PubMed Health⌕ Search

Biomedical subjects

J A Palma

Publications and source records attributed to J A Palma.

At least 19 recordsLinked to original sources

Electrocardiographic characterization in Trypanosoma cruzi reinfected mice.

Chagas' disease, caused by Trypanosoma cruzi, affects approximately 20 million people. There are 3 stages in the disease: acute, intermediate and chronic, the diversity and severity of the symptoms range from a mild electrocardiographic alteration to sudden death. We have previously demonstrated that when reinfections were carried out in the acute phase they produce greater cardiac damage. The aim of the present work was to investigate whether T. cruzi reinfected mice present electrocardiographic abnormalities that could be characteristic and only achieved after reinfections. Of the mice reinfected during the acute phase 100% showed abnormalities from days 90 post-infection, with a predominance of auricle ventricle blocks (67-71%). All the mice reinfected during the chronic infection showed electrocardiographic alteration after 30 days post-first reinfection. Of the mice infected, without reinfection, 60% exhibited electrocardiographic dysfunction at 90 days post-infection. Our results demonstrated that when the host was reinfected in the acute phase, more serious electrocardiographic alterations were developed than when the reinfections were carried out in the chronic stage. Sudden death described in some chagasic patients, might be related to some of the findings described here.

Animals↗

He-Ne laser on microcrystalline arthropathies.

OBJECTIVE: The objective of this work is to assess the anti-inflammatory capacity of He-Ne laser therapy as determined by the plasmatic levels of inflammatory markers, fibrinogen, and TNFalpha and by histopathological study in rats with arthropathy induced by calcium pyrophosphate crystals. BACKGROUND DATA: Microcrystalline arthropathies are a group of diseases characterized by the deposit of different crystals in joints. MATERIALS AND METHODS: Two milligrams of dicalcium pyrophosphate crystals (DCPP) were injected in both joints of the lower limbs of rats during 2 days. A group was treated with laser of He-Ne (6 mW) on the injected joints during 3 consecutive days. After 96 h of the first injection, animals were sacrificed to determine TNFalpha using the ELISA method and fibrinogen was assessed using spectrophotometry. Sections from the lower limbs were used for histopathology. RESULTS: A statistically significant increase (p < 0.001) in plasma fibrinogen levels and TNFalpha was noted between the control group and the laser-treated group. The histological transversal section of a posterior limb joint of a rat injected with DCPP showed fibroadipose tissue with diffuse chronic infiltrate. The histopathology of the group of rats injected with DCPP and subsequently treated with He-Ne laser showed no inflammatory response. CONCLUSION: He-Ne laser treatment in the microcrystalline arthropathy induced in rats by DCPP injection might have an antiinflammatory effect, evaluated by fibrinogen plasma levels and TNF-alpha (inflammatory markers) and by the histopathology regressive process.

Analysis of Variance↗

Thioridazine treatment modifies the evolution of Trypanosoma cruzi infection in mice.

Thioridazine, a tricyclic drug, is known to have a direct effect on Trypanosoma cruzi, disrupting the parasites' mitochondria and kinetoplasts. In the present study, the drug was used orally, at 80 mg/kg.day for 3 days, to treat mice inoculated with low numbers of T. cruzi. The drug caused no apparent toxicity in the host. It cleared trypomastigotes from the bloodstream, prevented the histological and functional alterations of the heart normally observed in the chronic phase of the experimental disease, and greatly reduced the mortality rate compared with that in untreated, infected controls. When checked 135 days post-infection, the density of cardiac beta receptors and the cardiac histology of the treated mice were indistinguishable from those of uninfected, untreated controls. The drug is already used to treat humans, as a neuroleptic drug. It appears to be able to prevent acute infection with T. cruzi evolving into chronic disease, at least in mice, and may be a useful base from which to design new agents for the treatment of Chagas disease.

Animals↗

Effects of diclofenac sodium and He:Ne laser irradiation on plasmatic fibrinogen levels in inflammatory processes.

OBJECTIVE: The aim of the present work was to determine the possible synergic effect on the concentration of plasma fibrinogen (PF) by injecting diclofenac sodium associated with laser therapy postsurgery. SUMMARY BACKGROUND DATA: Nonsteroidal anti-inflammatory drugs (NSAIDs) and He:Ne laser irradiation as a therapy were used to inhibit the effects generated by inflammation. Tissue injury produces significant increases in PF levels, which are reduced to normal values by administration of NSAIDs or laser irradiation of the injured zone. MATERIALS AND METHODS: Rate were divided into groups in which different presurgical and postsurgical treatment were used; the inflammation was induced by laparotomy. RESULTS: Parenteral diclofenac or He:Ne laser irradiation used separately in normal rats did not produce changes in the PF levels. Diclofenac and laser irradiation combined postsurgery produced a significant reduction of PF levels compared with normal values, or with groups that were injected or irradiated postsurgically. CONCLUSION: The inflammatory response could be reduced by the effect of the diclofenac sodium upon the COX-2/COX-1 inhibitory relation associated with the photobiological effect of the He:Ne laser.

Animals↗

In vitro synthesis of prostaglandin E2 by synovial tissue after helium-neon laser radiation in rheumatoid arthritis.

This paper reports the effect of helium-neon laser radiation (power of 5 mW and 632.8 nm wave length) on the synthesis of PGE2 in vitro in synovial tissue of biopsy samples of knee joints in patients with chronic rheumatoid arthritis stages II or III. Twelve patients were studied. Each patient received 15 applications of He-Ne laser. Eleven points for He-Ne laser applications were selected in one of the affected knees. The energy density used was 8 J/cm2 per application point. The He-Ne laser therapy reduced the synthesis of PGE2. The analysis of the data revealed a statistically significant difference between the levels of the synthesis of PGE2 before treatment (17.69 +/- 2.65 ng mg-1 of dry tissue h-1) and after treatment (13.85 +/- 2.73 ng mg-1 of dry tissue h-1), with p < 0.01 comparing mean values. This was also accompanied by relief of pain (91.6%), and a favorable subjective report from the patient. We conclude that PGE2 is a quantifiable parameter that could explain what causes pain relief in patients with rheumatoid arthritis that are treated with He-Ne laser.

Aged↗

Cardiac beta receptors' density or affinity modified by different Trypanosoma cruzi amount.

Chagas' disease presents complex physiopathogenic mechanism, many of them poorly understood, that in our country generally produce cardiac lesions. The acute phase related with the presence of the parasite is usually asymptomatic. This report studies if the amount of T. cruzi that induced acute infection could modify the myocardiopathy evolution. Previous works have shown that Albino Swiss mice inoculated with 45 tripomastigotes (AcL) presented alterations in the cardiac pharmacological response to adrenergic agonist and antagonist studied at 30 days post-infection (p.i). Mice inoculated with 7 x 10(4) parasites/animal showed similar behaviour at 7 days p.i. We studied the involvement of the affinity and density of cardiac beta receptors in both acute groups by binding with 3H/DHA. The AcH group presented less cardiac beta receptors number (p < 0.001), but their affinity was conserved. The AcL model presented significantly less affinity (p < 0.01) but density was not different from non infected animals. beta receptors' affinity of both infected groups were similar, but AcH density was significantly diminished when compared with AcL. These studies demonstrates that the amount of T. cruzi received by the host determines and acelerates the evolution of the chagasic myocardiopathy.

Acute Disease↗

Isometric developed tension and histopathology of myocardium of chagasic mice. II.

In a preceding paper we reported the evolution of chagasic cardiopathy in mice inoculated with low number of T. cruzi from 2 days to 75 days post-infection (p.i.). The present work analyzed the contractility, pharmacological response and histopathology of myocardium isolated from chronic chagasic mice from 90 days until 180 days. p.i. Myocardium contractile force reached values similar to controls until 165 days p.i. From this to the end contractility was significantly lower. At 90 days p.i. NE provoked negative inotropic effect or had no effect in 13% of the cases tested. The others had a reactivity to NE similar to normal ventricles. From 105 days until 180 days p.i. NE induced to a positive inotropic effect significantly lower than in normal. ACh effect was significantly smaller from 165 days to the end. Previously ACh ventricles responses were as control. The effects of dibenamine, propranolol and atropine (10-6M) on chagasic ventricles were similar to those observed in normal tissues. At 90 days p.i. the histopathology showed focalized inflammatory infiltrates. At 180 days p.i. fibers fragmentations and loss of typical striated characteristic of cardiac tissue. The abnormal pharmacological response described could be attributed to alterations in cardiac beta and muscarinic receptors probably due to a lower oxygen support. The present paper shows that during chronic Chagas' disease myocardial function and pharmacological reactivity are seriously and definitively compromised.

Acetylcholine↗

Isometric developed tension and histopathology of myocardium of chagasic mice. I.

Cardiac disease is usually the most serious complication of human infection with Trypanosoma cruzi in our country. This report studies the evolution of the chagasic cardiopathy in mice inoculated with low number of parasites during acute and indeterminate stages in different aspects: contractility, histopathology and pharmacological response. From 2-45 days post infection (p.i.) (acute stage) myocardium contractile force reached higher values than in controls, but norepinephrine (NE) response was significantly lower. Acetylcholine (ACh) caused a negative inotropic effect similar to the observed in control group. In this period cardiac damage evolved to an acute interstitial myocarditis. In the indeterminate phase (45-75 days p.i.) of this parasitosis NE produced either small inotropic effect, negative inotropic effect or had no effect on the ventricles tested. A significantly low ACh effect, sub-endocardiac perivascular fibrosis and necrosis in wall bases were also observed. The abnormal pharmacological response described could be ascribed to modifications in cardiac beta and muscarinic receptors number or affinity. The present results showed that in myocardium isolated from T. cruzi infected mice the histopathology, contractility and pharmacological response were altered from 48 h p.i. reaching a maximum disorder at 60 days p.i.

Acetylcholine↗

[Arterial hypertension in childhood and adolescence].

One thousand six hundred and ninety-eight children and adolescents four to eighteen years-old were studied, eight hundred and forty of them were males and eight hundred and fifty-eight females. No individual following, was performed. Two determinations of both systolic and diastolic pressure were registered after a fifteen minutes rest, and the average figures of both, of them was registered. The group analyzed belonged to upper middle class and the hypertension figures were: females 28 (3.26%) and males 30 (3.57%). The influence of bodily area was observed en hypertensive patients. Those located between the average +/- two standard deviations were considered as normal. (95% of the cases).

Adolescent↗

CO2 laser in decubitus ulcers: a comparative study.

This is a comparative study of conventional surgery (knife/electric knife) and CO2 laser surgery and their effect on the outcome of stage III (including muscle) and stage IV (including bone) decubitus ulcers with an average area of 400 cm2. It is a prospective clinical study done with two groups of patients of similar age, economic and social background, as well with similar types of decubitus ulcers. Thirty patients were studied in each group. The study demonstrated a statistically significant difference in favor of the patients treated with CO2 laser with regard to operative blood loss, 0.5 cc/cm2 or 20% (P less than .01), infection rate (chi 2 test, P less than .01), and difference (60%) in recovery time (P less than .01). This translated into an average saving of 23 hospitalization days per patient. It also showed a difference, though not statistically significant, favoring the group treated with laser with respect to survival and full recovery. This probably is attributable to the lowered blood loss and infection rate as well as improved operative time and analgesia.

Aged↗

Interactions of prostaglandin E1, bradykinin and histamine and the increase of plasma fibrinogen in rats.

Considering that tissue injury caused by laparotomy significantly increases the liver synthesis of plasma fibrinogen, and that PGE1, bradykinin and histamine are released into the injured tissues, the effect of above mentioned inflammatory agents and of the adrenal medulla on plasma fibrinogen levels in rats was studied. The subcutaneous administration of PGE1, bradykinin or histamine does not modify plasma fibrinogen levels acting independently comparing with non-injected animals or injected with the drug vehicle. Bradykinin + histamine did not modify plasma fibrinogen levels either. However the administration of prostaglandin E1 + bradykinin + histamine reproduced the increase of fibrinogen characteristics of laparotomy. This increase was partially but significantly inhibited in rats that had undergone bilateral removal of the adrenal medulla or administration of PGE1 + bradykinin + histamine + bupivacaine (a local anesthetic), but it was not modified when the adrenal medullectomy was unilateral. It is concluded that plasma fibrinogen increase is obtained only when PGE1 acts in presence of bradykinin or histamine and the adrenal medulla should be partially responsible for said increase.

Alprostadil↗

Rôle of histamine on plasma fibrinogen levels in rats with surgical injury (laparotomy).

The probable rôle of endogenous histamine in the increase of plasma fibrinogen in rats submitted to tissue injury (laparotomy) was studied. In laparotomized rats with 10 mg kg-1 day-1 of diphenhydramine (a H1-histamine receptor blocker) plasma fibrinogen decreased significantly as compared to the group of rats laparotomized only (P less than 0.02), reaching values similar to those observed in rats laparotomized with removal of the adrenal medulla or laparotomized with severing of splanchnic nerves. There is a significant difference between these latter groups and the normal noninjured group (P less than 0.01). Plasma fibrinogen did not modify (as compared with the uninjured group) in rats injected only with histamine (1 mg kg-1 day-1) or with diphenhydramine. Taking into account the results obtained and the mechanism of action of diphenhydramine, it would seen that endogenous histamine takes part in the increase of plasma fibrinogen in laparotomized rats, perhaps indirectly through stimulation of the adrenal medulla secretion.

Adrenal Medulla↗

Effects of indomethacin on plasma fibrinogen levels in rats with tissue injury.

The present investigation was designed to study the effect of indomethacin (5 mg kg-1 day-1) on plasma fibrinogen levels in laparotomized rats. Whereas tissue injury significantly increased plasma fibrinogen when compared to normal uninjured rats, indomethacin completely blocked that effect. Conversely, indomethacin did not prevent fibrinogen increase in laparotomized rats injected with epinephrine, with spinal cord transection + epinephrine or with adrenal medullectomy + epinephrine. Indomethacin or epinephrine administration to normal rats did not modify plasma fibrinogen. Taking into account that epinephrine is a key hormone in plasma fibrinogen response in laparotomized rats, and according to our results, prostaglandins might act by two possible pathways: 1) by decreasing of the pain threshold of the sensory nerve endings and stimulating sympathetic adreno-medullar system; 2) by entering into the blood stream and enhancing epinephrine action on plasma fibrinogen. It would appear that indomethacin inhibits both pathways.

Animals↗

Effects of diethylstilbestrol, 17 beta estradiol, and progesterone on plasma fibrinogen levels in rats submitted to tissue injury (laparotomy).

Participation of estrogens (17 beta estradiol, diethylstilbestrol) and progesterone in the increase of plasma fibrinogen levels in female rats submitted to tissue injury (laparotomy) was studied. Ovariectomy avoided the increase of fibrinogen observed in laparotomized rats, while the administration of 17 beta estradiol or diethylstilbestrol to laparotomized-ovariectomized rats increased fibrinogen to levels similar to those observed in the group of laparotomized rats without other treatment. On the other hand, progesterone inhibited the increase of fibrinogen which is typical of laparotomy in both groups: one of laparotomized rats and the other of laparotomized rats injected with estrogens. Neither estrogens nor progesterone modify plasma fibrinogen levels in uninjured rats. It is concluded that estrogens might participate in the fibrinogen increase observed after tissue injury in female rats, and on the contrary, the administration of progesterone would render that increase null.

Animals↗

Effects of the administration of progesterone and adrenal medullectomy on the plasma fibrinogen levels in rats with surgical injury (laparotomy).

The probable rôle played by the adrenal medulla in the decrease of plasma fibrinogen due to the administration of progesterone (0.5 mg kg-1 day-1 during 72 h) in rats submitted to surgical injury (laparotomy) was studied. The results obtained lead to assume that the decrease of plasma fibrinogen observed in laparotomized rats injected with progesterone is indirectly produced through inhibition of the adrenal medulla. The action of progesterone on the plasma fibrinogen would be a pharmacological effect of the drug, since in doses of 0.10 mg kg-1 day-1 the decrease of the fibrinogen is not observed in laparotomized rats. The administration of progesterone in non injured rats does not modify the plasma fibrinogen as compared to the group of non injected rats.

Adrenal Medulla↗

Effects of epinephrine on plasma fibrinogen levels in rats submitted to tissue injury.

Tissue injury (laparotomy) produces an increase in plasma fibrinogen. This increase is inhibited by the removal of the adrenal medulla, but injection of epinephrine in laparotomized-medullectomized rats returns fibrinogen levels to values similar to those observed in only laparotomized rats. Epinephrine administration to laparotomized rats increases the fibrinogen compared with the group of laparotomized rats without treatment, but epinephrine by itself does not modify plasma fibrinogen levels in uninjured rats. Epinephrine is apparently responsible for the increase of plasma fibrinogen in rats subjected to tissue injury, probably through beta adrenergic stimulation.

Adrenal Medulla↗