Pharmacological characterization of rat paw edema induced by Cerastes gasperettii (cerastes) venom

Inflammatory response induced by the venom of the Arabian sand viper Cerastes gasperettii was studied by measuring rat hind-paw edema. Cerastes gasperettii venom (CgV, 3.75-240 µg/paw), heated for 30s at 97°C, caused a marked dose and time-dependent edema in rat paw. Response was maximal 2h after venom administration and ceased within 24h. Heated CgV was routinely used in our experiments at the dose of 120 µg/paw. Among all the drugs and antivenoms tested, cyproheptadine and 5-nitroindazole were the most effective in inhibiting edema formation. Aprotinin, mepyramine, dexamethasone, diclofenac, dipyridamole, Nomega-nitro-L-arginine, quinacrine, and nordihydroguaiaretic acid showed statistically (p 0.001) significant inhibitory effect, but with variations in their inhibition degree. Equine polyspecific and rabbit monospecific antivenoms significantly (p 0.001) reduced edema when locally administered (subplantar) but were ineffective when intravenously injected. We can conclude that the principal inflammatory mediators were serotonin, histamine, adenosine transport factors, phosphodiesterase (PDE), cyclooxygenase, lipoxygenase and phospholipase A2 (PLA2), in addition to other prostaglandins and cytokines.

Pharmacological characterization of rat paw edema induced by Cerastes gasperettii (cerastes) venom

Inflammatory response induced by the venom of the Arabian sand viper Cerastes gasperettii was studied by measuring rat hind-paw edema. Cerastes gasperettii venom (CgV, 3.75-240 µg/paw), heated for 30s at 97°C, caused a marked dose and time-dependent edema in rat paw. Response was maximal 2h after venom administration and ceased within 24h. Heated CgV was routinely used in our experiments at the dose of 120 µg/paw. Among all the drugs and antivenoms tested, cyproheptadine and 5-nitroindazole were the most effective in inhibiting edema formation. Aprotinin, mepyramine, dexamethasone, diclofenac, dipyridamole, Nomega-nitro-L-arginine, quinacrine, and nordihydroguaiaretic acid showed statistically (p 0.001) significant inhibitory effect, but with variations in their inhibition degree. Equine polyspecific and rabbit monospecific antivenoms significantly (p 0.001) reduced edema when locally administered (subplantar) but were ineffective when intravenously injected. We can conclude that the principal inflammatory mediators were serotonin, histamine, adenosine transport factors, phosphodiesterase (PDE), cyclooxygenase, lipoxygenase and phospholipase A2 (PLA2), in addition to other prostaglandins and cytokines.

Pharmacological characterization of rat paw edema induced by Naja haje arabica venom

This investigation was performed in order to assess the inflammatory response induced by Naja haje arabica venom (NhaV) in rat hind paw. The inflammatory response was estimated by measuring the edema with a Plethysmometer. The venom (0.625-10mug/paw) produced a dose and time-dependent increase in non-hemorrhagic paw edema. The response to NhaV was maximal within 15 min and disappeared in 24 h. Five mug/paw of NhaV was chosen to test the effect of various drugs on the edema induced by this venom. Quinacrine (QNC), a phospholipase A2 (PLA2) inhibitor, and dipyridamole (DPM), an adenosine transport inhibitor, attenuated venom-induced edema in rat paw (P<0.001). Commercially available antivenom was ineffective when administered intravenously, whereas its local administration with NhaV attenuated the edema formation (P<0.001). In conclusion, NhaV-induced edema in rat paw involves PLA2 and adenosine mechanisms. Additionally, the use of polyspecific antivenom, intravenously, was ineffective in preventing NhaV-induced edema.(AU)

Pharmacological characterization of rat paw edema induced by Naja haje arabica venom

This investigation was performed in order to assess the inflammatory response induced by Naja haje arabica venom (NhaV) in rat hind paw. The inflammatory response was estimated by measuring the edema with a Plethysmometer. The venom (0.625-10mug/paw) produced a dose and time-dependent increase in non-hemorrhagic paw edema. The response to NhaV was maximal within 15 min and disappeared in 24 h. Five mug/paw of NhaV was chosen to test the effect of various drugs on the edema induced by this venom. Quinacrine (QNC), a phospholipase A2 (PLA2) inhibitor, and dipyridamole (DPM), an adenosine transport inhibitor, attenuated venom-induced edema in rat paw (P 0.001). Commercially available antivenom was ineffective when administered intravenously, whereas its local administration with NhaV attenuated the edema formation (P 0.001). In conclusion, NhaV-induced edema in rat paw involves PLA2 and adenosine mechanisms. Additionally, the use of polyspecific antivenom, intravenously, was ineffective in preventing NhaV-induced edema.

Circulatory shock in horses / Choque circulatório em equinos

Circulatory shock can be defined as an acute circulatory failure with an inadequate tissue delivery of oxygen and nutritive substrates to the tissues, resulting in generalised cellular hypoxia. Shock can be classified as cardiogenic, obstructive, hypovolaemic, or distributive. The pathophysiologic consequences of inadequate tissue perfusion are directly related to cell ischemia, inadequate O2 delivery, and the production of proinflammatory mediators. If abnormalities of tissue perfusion are allowed to persist, the function of vital organs will be impaired. The subsequent reperfusion will exacerbate organ dysfunction and, in severe cases, may culminate in multiple organ dysfunction syndrome. Early recognition of equine that are shocked and immediate provision of effective circulatory support is therefore essential. In all cases the objective is to restore oxygen delivery to the tissues while correcting the underlying cause. Delays in making the diagnosis and initiating treatment, as well as suboptimal resuscitation, contribute to the development of peripheral vascular failure and irreversible defects in oxygen use which can culminate in vital organ dysfunction. 

Choque circulatório pode ser definido como uma falha circulatória aguda com liberação inadequada de oxigênio e nutrientes aos tecidos, resultando em hipóxia celular. O choque pode ser classificado como cardiogênico, obstrutivo, hipovolêmico ou distributivo. As consequências fisiopatológicas da perfusão tecidual inadequada estão diretamente relacionadas à isquemia celular, liberação inadequada de O2 e produção de potentes mediadores inflamatórios. Caso as anormalidades de perfusão tecidual se perpetuem, a função de vários órgãos se torna inadequada. A consequente reperfusão poderá exacerbar a disfunção orgânica e, nos casos graves, culminar na síndrome da disfunção orgânica múltipla. O reconhecimento precoce de equinos em choque circulatório e o fornecimento imediato de suporte circulatório efetivo são essenciais. Em todos os casos o objetivo é restaurar a perfusão e a liberação de oxigênio aos tecidos, enquanto se corrige a causa primária. A demora em fazer o diagnóstico e iniciar o tratamento, bem como a ressuscitação sub-ótima, contribuem para o desenvolvimento de falha vascular periférica e alterações irreversíveis na utilização de oxigênio, culminando na disfunção orgânica.