Platelet-activating factor and cytokine interactions in shock

Effect of PF 10040 on PAF‐induced airway responses in neonatally immunized rabbits

“…The local administration of PF 10040 into rabbit skin has recently been shown to inhibit oedema formation induced by PAF (Rossi et al, 1992) (Hosford et al, 1989) as this biological response induced by PAF is known to be a platelet dependent phenomenon (Coyle et al, 1990). It is plausible that we failed to inhibit PAF-induced bronchoconstriction with PF 10040 because we did not achieve high enough local concentrations of the drug in the airways.…”

Effect of PF 10040 on PAF‐induced airway responses in neonatally immunized rabbits

“…The local administration of PF 10040 into rabbit skin has recently been shown to inhibit oedema formation induced by PAF (Rossi et al, 1992) (Hosford et al, 1989) as this biological response induced by PAF is known to be a platelet dependent phenomenon (Coyle et al, 1990). It is plausible that we failed to inhibit PAF-induced bronchoconstriction with PF 10040 because we did not achieve high enough local concentrations of the drug in the airways.…”

Novel low‐molecular‐weight superoxide dismutase mimic deferoxamine‐manganese improves survival following hemorrhagic and endotoxic shock

“…The high incidence of mortality associated with hemorrhagic and endotoxic shock remains a serious and complicated problem [Holcroft et al, 1989;van Deventer et al, 19881. Intravenous fluid administration alone does not ensure uncomplicated resuscitation and survival [Rackow et al, 19831, suggesting that hemodynamic compensation alone may not be adequate. In addition, a number of pharmacological agents have been shown to improve survival following circulatory shock [Hosford et al, 1989;Feuerstein and Hallenbeck, 19871, further suggesting that a variety of biochemical and cellular events lead to organ dysfunction and death. Moreover, it now appears that oxygen-derived free radicals contribute to the pathology of circulatory shock [Poli et al, 1989;Cunningham and Keaveny, 1978;Crowell et al, 19691 and, although it is not yet clear how free radicals are produced during shock, the administration of the enzyme superoxide dismutase (SOD), which catalyzes the dismutation of the superoxide radical (OF) to hydrogen peroxide (H202), has been shown to improve survival in models of circulatory shock [Broner et al, 1988;Kunimoto et al, 19871. Despite the possibility that SOD may provide therapeutic benefit during circulatory shock there are some obvious practical limitations to using the enzyme clinically, which has led investigators to search for a biologically active, synthetic replacement for SOD.…”

Effect of PF 10040 on PAF‐induced airway responses in neonatally immunized rabbits

“…The local administration of PF 10040 into rabbit skin has recently been shown to inhibit oedema formation induced by PAF (Rossi et al, 1992) (Hosford et al, 1989) as this biological response induced by PAF is known to be a platelet dependent phenomenon (Coyle et al, 1990). It is plausible that we failed to inhibit PAF-induced bronchoconstriction with PF 10040 because we did not achieve high enough local concentrations of the drug in the airways.…”

Novel low‐molecular‐weight superoxide dismutase mimic deferoxamine‐manganese improves survival following hemorrhagic and endotoxic shock

“…The high incidence of mortality associated with hemorrhagic and endotoxic shock remains a serious and complicated problem [Holcroft et al, 1989;van Deventer et al, 19881. Intravenous fluid administration alone does not ensure uncomplicated resuscitation and survival [Rackow et al, 19831, suggesting that hemodynamic compensation alone may not be adequate. In addition, a number of pharmacological agents have been shown to improve survival following circulatory shock [Hosford et al, 1989;Feuerstein and Hallenbeck, 19871, further suggesting that a variety of biochemical and cellular events lead to organ dysfunction and death. Moreover, it now appears that oxygen-derived free radicals contribute to the pathology of circulatory shock [Poli et al, 1989;Cunningham and Keaveny, 1978;Crowell et al, 19691 and, although it is not yet clear how free radicals are produced during shock, the administration of the enzyme superoxide dismutase (SOD), which catalyzes the dismutation of the superoxide radical (OF) to hydrogen peroxide (H202), has been shown to improve survival in models of circulatory shock [Broner et al, 1988;Kunimoto et al, 19871. Despite the possibility that SOD may provide therapeutic benefit during circulatory shock there are some obvious practical limitations to using the enzyme clinically, which has led investigators to search for a biologically active, synthetic replacement for SOD.…”

Effect of PF 10040 on PAF‐induced airway responses in neonatally immunized rabbits

“…The local administration of PF 10040 into rabbit skin has recently been shown to inhibit oedema formation induced by PAF (Rossi et al, 1992) (Hosford et al, 1989) as this biological response induced by PAF is known to be a platelet dependent phenomenon (Coyle et al, 1990). It is plausible that we failed to inhibit PAF-induced bronchoconstriction with PF 10040 because we did not achieve high enough local concentrations of the drug in the airways.…”

Novel low‐molecular‐weight superoxide dismutase mimic deferoxamine‐manganese improves survival following hemorrhagic and endotoxic shock

“…The high incidence of mortality associated with hemorrhagic and endotoxic shock remains a serious and complicated problem [Holcroft et al, 1989;van Deventer et al, 19881. Intravenous fluid administration alone does not ensure uncomplicated resuscitation and survival [Rackow et al, 19831, suggesting that hemodynamic compensation alone may not be adequate. In addition, a number of pharmacological agents have been shown to improve survival following circulatory shock [Hosford et al, 1989;Feuerstein and Hallenbeck, 19871, further suggesting that a variety of biochemical and cellular events lead to organ dysfunction and death. Moreover, it now appears that oxygen-derived free radicals contribute to the pathology of circulatory shock [Poli et al, 1989;Cunningham and Keaveny, 1978;Crowell et al, 19691 and, although it is not yet clear how free radicals are produced during shock, the administration of the enzyme superoxide dismutase (SOD), which catalyzes the dismutation of the superoxide radical (OF) to hydrogen peroxide (H202), has been shown to improve survival in models of circulatory shock [Broner et al, 1988;Kunimoto et al, 19871. Despite the possibility that SOD may provide therapeutic benefit during circulatory shock there are some obvious practical limitations to using the enzyme clinically, which has led investigators to search for a biologically active, synthetic replacement for SOD.…”