Effects of prolonged cold injury on the subcutaneous microcirculation of the hamster

Abstract

An animal model is described allowing for direct measurements of local tissue PO2, microhemodynamics and vascular density in the event of a prolonged non freezing cold injury. The model consists of implanting a transparent skin fold chamber in the dorsal skin fold in hamsters and of inserting two permanent indwelling catheters in jugular vein and carotid artery, respectively. The microcirculation was studied using a Wild Photomacroscope for photography and a platinum multiwire electrode for measurements of local PO2 in the conscious animal. After 72 h of recovery from anesthesia and surgery, the experimental was started with the animal immobilized. The decrease of local s.c. temperature was achieved by perfusing a heat exchanger with distilled H2O and Isopropanol 70% (1:1) at a rate of 81/min with the heat exchanger located directly beneath the aluminium frame of the chamber. With this technique, a decrease in local tissue temperature from 28 degrees C to 15 degrees C could be obtained within 15 min and was kept constant for 60 min. After photography of the microcirculation and local PO2-measurements, the local temperature was further reduced to 5 degrees C with 15 min. Sixty minutes later, the area exposed was slowly rewarmed from a level of 5 degrees C within 30 min. This procedure was repeated in intervals of 24 h over a period of five days. During the course of the experiments, local PO2 values shifted toward hypoxic or even anoxic values. Intravital microscopic observation revealed aggregate formation, stasis and obstruction of capillary flow associated with pronounced tissue anoxia after five cold exposures. This event resulted inevitably in tissue necrosis and scar formation after seven consecutive exposures to cold. It is concluded that this model can be used to study the effects of local non freezing cold injury in a precisely reproducible manner.

A Novel Phenomenon Predicting the Entry into a State of Hibernation in Syrian Hamsters (Mesocricetus auratus)

“…Eventually, these results and further studies may provide more insight into the association between peripheral/core body temperatures and the induction of hibernation, with possible consequences for the understanding of injuries due to hypothermia [5], low temperature organ preservation techniques and induced or re-routed blood circulation [2,10]. a) Data are represented as the mean ± SD of body temperature for the period of days taken to reach the dropping point after logger implantation as shown in Table 2.…”

Cold nerve injury is enhanced by intermittent cooling

“…17 Studies measuring tissue oxygen tension in nonfreezing cold injury models have demonstrated hypoxia and local tissue anoxia, both subcutaneously and intramuscularly, during cooling. 7,23 Cold injury is also known to reduce blood flow, induce vasopressor changes, 8 increase the viscosity of the blood, 24 and cause platelet aggregation. 10,33 It has also been pointed out that, although hypothermia reduces the rate of cellular metabolism, the poor perfusion of capillaries results in insufficient oxygen being released to meet the needs of surrounding tissues.…”

Microvascular ultrastructure in non-freezing cold injuries

“…Pronounced inflammatory reactions after infliction of a non-freezing cold injury provoke transient or permanent tissue damage [12]. Such effects on tissue integrity are explained on the basis of rheological changes, which include variations of local hematocrit and a tendency of red blood cells to aggregate.…”

“…While the experimental evidence of a significant microhemodynamic impact seems poor at present for the first of these two factors, the enhanced capability of white blood cells and platelets to adhere to the vascular endothelium may lead to an elevation of local flow resistance and thereby enhance perfusion heterogeneity [15]. The latter phenomenon could be of particular significance during a chronic exposure to low temperatures, because the microvasculature would be plugged by blood cells, resulting in tissue hypoxia [12,23]. The mechanism of such microvascular occlusion, however, remains obscure, because an analysis of capillary ultrastructure during chronic, repeated cold exposure is not available.…”

“…It should be noted that the changes in flow observed in an earlier study [12] affected microvascular regions of approximately 300 • 200 ~tm, while well-perfused capillaries were frequently seen in the immediate neighborhood of ischemic regions. As a consequence, the simultaneous use of intravital and electron microscopy is essential for such studies in order to elucidate the pathomechanism of this injury.…”