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Publications (2)3.92 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The response of peripheral blood vessels to adrenergic and cholinergic agonists was examined 1, 3, 7, and 21 d after hens were treated with a single intramuscular injection of 2.5 mg/kg cyclic phenyl saligenin phosphate (PSP) or 0.10 mg/kg paraoxon (PXN). These two organophosphates (OPs) cause different clinical effects in exposed animals, as PSP causes organophosphate-induced delayed neuropathy (OPIDN) and PXN causes acute poisoning through inhibition of acetylcholinesterase. For these studies, the ischiadic artery was cannulated both prograde and retrograde and the blood was shunted through a pump to maintain a constant flow. Alterations in pressure measured at the pump outflow were used to indicate changes in limb vascular resistance. Dose-response curves were generated for the response to intravenous administration of acetylcholine (ACh), phenylephrine (PE), or salbutamol (SAL) (10(-8) to 10(-4) mol/kg). Acetylcholine at 10(-8) to 10(-7) mol/kg caused an increase in vascular resistance, whereas concentrations of 10(-5) to 10(-4) mol/kg caused a decrease in vascular resistance in hens given PSP 1 and 3 d previously. The response of PXN-treated hens to ACh was not significantly altered from that of vehicle-treated hens. The resistance generated in response to PE, an alpha 1-adrenergic agonist, in PSP-treated hens was greater than levels in vehicle-treated hens on d 1 and 3 and greater than the response seen in hens treated with PXN. Salbutamol, a beta 2-adrenergic agonist, at concentrations of 10(-7) to 10(-4) mol/kg caused an increase in resistance 1 and 3 d after PSP and a decrease on d 7. The responses to SAL were different in PXN-treated hens, as these hens demonstrated a lesser increase in resistance at concentrations of 10(-8) to 10(-7) mol/kg and a decrease in resistance at 10(-5) to 10(-4) mol/kg 1 d after administration of PXN. These observations indicate that response to vasoactive agents is altered in OP-treated hens and that responses differ between a compound capable of causing OPIDN (PSP) and a compound that only causes acute effects (PXN).
    Journal of Toxicology and Environmental Health 03/1995; 44(2):167-87. · 1.81 Impact Factor
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    ABSTRACT: Cardiovascular parameters, including limb venous flow and arterial blood pressure, were measured 1, 3, 7, and 15-21 days after a single 2.5 mg/kg intramuscular injection of phenyl saligenin cyclic phosphate (PSP) was administered to hens. All hens given the organophosphate developed clinical signs of delayed neuropathy by Day 10 and these signs were maximal by Day 20 after PSP administration. Resistance to blood flow was increased in the legs of hens given PSP prior to the onset of clinical signs of organophosphorus-induced delayed neuropathy (OPIDN). This did not occur in hens given an OP that did not cause OPIDN (paraoxon). PSP administration also resulted in significant decreases in the activities of brain neurotoxic esterase (NTE) and plasma cholinesterase, as well as decreases in body weight prior to evidence of clinical signs of OPIDN. When maximal signs of OPIDN were present, activities of brain NTE and plasma cholinesterase had returned to control levels. Limb venous flow and arterial blood pressure were elevated in PSP-treated hens when maximal clinical signs were evident (Days 15-21). Body weight and arterial PCO2 were also significantly decreased in hens with OPIDN and hematocrit significantly increased. Administration of this neuropathy-inducing organophosphate was, therefore, capable of altering hemodynamic and hematologic parameters before and after onset of OPIDN.
    Pesticide Biochemistry and Physiology 03/1993; 45(3):220–227. · 2.11 Impact Factor