MSJA • RESEARCH free radicals (10, 11). Even though leukocytes and endothelial cells possess several defenses against oxidative stress, a voluminous quantity of oxygen free radicals can lead to oxidative injury and vascular dysfunction in vivo (12, 13).
Reperfusion in the coronary microvasculature In another experiment that drew upon the animal model work of (2), male dogs were anaesthetised with intravenous thiopental sodium (20 mg/kg) and α-chloralose (100 mg/kg), and mechanically ventilated (9).
During the procedure, a catheter was placed into the left atrium. The left anterior descending coronary artery in fourteen dogs was then obstructed proximally. Ischaemia was established by cyanosis and akinaesia of the left ventricular wall, supporting the findings of (14, 15). Three groups of animals were studied as seen in Fig 1 below. The ischaemiareperfusion group (n=9) underwent 60 minutes of ischaemia and 120 minutes of reperfusion. The ischaemia-control (I-Ctl) group (n=5) experienced 180 minutes of ischaemia with no subsequent reperfusion. The control group (n=5) underwent no ischaemia for 180 minutes.
The coronary microvasculature (average diameter between 25 and 130 µm) was visualised with a fluorescence microscope (9). Leukocytes were then labeled by infusing acridine orange for two minutes into the left atrium before each measurement. Images were then recorded two minutes after the acridine orange infusion ceased at the following time points: 15 and five minutes before the protocol was begun (period 1); 10, 30 and 55 minutes of the first hour of the protocol (period 2); and 10, 60, and 120 minutes into the second and third hours of the protocol (period 3) (Figure 1). From Figure 1 it can be seen that
Figure 1 Illness Perception Questionnaire. Fluorescence measurements (gray level of vessel wall minus gray level of background) along the walls of coronary microvessels over 195 minutes. Starting at time 0, the ischaemia-reperfusion group ( , n=9) was subjected to 60 minutes of ischaemia (period 2) and then reperfused for 120 minutes (period 3). The ischaemia-control group ( , n=5) was subjected to 180 minutes of ischaemia only starting at time 0 (periods 2 and 3). The control group ( , n=5) was not subjected to ischaemia and was perfused under baseline conditions for the duration of the protocol. The vertical dashed line labeled “Ischaemia” indicates the time of onset of ischaemia for the ischaemia-reperfusion and ischaemia-control groups. The vertical dashed line labeled “Reperfusion” indicates the time of onset of reperfusion for the ischaemiareperfusion group. Although there were no differences between the three groups during period 2, fluorescence was significantly greater in the ischaemia-reperfusion group than in the ischaemia-control or control groups during period 3. Fluorescence in the ischaemia-reperfusion group during period 3 (reperfusion) was also significantly greater than fluorescence in the same group during period 2 (ischaemia). Values are mean ± SEM. Based on (9). MSJA • Volume 5 Issue 1 • 2013
27