Skeletal muscle perfusion during prolonged 2.03% end-tidal isoflurane-O2 anesthesia in isocapnic ponies

Effects of 1.55 minimum alveolar concentration isoflurane O2 anesthesia (2.03% end-tidal isoflurane) on blood flow in the up-(nondependent) and down-(dependent) positioned skeletal muscles were studied at 60, 120, and 180 minutes in 6 healthy isocapnic ponies in right lateral recumbency on a nonpadded hardwood floor. Measurements were made, using 15-micron diameter radionuclide-labeled microspheres injected into the left ventricle, and comparisons were made with data obtained from ponies in the conscious state. Isoflurane administration caused a sharp reduction in cardiac output and systemic pressure (P less than 0.01), but total peripheral resistance did not change significantly. In the triceps brachii, gluteus medius, biceps femoris, and vastus lateralis of both sides, blood flow decreased significantly during 1.55 minimum alveolar concentration isoflurane anesthesia (P less than 0.01), and fluctuations did not occur with increasing duration of anesthesia. In masseter muscles, perfusion values during the 3 hours of anesthesia were not significantly different from values in awake ponies. Despite the fact that 4 ponies developed marked edema of the dependent masseter muscle, 1 pony without masseter edema developed postanesthetic forelimb lameness and 2 of the 4 ponies with masseter edema had generalized hind limb weakness after anesthesia; significant differences in blood flow between up- and down-positioned muscles were not observed. During isoflurane-O2 anesthesia in ponies, a sharp significant decrease in skeletal muscle blood flow was observed (P less than 0.01). Decreased equine skeletal muscle perfusion during isoflurane anesthesia also may be accompanied by accentuated O2 loss from the arterial blood via the countercurrent O2 exchange between large arterioles and venules.