Abstract

Cerebral cortical blood flow, electrical activity, and extracellular fluid (ECF) pH and K+ ion activities were measured in anesthetized cats (0.7% halothane 65% N2O in O2) subjected to hypotension (mean BP 30-32 and 26-28 mmHg), induced by either practolol and trimetaphan (TMP) or practolol and nitroprusside (NTP). Limited blood withdrawal was also necessary to achieve these blood pressure (BP) levels. Cerebral cortical blood flow during hypotension was greater with NTP than with TMP, and hyperemia occurred in the recovery phase after NTP but not TMP. Electrical activity also was maintained better with NTP. ECF K+ increased in five of six TMP experiments but in only one of six NTP experiments. Values of K+ greater than 15 mM were only seen in the TMP group. Release of K+ into the ECF space occurred at values of cerebral cortical oxygen delivery below 3 ml 100 g-1 min-1. ECF K+ partially recovered after the end of hypotension in all except the experiment with the highest value. A progressive and severe cerebral acidosis was seen in all experiments during induced hypotension, and values below pH 6.50 were present at the stage of K+ increase in the ECF space. It is concluded that the ability of cell membranes in the cat's cortex to maintain normal ionic gradients is depressed by hypotension to these levels with TMP, but not with NTP, and that this difference is related to better-maintained oxygen supply values during NTP hypotension.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.