“…However, in chloralose anaesthetised rats, control MAP, and the pressor response to yet another non‐selective inhibitor, (N G ‐nitro‐L‐arginine), were not significantly different from those in conscious animals (23). In other experiments in endotoxaemic rats in the present model, we have indeed observed a marked increase in blood pressure in response to L‐NAME (24). Our conclusion is that in our setting there was no important interference with the response to NO from anaesthesia.…”
Aminoguanidine at 20 mg kg(-1) did not reverse the haemodynamic changes induced by LPS. Neither did the drug affect the tissue plasma clearance of albumin or the tissue plasma volume.
“…However, in chloralose anaesthetised rats, control MAP, and the pressor response to yet another non‐selective inhibitor, (N G ‐nitro‐L‐arginine), were not significantly different from those in conscious animals (23). In other experiments in endotoxaemic rats in the present model, we have indeed observed a marked increase in blood pressure in response to L‐NAME (24). Our conclusion is that in our setting there was no important interference with the response to NO from anaesthesia.…”
Aminoguanidine at 20 mg kg(-1) did not reverse the haemodynamic changes induced by LPS. Neither did the drug affect the tissue plasma clearance of albumin or the tissue plasma volume.
“…The data, however, should be regarded with some caution as the drug might have influenced constitutive NOS isoforms as well. Notwithstanding, the action on such NOS cannot have been pronounced as we, in other experiments (32), observed a pronounced pressor response to the non‐selective NOS inhibitor N ω ‐nitro‐L‐arginine‐methyl‐ester (L‐NAME). On the other hand, AG in non‐septic animals slightly increases arterial pressure and is inert on NOx levels (25).…”
AG inhibited NO formation in a dose-dependent way. Yet, AG had no haemodynamic effects, suggesting a minor cardiovascular influence of iNOS in this endotoxin model, in parallel to what has been found in microbial sepsis.
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