Reference

Thermoregulatory defect in rats during anesthesia

Thermoregulatory defect in rats during anesthesia. Hitt, Ben A.; Mazze, Richard I.; Cook, Thomas L.; Beppu, William J.; Kosek, Jon C. 13838-16-9 and 76-38-0 are cas registry numbers. These chemicals are also mentioned in this article. (Dep. Anesth., VA Hosp., Palo Alto, Calif., USA). Anesth. Analg. (Cleveland), 56(1), 9-15 (English) 1977. CODEN: AACRAT. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Eighty-six percent (43/50) of Fischer 344 rats treated with phenobarbital Na (I) [57-30-7] (1 mg/mL in drinking water) and exposed to either sevoflurane [28523-86-6] or enflurane [13838-16-9], in the presence of either soda lime or exogenous heat, died within a few h after exposure. Fischer 344 rats and rats of other strains drinking I water and exposed to methoxyflurane [76-38-0] were affected, but to a lesser degree. Rats drinking ordinary tap water and I-treated rats not exposed to either soda lime or exogenous heat were unaffected. Guinea pigs and mice also were unaffected. Thus, the toxic response represents a species-specific thermoregulatory defect, pptd. by heat and occurring in rats treated with I in combination with sevoflurane, enflurane, or methoxyflurane. .

Regional brain blood flow and cerebral cortical oxygen consumption during sevoflurane anesthesia in healthy isocapnic swine

Regional brain blood flow and cerebral cortical oxygen consumption during sevoflurane anesthesia in healthy isocapnic swine. Manohar, Murli (Coll. Vet. Med., Univ. Illinois, Urbana, IL 61801, USA). J. Cardiovasc. Pharmacol., 8(6), 1268-75 (English) 1986. CODEN: JCPCDT. ISSN: 0160-2446. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Regional distribution of brain blood flow was examd. in previously catheterized healthy isocapnic swine while awake (control), and during 1.0 and 1.5 min. alveolar concn. (MAC-2.66 and 3.99% end-tidal, resp.) sevoflurane [28523-86-6] anesthesia using radionuclide-labeled 15-mm diam. microspheres that were injected into the left atrium. In 6 addnl. pigs, the superior sagittal sinus was also catheterized so that cerebral cortical O2 consumption could be ascertained during these conditions. Control values of blood flow in the cerebral cortical gray matter, white matter, and caudate nuclei were 117, 38, and 105 mL/min/100 g, resp. At 1.0 MAC sevoflurane, blood flow in these regions decreased to 66, 76, and 75% of resp. control values, and these values were not different from those recorded at 1.5 MAC anesthesia. Cerebral cortical O consumption decreased by 50 and 52% at 1.0 and 1.5 MAC sevoflurane anesthesia, but the Hb-O satn. in the cerebral cortical venous drainage (57% and 69% at 1.0 and 1.5 MAC) consistently exceeded the control value (42%), suggesting that cortical O supply during both levels of sevoflurane anesthesia remained adequate. In cerebellum, blood flow decreased from 86 (control) to 68 mL/min/100 g with 1.0 MAC sevoflurane, but returned toward the control value at 1.5 MAC anesthesia. The thalamohypothalamic perfusion decreased to 59 and 75% of the control value with 1.0 and 1.5 MAC sevoflurane anesthesia. The pontine and medullary blood flows decreased to 81 and 84% of the resp. control values only with 1.0 MAC sevoflurane. Vascular resistance did not decrease in any region of the brain with 1.0 MAC anesthesia; however, vasodilatation occurred in the cerebral white matter, cerebellum, pons, and medulla during 1.5 MAC sevoflurane anesthesia.