Taponamiento cardiaco como forma de presentación del cáncer de pulmón / Cardiac tamponade as a form of presentation of lung cancer

El taponamiento cardiaco es un evento grave que requiere un rápido diagnóstico y tratamiento. Obedece a diversas causas que no siempre son evidentes. Dentro de estas, los procesos neoplásicos y en particular los de pulmón, deben tenerse siempre en cuenta. El objetivo de este trabajo es ejemplificar que el taponamiento cardiaco puede ser la forma de manifestación de un cáncer de pulmón. Los dos casos que se presentan comenzaron clínicamente con disnea y dolor torácico, y se detectó al examen físico ingurgitación venosa yugular, ruidos cardiacos apagados, taquicardia e hipotensión arterial. Se constató microvoltaje en el electrocardiograma y aumento del área cardiaca en radiografía de tórax. Se comprobó el diagnóstico de taponamiento cardiaco mediante ecocardiograma. En ambos pacientes se efectuó una ventana pericárdica con obtención de biopsia pericárdica, en la cual se definió el diagnóstico de neoplasia de pulmón. En conclusión, ante todo taponamiento cardiaco de causa no clara, siempre debe sospecharse su origen neoplásico y, en particular, el cáncer de pulmón

Cardiac tamponade is a serious event requiring immediate diagnosis and treatment. It may result from a variety of causes which are not always self-evident. Among these causes, neoplastic processes, particularly lung neoplasias, should always be considered. The objective of the present study is to show that cardiac tamponade may be the form of presentation of lung cancer. In the two cases presented, the initial clinical symptoms were dyspnea and chest pain. The physical examination revealed jugular ingurgitation, muffled cardiac sounds, tachycardia and arterial hypotension. The electrocardiogram showed the presence of microvoltage, and the chest x-rays an increase in cardiac area. The diagnosis of cardiac tamponade was verified by echocardiography. A pericardial window was performed in both patients and a pericardial biopsy was obtained, by means of which the diagnosis of lung neoplasia was defined. It is concluded that in the presence of a cardiac tamponade of unclear cause, a neoplastic origin should always be suspected, particularly lung cancer

Taponamiento cardiaco como forma de presentación del cáncer de pulmón / Cardiac tamponade as a form of presentation of lung cancer

El taponamiento cardiaco es un evento grave que requiere un rápido diagnóstico y tratamiento. Obedece a diversas causas que no siempre son evidentes. Dentro de estas, los procesos neoplásicos y en particular los de pulmón, deben tenerse siempre en cuenta. El objetivo de este trabajo es ejemplificar que el taponamiento cardiaco puede ser la forma de manifestación de un cáncer de pulmón. Los dos casos que se presentan comenzaron clínicamente con disnea y dolor torácico, y se detectó al examen físico ingurgitación venosa yugular, ruidos cardiacos apagados, taquicardia e hipotensión arterial. Se constató microvoltaje en el electrocardiograma y aumento del área cardiaca en radiografía de tórax. Se comprobó el diagnóstico de taponamiento cardiaco mediante ecocardiograma. En ambos pacientes se efectuó una ventana pericárdica con obtención de biopsia pericárdica, en la cual se definió el diagnóstico de neoplasia de pulmón. En conclusión, ante todo taponamiento cardiaco de causa no clara, siempre debe sospecharse su origen neoplásico y, en particular, el cáncer de pulmón(AU)

Cardiac tamponade is a serious event requiring immediate diagnosis and treatment. It may result from a variety of causes which are not always self-evident. Among these causes, neoplastic processes, particularly lung neoplasias, should always be considered. The objective of the present study is to show that cardiac tamponade may be the form of presentation of lung cancer. In the two cases presented, the initial clinical symptoms were dyspnea and chest pain. The physical examination revealed jugular ingurgitation, muffled cardiac sounds, tachycardia and arterial hypotension. The electrocardiogram showed the presence of microvoltage, and the chest x-rays an increase in cardiac area. The diagnosis of cardiac tamponade was verified by echocardiography. A pericardial window was performed in both patients and a pericardial biopsy was obtained, by means of which the diagnosis of lung neoplasia was defined. It is concluded that in the presence of a cardiac tamponade of unclear cause, a neoplastic origin should always be suspected, particularly lung cancer(AU)

Ozone/oxygen mixture modifies the subcellular redistribution of Bax protein in renal tissue from rats treated with cisplatin.

BACKGROUND: Cellular events in cisplatin-mediated nephrotoxicity include apoptosis induction, decreased protein synthesis, changes in the subcellular redistribution of Bax mitochondrial dysfunction, DNA injury, increased lipid peroxidation, depletion of glutathione and decrease in enzymatic activity of renal antioxidant enzymes. In previous papers we have shown that intra-rectal (i.r.) ozone/oxygen mixture protected and induced a significant recovery in cisplatin-induced renal damage and was related to a significant increase in the antioxidant system in renal tissue. METHODS: This study was undertaken to examine the effect of the ir applications of ozone/oxygen mixture in the renal expression pattern of Bax proteins in rats treated with cisplatin. A group of male Sprague-Dawley rats was pretreated with 15 i.r. applications of ozone/oxygen (1.1 mg/kg) before intraperitoneal injection of cisplatin (6 mg/kg). Another group was treated with five i.r. applications of ozone/oxygen mixture after cisplatin administration. Serum creatinine was measured thereafter. Subcellular distribution of Bax in renal tissue was analyzed by immunohistochemistry. RESULTS: Ozone pretreatment prevented the increase in serum creatinine levels and completely inhibited the acute tubular necrosis induced by cisplatin in renal tissue, diminishing the expression of Bax. Ozone treatment after cisplatin application reduced the increase in serum creatinine levels and the renal necrosis, inducing a lesser decrease of the Bax expression in cisplatin-treated kidneys. CONCLUSIONS: Expression of Bax in renal tissue seems to play an important role in the protection and recovery in cisplatin-nephrotoxicity achieved by ozone/oxygen mixture.

Ozone therapy on rats submitted to subtotal nephrectomy: role of antioxidant system.

Chronic renal failure (CRF) represents a world health problem. Ozone increases the endogenous antioxidant defense system, preserving the cell redox state. The aim of this study is to evaluate the effect of ozone/oxygen mixture in the renal function, morphology, and biochemical parameters, in an experimental model of CRF (subtotal nephrectomy). Ozone/oxygen mixture was applied daily, by rectal insufflation (0.5 mg/kg) for 15 sessions after the nephrectomy. Renal function was evaluated, as well as different biochemical parameters, at the beginning and at the end of the study (10 weeks). Renal plasmatic flow (RPF), glomerular filtration rate (GFR), the urine excretion index, and the sodium and potassium excretions (as a measurement of tubular function) in the ozone group were similar to those in Sham group. Nevertheless, nephrectomized rats without ozone (positive control group) showed the lowest RPF, GFR, and urine excretion figures, as well as tubular function. Animals treated with ozone showed systolic arterial pressure (SAP) figures lower than those in the positive control group, but higher values compared to Sham group. Serum creatinine values and protein excretion in 24 hours in the ozone group were decreased compared with nephrectomized rats, but were still higher than normal values. Histological study demonstrated that animals treated with ozone showed less number of lesions in comparison with nephrectomized rats. Thiobarbituric acid reactive substances were significantly increased in nephrectomized and ozone-treated nephrectomized rats in comparison with Sham group. In the positive control group, superoxide dismutase (SOD) and catalase (CAT) showed the lowest figures in comparison with the other groups. However, ozone/oxygen mixture induced a significant stimulation in the enzymatic activity of CAT, SOD, and glutathione peroxidase, as well as reduced glutathione in relation with Sham and positive control groups. In this animal model of CRF, ozone rectal administrations produced a delay in the advance of the disease, protecting the kidneys against vascular, hemorheological, and oxidative mechanisms. This behavior suggests ozone therapy has a protective effect on renal tissue by downregulation of the oxidative stress shown in CRF.

Protection by ozone preconditioning is mediated by the antioxidant system in cisplatin-induced nephrotoxicity in rats.

BACKGROUND: Acute renal failure is a dose-limiting factor of cisplatin chemotherapy. Here, we show the protective effect of ozone oxidative preconditioning against cisplatin-induced renal dysfunction in rats. Ozone oxidative preconditioning is a prophylactic approach, which favors the antioxidant-pro-oxidant balance for preservation of the cell redox state by increasing antioxidant endogenous systems in various in vivo and in vitro experimental models. AIMS: To analyze the protective role of ozone oxidative preconditioning against cisplatin-induced nephrotoxicity. METHODS: Male Sprague-Dawley rats were pretreated with 15 intrarectal applications of ozone/oxygen mixture at 0.36, 0.72, 1.1, 1.8 and 2.5 mg/kg before cisplatin intraperitoneal injection (6 mg/kg). Serum and kidneys were extracted and analyzed 5 days after cisplatin treatment for determinations of the renal content of glutathione, thiobarbituric acid-reactive substances, renal concentration and enzymatic activities of catalase, superoxide dismutase and glutathione peroxidase. RESULTS: Ozone pretreatment prevented the increase in serum creatinine levels, the glutathione depletion and the inhibition of superoxide dismutase, catalase and glutathione peroxidase activities induced by cisplatin in the rat kidney. Also, the renal content of thiobarbituric acid-reactive substances was decreased by ozone therapy. These protective effects of ozone were dose dependent. CONCLUSIONS: Intrarectal ozone therapy prevented effectively the renal antioxidant unbalance induced by cisplatin treatment.

Reversion by ozone treatment of acute nephrotoxicity induced by cisplatin in rats.

BACKGROUND: Ozone therapy has become a useful treatment for pathological processes, in which the damage mediated by reactive oxygen species is involved. Several lines of evidence suggest that cisplatin-induced acute nephrotoxicity is partially mediated by reactive oxygen species AIMS: To analyze the effect of ozone administration after cisplatin-induced acute nephrotoxicity. METHODS: Male Sprague-Dawley rats were treated with five intra-rectal applications of ozone/oxygen mixture at 0.36, 1.1 and 1.8 mg/kg after cisplatin intraperitoneal injection (6 mg/kg). Serum and kidneys were taken off 5 days after cisplatin treatment. Creatinine was measured in the serum and the activities of antioxidant enzymes and thiobarbituric acid reactive substances and glutathione content were analyzed in renal homogenate. RESULTS: Ozone treatment diminished the increase in serum creatinine levels, the glutathione depletion and also reversed the inhibition of superoxide dismutase, catalase and glutathione peroxidase activities induced by cisplatin in the rat kidney. Also, the renal content of thiobarbituric reactive substances was decreased by ozone/oxygen mixture applied after cisplatin. CONCLUSION: Intrarectal applications of ozone reversed the renal pro-oxidant unbalance induced by cisplatin treatment by the way of stimulation to some constituents of antioxidant system in the kidney, and thereby it decreased the renal damage.