Effects of chemical castration using 20% CaCl2 with 0.5% DMSO in tomcats: Evaluation of inflammatory reaction by infrared thermography and effectiveness of treatment.

This study used infrared thermography to monitor the immediate inflammatory reaction to an intratesticular injection of 20% (calcium chloride) CaCl2 with 0.5% dimethyl sulfoxide (DMSO) for chemical castration and to provide evidence of the treatment's clinical viability. Six animals received a 0.25 mL intratesticular injection of 20% CaCl2 with 0.5% DMSO in each testis. Thermographic imaging, testicular measurement, penile spine evaluation, electroejaculation, and sperm analysis were performed before the injection. Eighty days post-injection, the cats were evaluated again, then received an orchiectomy followed by histological analysis. Infrared thermography of the testicular area was performed before (M0) and after anesthesia (M0A); after electroejaculation (M0E); 10 min (M1), 1 h, (M2) and 6 h (M3) after the injection for seven consecutive days (M4-10); after 15 (M11) and 30 days (M12); and after 80 days, before and after anesthesia and after electroejaculation (M13, M13A and M13E). No cats had a significant increase in testicular temperature or behavioral changes. All animals were azoospermic and had a 50% reduction in total testicular volume after 80 days. Histologically, the testes showed different degrees of degeneration, necrosis, calcification and replaced connective tissue, as well as Leydig cell hyperplasia in 7/12 of the testes. Infrared thermography efficiently diagnosed and monitored scrotal inflammation caused by intratesticular injection of 20% CaCl2 solution with 0.5% DMSO, and it is suggested that a single injection of this compound can cause azoospermia after 80 days. We concluded by infrared thermography with a clinical exam, that the adverse reactions were minimal and did not interfere with animal welfare.

Calcium supplementation during sepsis exacerbates organ failure and mortality via calcium/calmodulin-dependent protein kinase kinase signaling.

BACKGROUND: Calcium plays an essential role in nearly all cellular processes. As such, cellular and systemic calcium concentrations are tightly regulated. During sepsis, derangements in such tight regulation frequently occur, and treating hypocalcemia with parenteral calcium administration remains the current practice guideline. OBJECTIVE: We investigated whether calcium administration worsens mortality and organ dysfunction using an experimental murine model of sepsis and explored the mechanistic role of the family of calcium/calmodulin-dependent protein kinases in mediating these physiological effects. To highlight the biological relevance of these observations, we conducted a translational study of the association between calcium administration, organ dysfunction, and mortality among a cohort of critically ill septic ICU patients. DESIGN: Prospective, randomized controlled experimental murine study and observational clinical cohort analysis. SETTING: University research laboratory and eight ICUs at a tertiary care center. PATIENTS: A cohort of 870 septic ICU patients. SUBJECTS: C57Bl/6 and CaMKK mice. INTERVENTIONS: Mice underwent cecal ligation and puncture polymicrobial sepsis and were administered with calcium chloride (0.25 or 0.25 mg/kg) or normal saline. MEASUREMENTS AND MAIN RESULTS: Administering calcium chloride to septic C57Bl/6 mice heightened systemic inflammation and vascular leak, exacerbated hepatic and renal dysfunction, and increased mortality. These events were significantly attenuated in CaMKK mice. In a risk-adjusted analysis of septic patients, calcium administration was associated with an increased risk of death, odds ratio 1.92 (95% CI, 1.00-3.68; p = 0.049), a significant increase in the risk of renal dysfunction, odds ratio 4.74 (95% CI, 2.48-9.08; p < 0.001), and a significant reduction in ventilator-free days, mean decrease 3.29 days (0.50-6.08 days; p = 0.02). CONCLUSIONS: Derangements in calcium homeostasis occur during sepsis that is sensitive to calcium administration. This altered calcium signaling, transduced by the calmodulin-dependent protein kinase kinase cascade, mediates heightened inflammation and vascular leak that culminates in elevated organ dysfunction and mortality. In the clinical management of septic patients, calcium supplementation provides no benefit and may impose harm.

Investigation of mechanisms involved in (-)-borneol-induced vasorelaxant response on rat thoracic aorta.

The monoterpene (-)-borneol is present in essential oils of several medicinal plants. The aim of this study was to evaluate (-)-borneol effects on rat thoracic aorta artery rings. The cumulative addition of (-)-borneol (10(-9) -3 × 10(-4) M) on a phenylephrine-induced pre-contraction (10(-6) M) promoted a vasorelaxant effect in a concentration-dependent manner and independent of vascular endothelium. A similar effect was obtained on KCl-induced pre-contractions (80 mM). (-)-Borneol (10(-5) -3 × 10(-4 ) M) inhibited contractions induced by cumulative addition of CaCl2 (10(-6) -3 × 10(-2) M) in depolarizing medium without Ca(2+) in a concentration-dependent manner. On S-(-) Bay K 8644-induced pre-contractions (10(-7) M), (-)-borneol did not induce significant changes compared with KCl-induced pre-contractions. In a Ca(2+) -free medium, (-)-borneol (10(-5) , 10(-4) or 10(-3) M) interfered in calcium mobilization from phenylephrine (10(-6) M)- or caffeine (20 mM)-sensitive intracellular stores. The involvement of K(+) channels was evaluated by tetraethylammonium (3 mM), 4-aminopyridine (1 mM) and glibenclamide (10(-5) M) pre-treatment, and (-)-borneol-induced vasorelaxation was markedly attenuated. Thus, this vasorelaxant effect can probably be attributed to calcium influx blockade through voltage-operated calcium channels (CaV L), calcium mobilization from intracellular stores and potassium channels activation.

Estudo histopatológico do efeito do tenoxicam e do seu diluente no endotélio venoso, em coelhos / Histopathologic study on the effect of tenoxicam and its diluent in the venous endothelium, in rabbits

Com o objetivo de avaliar pela histopatologia o efeito do tenoxicam e do seu diluente no endotélio venoso, foram utilizados 48 coelhos (Oryctolagus cuniculus), rancos, da linhagem Nova Zelândia, machos, com idade acima de 10 semanas, com peso variando entre 2350 e 3500 gramas, divididos em dois grupos, denominados Experimento e Controle, que foram observados nos tempos de 6, 12 e 24 horas. Administrou-se nas venae auriculares dextra e sinistra, diluente ou tenoxicam/diluente no Grupo Experimento e cloreto de sódio a 0,9 por cento no Grupo Controle. Não se observou diferença estatisticamente significante entre o peso dos animais do Grupo Experimento e do Grupo Controle, antes da realização do procedimento. No que se refere à presença ou ausência de trombose, observamos que: após administração do diluente no Grupo Experimento, 19,4 por cento das venae apresentaram trombos; após administração do tenoxicam com o diluente no Grupo Experimento, a incidência de trombose foi também de 19,4 por cento; no Grupo Controle, em que foi injetado cloreto de sódio a 0,9 por cento, nenhuma das venae apresentou trombos. Os resultados observados permitem concluir que o tenoxicam com o seu diluente comercial ou o seu diluente isolado podem acarretar trombose nas venae em que foram injetados.

Effect of calcium addition and acidification on the quality characteristics of canned okra (Hibiscus esculentus L).

A study was conducted on calcium chloride treatments of canned okra acidified by adding either acetic, citric, lactic, malic or tartaric acids or by lactic fermentation. The quality of the processed okra was determined by physical, chemical, microbiological and sensory analyses after a two month storage period at room temperature. The results indicated the possibility of processing high quality canned okra by small canneries, with low cost equipment and low energy requirements. The acidification procedures ensure minimal risk of botulism.

Influence of calcium on the blood pressure and renal effects of stevioside

The effect of verapamil (V, 0.015 mg/min, iv) or Ca Cl2 (800 mEq/l, 0.025 ml kg-1 min-1,iv) on renal function and mean arterial pressure (MAP) were evaluated in male Wistar rats weighing 280-320 g during treatment with stevioside (S, 16 mg kg-1 h-1, iv). Verapamil administered to 10 rats significantly increased the hypotensive effect of stevioside on MAP (control 124 ñ 0.77; S, 96 ñ 1.50; S+V, 67 ñ 0.70 mm Hg) and fractional sodium excretion (control 0.76 ñ 0.05; S, 1.56 ñ 0.10; S+V, 2.72 ñ 0.25%). Urinary flow, reported as percent glomerular filtration rate (V/GRF), and renal plasma flow (RPF) increased slightly but not significantly during stevioside plus verapamil administration. In contrast, infusion of CaCl2 in 10 rats pretreated with stevioside induced a marked attenuation of MAP (control 119 ñ 1.83; S, 70 ñ 1.12; S ñ CaCl2, 109 ñ 1.60 mmHg) and RPF (control, 16.73 ñ 3.76; S, 34.33 ñ 2.55; S+CaCl2, 17.20 ñ 2.87 ml min-1 Kg-1). The diuresis and natriuresis induced by stevioside were also inhibited by simultaneous administration of CaCl2. These data are consistent with the view that stevioside acts on arterial pressure and renal function as a calcium antagonist, as is the case for verapamil

Efecto de la ligadura del conducto pancreático principal en la pancreatits necrohemórragica experimental / Effect of the ligation of the pancreatic duct in experimental necrohemorrhagic prancreatitis

Se presenta una serie compuesta por 10 perros, a quienes de 20 minutos de provocarles una pancreatitis aguda grave mediante la inyección intracanalicular de 2 a 4 cm3 de cloruro de calcio, se procedió a ligar el conducto pancreático principal. Se quiso comenzar a investigar el nivel del árbol canalicular en donde el bloqueo desempeña su acción. Al morir los 10 animales se demostró que la simple obturación del conducto por la ligadura no reemplaza la acción obtenida prolamina o Tissucol

Efecto de la ligadura del conducto pancreático principal en la pancreatits necrohemórragica experimental / Effect of the ligation of the pancreatic duct in experimental necrohemorrhagic prancreatitis

Se presenta una serie compuesta por 10 perros, a quienes de 20 minutos de provocarles una pancreatitis aguda grave mediante la inyección intracanalicular de 2 a 4 cm3 de cloruro de calcio, se procedió a ligar el conducto pancreático principal. Se quiso comenzar a investigar el nivel del árbol canalicular en donde el bloqueo desempeña su acción. Al morir los 10 animales se demostró que la simple obturación del conducto por la ligadura no reemplaza la acción obtenida prolamina o Tissucol (AU)

Tratamiento de la pancreatitis aguda experimental: demostración de la acción física del bloqueo ductal / Treatment of experimental acute pancreatitis: demostration of the physical effect of ductal blockage

Las experiencias preliminares empleando el bloqueo ductal pancreático mediante la aplicación de Ethibloc, para el tratamiento de la pancreatitis aguda experimental demostraron la reducción de la mortalidad del 100% al 12,5%. En una segunda etapa, el empleo de Tissucol en reemplazo del Ethibloc, mostró interesantes resultados que permiten sospechar que la acción del bloqueo ductal es de origen físico. Sin embargo, quedaban dudas por la presencia de derivados proteicos en ambas sustancias. Con el objeto de despejar dicho interrogante se realizó el bloqueo a un grupo de 10 perros empleando una tercera sustancia, físicamente similar pero inorgánica. La pancreatitis grave se provocó también con clouro de calcio al 20% y a los 20 a 30 minutos, y una vez comprbada la lesión hemorrágica se inyectaron 5 cm3 de una silicona denominada Xantopren. La evolución fue más tórpida que en las experiencias anteriores. Seguramente debido a que esta sustancia no se reabsorbe como el Erthibloc o el Tissucol. Murió un solo perro al primer día del postoperatorio, dentro del período en que mueren todos los animales con pancreatitis aguda por cloruro de calcio. De esta forma quedaría confirmado que el mecanismo de la acción terapéutica de este nuevo procedimiento, es realmente físico

Tratamiento de la pancreatitis aguda experimental: demostración de la acción física del bloqueo ductal / Treatment of experimental acute pancreatitis: demostration of the physical effect of ductal blockage

Las experiencias preliminares empleando el bloqueo ductal pancreático mediante la aplicación de Ethibloc, para el tratamiento de la pancreatitis aguda experimental demostraron la reducción de la mortalidad del 100% al 12,5%. En una segunda etapa, el empleo de Tissucol en reemplazo del Ethibloc, mostró interesantes resultados que permiten sospechar que la acción del bloqueo ductal es de origen físico. Sin embargo, quedaban dudas por la presencia de derivados proteicos en ambas sustancias. Con el objeto de despejar dicho interrogante se realizó el bloqueo a un grupo de 10 perros empleando una tercera sustancia, físicamente similar pero inorgánica. La pancreatitis grave se provocó también con clouro de calcio al 20% y a los 20 a 30 minutos, y una vez comprbada la lesión hemorrágica se inyectaron 5 cm3 de una silicona denominada Xantopren. La evolución fue más tórpida que en las experiencias anteriores. Seguramente debido a que esta sustancia no se reabsorbe como el Erthibloc o el Tissucol. Murió un solo perro al primer día del postoperatorio, dentro del período en que mueren todos los animales con pancreatitis aguda por cloruro de calcio. De esta forma quedaría confirmado que el mecanismo de la acción terapéutica de este nuevo procedimiento, es realmente físico (AU)