6-Keto-PGE1

6-Keto-PGE1 (6-keto-Prostaglandin E1) is a biologically active derivative of PGE1. 6-Keto-PGE1 inhibits adenosine diphosphate-induced platelet aggregation. 6-Keto-PGE1 reduces cardiac afterload, decreases the accumulation of plasma myocardial depressant factor (MDF), lowers arterial blood pressure, dilates vascular beds, inhibits the vasoconstrictive response of vascular smooth muscle, and increases pulmonary compliance. 6-Keto-PGE1 directly stabilizes isolated cat liver lysosomes and significantly reduces the release of β-glucuronidase and cathepsin D. 6-Keto-PGE1 prolongs the survival time of traumatized rats and exerts protective effects through hemodynamic and cytoprotective actions. 6-Keto-PGE1 reduces central airway resistance. 6-Keto-PGE1 can be used in studies related to traumatic shock^[1][2][3]. In Vitro:6-Keto-PGE1 (1 μg/mL; 30 min) directly stabilizes isolated cat liver lysosomes, significantly reducing the release of β-glucuronidase and cathepsin D^[1]. In Vivo:6-Keto-PGE1 (250 ng/kg/min; i.v.; continuous infusion; starting 15 min after trauma for experiment duration) significantly prolongs survival time to 2.6 hours in rats with traumatic shock, while reducing plasma levels of cathepsin D and MDF and stabilizing mean arterial blood pressure^[1].
6-Keto-PGE1 (250 ng/kg/min; i.v.; continuous infusion; 5 hours) produces a modest, sustained decrease in mean arterial blood pressure (23 mmHg total reduction at 5 hours) without altering heart rate in healthy sham-operated rats^[1].
6-Keto-PGE₁ (1 μg/min; i.a.; infusion) significantly reduces mesenteric perfusion pressure by ~27-31% and reversibly inhibits vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine, and angiotensin II in the feline mesenteric vascular bed^[2].
6-Keto-PGE1 (0.3-10 μg; i.v.; rapid injection) acts as a potent bronchodilator in 5-HT-induced bronchoconstricted cats, reducing central airway resistance 3-10 times more potently than PGI2, with minimal pulmonary vasomotor activity, and its effects are independent of cyclooxygenase pathway stimulation^[3].