Cause of death in tourniquet shock in rats

Meer, C. van der; Valkenburg, P.W.; Ariëns, A.Th.; Benthem, RM van

doi:10.1152/ajplegacy.1966.210.3.513

Cited by 26 publications

(3 citation statements)

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“…Thus, multiple studies of blood flow in advanced ischemia document that a close down of the microcirculation follows 6 h or more of complete ischemia [18,36]. This is past the point of muscle tolerance of ischemia, as noted previously [33].…”

Section: No Reflow Phenomenonmentioning

confidence: 74%

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The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review

Blaisdell

2002

Cardiovascular Surgery

132

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There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response, which follows reperfusion. consists of limb swelling with its potential for aggravating tissue injury and the systemic response, which results in multiple organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical studies show that irreversible muscle cell damage starts after 3 h of ischemia and is nearly complete at 6 h. These muscle changes are paralleled by progressive microvascular damage. Microvascular changes appear to follow rather than precede skeletal muscle damage as the tolerance of capillaries to ischemia vary with the tissue being reperfused. The more severe the cellular damage the greater the microvascular changes and with death of tissue microvascular flow ceases within a few hours—the no reflow phenomenon. At this point tissue swelling ceases. The inflammatory responses following reperfusion varies greatly. When muscle tissue death is uniform, as would follow tourniquet ischemia or limb replantation, little inflammatory response results. In most instances of reperfusion, which follows thrombotic or embolic occlusion, there will be a variable degree of ischemic damage in the zone where collateral blood flow is possible. The extent of this region will determine the magnitude of the inflammatory response, whether local or systemic. Only in this region will therapy be of any benefit, whether fasciotomy to prevent pressure occlusion of the microcirculation, or anticoagulation to prevent further microvascular thrombosis. Since many of the inflammatory mediators are generated by the act of clotting, anticoagulation will have additional benefit by decreasing the inflammatory response. In instances in which the process involves the bulk of the lower extremity, amputation rather than attempts at revascularization may be the most prudent course to prevent the toxic product in the ischemic limb from entering the systemic circulation.

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Section: No Reflow Phenomenonmentioning

confidence: 74%

“…It is here in the severely injured tissue that inflammatory mediators are most likely generated that can have a local or systemic effect. It is the amount of reperfused damaged or devitalized tissue that will determine morbidity [33,37].…”

Section: Local Inflammatory Responsementioning

confidence: 99%

The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review

Blaisdell

2002

Cardiovascular Surgery

132

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“…While we were completing our experiments, Van der Meer et al [26] published a paper in which they concluded that Ihe principal cause of death in tourniquet shock is K+ intoxication and that the fall in blood pressure is of secondary importance. Furthermore, they reported that Ihe EGG changes and heart arrhythmia closely resemble those found after K+ intoxication.…”

Section: Discussionmentioning

confidence: 97%

Effect of Adrenalectomy and Complete Blockade of Adrenergic Function on Mortality from Histamine, Endotoxin, Formalin and Tourniquet Stress in Rats

Krawczak¹,

Brodie²

1970

Pharmacology

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Lesions of the kidney in tourniquet shock: Ultrastructural study

1984

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Light microscope and ultrastructural changes in the rat kidney in tourniquet shock are described. The animals (24) were divided into two series; in the first one, the hind limb was kept at room temperature; in the second series, prerefrigeration was used. The effects of different ischemia were studied (2,4,8, and 12 hours for warm ischemia; 4,8,12, and 16 hours for cold ischemia). The animals were sacrificed at 3, 10, and 30 days. Pathological changes were evident, consisting in an increase of cytosomes in the proximal tubules and apical vacuolation in collecting ducts; numerous cytosomes including myelin-like structures were also seen. Large differences between warm and cold ischemia alterations were found. The changes in the tubules were clearly less important in cold ischemia. The authors conclude that there is a protective effect in regard to prevention of renal pathology affordable by prerefrigeration of a limb for reimplantation.

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Cause of death in tourniquet shock in rats

Cited by 26 publications

References 0 publications

The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review

The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review

Effect of Adrenalectomy and Complete Blockade of Adrenergic Function on Mortality from Histamine, Endotoxin, Formalin and Tourniquet Stress in Rats

Lesions of the kidney in tourniquet shock: Ultrastructural study

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