Menger M D, Hammersen F, Barker J, Feifel G, Messmer K
Dept. of General Surgery, University of the Saarland, Homburg, Saar/FRG.
Adv Exp Med Biol. 1988;222:631-6. doi: 10.1007/978-1-4615-9510-6_78.
In order to study changes in functional capillary density and tissue PO2 in chronically ischemic skeletal muscle, a new model, using the Syrian golden hamster was developed. In the hamster dorsal skin fold, which receives its vascular supply from two cranial and two caudal feeding arteries, a double frame chamber was implanted and ischemia was induced in the cranial part by heat coagulation of the cranial arteries outside of the chamber. This technique allows for analysis of microvascular hemodynamics and local tissue PO2 prior to and during a prolonged period of ischemia in skin muscle. As result of ischemia the diameters of the arterioles increased (p less than 0.001) over the whole 11 day observation period. Functional capillary density decreased significantly (p less than 0.01) during the first 7 days, while capillary RBC-velocity was reduced throughout the 11 days of observation. RBC-velocity in collecting venules was diminished significantly throughout the postischemic observation period. The diameters of the collecting venules first increased upon ischemia (p less than 0.001) but were found decreased at 4, 7 and 11 days. Measurements of tissue PO2 demonstrated a marked decrease from a mean PO2 of 20.5 mmHg prior, to 9.5 mmHg following induction of ischemia. The model allows for induction of chronic ischemia and is suitable to study the effect of therapeutic measures on the microcirculation in chronically ischemic skeletal muscle in vivo.
