniques to evaluate changes in the microvascular patency of rat hindpaws cooled to four different subzero temperatures. Left hindpaws of anesthetized rats in group 1 were cooled to -5 degrees C, in group 2 to -15 degrees C, in group 3 to heat of fusion (HOF), and in group 4 to HOF and then to -15 degrees C. Although freezing did not take place in the hindpaws of groups 1 and 2, initiation of freezing in the tissues, as indicated by HOF, did occur in groups 3 and 4. Cooled hindpaws were rapidly rewarmed. Right hindpaws served as controls. Microvascular corrosion casts were made from the left and right hindpaws of all animals. There was no significant difference when the mean cast weights of cooled hindpaws from groups 1, 2, and 3 were compared to the mean cast weights of their respective control hindpaws. In group 4, there was a significant difference (P less than 0.05) when the mean cast weight of the cooled hindpaws (47.69 +/- 9.05, mg +/- SEM) was compared to that of the control hindpaws (80.63 +/- 12.23). Since, in this acute experiment, a loss of vascular integrity occurred when the hindpaws in group 4 were cooled to -15 degrees C after reaching HOF, the initiation of freezing alone was not sufficient to reduce mean cast weight.

Animals↗

[Wilson's disease: computed tomography and magnetic resonance imaging].

Wilson's disease is an autosomal recessive hereditary disease in which the capacity of biliary copper excretion is reduced, resulting in a toxic accumulation of this metal in the liver, brain and other organs. The neuroimaging techniques, computed tomography (CT) and nuclear magnetic resonance (NMR), have been incorporated to the diagnostic workup in patients with suspected Wilson's disease (WD). We report two patients with WD in whom CT and NMR were carried out for the evaluation of the central nervous system (CNS). The lesions appeared as hypodense areas in CT or signal abnormalities in NMR over the involved structures: putamen, caudate nucleus, cerebellar dental nucleus, red nucleus and subcortical white matter. In one of the patients, hypointense signal areas were found over both putamen nuclei in T-2 times of NMR, which might correspond to cavitary necrosis or copper deposition. The lesion distribution suggests that vascular lesions might play a role in the mechanisms of tissue damage. These findings show that CT and NMR are very helpful to evaluate WD. NMR images are quite characteristic of this disorder.

Adolescent↗

An evaluation of the ability of the peripheral vasodilator buflomedil to improve vascular patency after acute frostbite.

The extent of microvascular damage from frostbite can be accurately demonstrated by vascular microcorrosion casting techniques (P. S. Daum, W. D. Bowers, Jr., J. Tejada, and M. P. Hamlet, Cryobiology 24, 65-73, 1987). In the present investigation, the peripheral vasodilator buflomedil was evaluated for its ability to ameliorate microcirculatory damage from acute experimentally induced freeze injury. This drug has been reported to decrease tissue loss in human frostbite patients when given intravenously during thawing (J. Foray, P. E. Baisse, J. P. Mont, and Cl. Cahen, Sem. Hop. Paris 56, 490-497, 1980). In seven groups of anesthetized rats, left hindpaws were cooled to heat of fusion; cooling continued until the temperature in the footpads fell to -15 degrees C. Prior to cooling, group 1 received a tail vein injection of 1 ml saline/kg, while group 2 received 10 mg buflomedil/kg. Immediately following cooling, group 3 received an injection of 10 mg buflomedil/kg. Hindpaws were rapidly rewarmed in a 40 degree C bath. During rewarming, left hindpaws from group 4 were immersed in deionized water, from group 5 in 24 mg buflomedil in deionized water, from group 6 in 30% dimethyl sulfoxide (Me2SO), and from group 7 in 24 mg buflomedil in 30% Me2SO. Right hindpaws served as controls. Vascular microcorrosion casts were made from left and right hindpaws of all groups. There was no significant difference in mean cast weights when frozen hindpaws of the seven groups were compared, although treatment with buflomedil increased the mean cast weight of control hindpaws from groups 3 and 7. It therefore appears that, in this acute model for frostbite, buflomedil does not improve vascular patency.

Animals↗

[Neurologic complications caused by use of cocaine, amphetamines and sympathomimetics].

Drug abuse has become a social and medical problem. Amphetamine and cocaine have a potent sympathicomimetic action, so they have important effects on the Central Nervous and Cardiovascular Systems. Their neurological complications are principally: psychic alterations, seizures and stroke (hemorrhagic and ischemic). The latter are the most important in the clinical practice. Their capacity to produce transit arterial hypertension and cerebral vascular constriction could be the physiopathological substrate of such alterations. Angiographic studies have shown lesions suggesting vasculopathy. In the last ten years cocaine abuse has become an authentic epidemic. We have reviewed its neurological complications, particularly the vascular ones--42 hemorrhagic and 24 ischemic--and the following conclusions were drawn: it should be considered as a risk factor in the younger age group; a short period of time between the last drug dose and the clinical picture is frequently seen; clinical features may appear with the first drug administration; no characteristic lesion in relation to the way of administration or consumption time was elicited.

Amphetamines↗