Irreversibility In Hemorrhagic Shock Research Articles

Determinants of the irreversibility of hemorrhagic shock: an exploratory simulation study

Determinants of the irreversibility of hemorrhagic shock: an exploratory simulation study

Transformation of neutrophils as indicator of irreversibility in hemorrhagic shock.

Recent evidence shows that the presence of circulating neutrophils (PMNs) influences the lethal course and extent of ischemic injury associated with hemorrhagic shock. The objective of this study was to use the Wiggers shock model to investigate the correlation between the appearance of activated circulating PMNs as measured by the spontaneous reduction of nitro blue tetrazolium [(NBT)-positive PMNs] and survival rate. Rats were maintained at 35-mmHg arterial pressure for 90 min and then observed over 24 h for survival. This protocol resulted in 50% mortality. In all animals in which levels of circulating NBT-positive PMNs before bleeding were greater than 225 cells/mm3, the experimental procedure was lethal. Animals that initially had low numbers of NBT-positive PMNs (to approximately 135 cells/mm3) and maintained low counts during the hypotensive period consistently survived. Animals, which before bleeding had low NBT-positive PMN counts but during the course of hypotension significantly elevated their circulating count, have low probability for survival. In those cases in which high NBT-positive PMN counts occurred only later in the course of the hypotensive period, the rats survived. These results suggest that the number of circulating NBT-positive PMNs is a singular index for the trend toward irreversibility in this shock model.

Effects of hemorrhagic shock on the microvasculature of skeletal muscle

The relationship between arteriolar and venular dimensions and the progressive failure of the homeostatic mechanisms leading to irreversibility in hemorrhagic shock was evaluated in mammalian skeletal muscle (rat cremaster). The small distribution arterioles (diameter = 17 μm) were observed to lose their tone and vasomotion at irreversibility although at 15 min after hemorrhage they exhibited enhanced vascular activity. Slowing of flow was seen to occur in the large venules (100 μm) and late in shock in smaller venules (25 μm). Venular dilatation was adjudged to be the vascular defect associated with the onset of irreversibility. Muscle surface pH and PO 2 followed a course similar to that seen in unanesthetized subjects. The red cell aggregation seen in the venules during the low flow state was generally reversed after reinfusion of the shed blood and restoration of arterial pressure.

Hemodialysis in the treatment of shock

It has been suggested repeatedly that toxins exist which account for irreversibility in hemorrhagic shock. 4'14 Recently, Schayer13 and llinshaw 7 have demonstrated a relationship between the production of histamine and the state of irreversibility in due to endotoxin. Catecholamines and other chemical mediators of small molecular weight have been s e r i o u s l y c o n s i d e r e d as the shock toxin. ~' I s , i s In the present investigation, hemodialysis was used in dogs subjected to produced by both hemorrhage and endotoxin in an attempt to test the shock toxin hypothesis. Furthermore, it was hoped that hemodialysis might prove to be a rational approach to therapy.

BIOCHEMICAL CHANGES DURING ACUTE PHYSIOLOGICAL FAILURE IN THE RAT: I. THE COENZYME A CONTENT OF THE COMPARTMENTS OF THE LIVER CELLS OF THE RAT DURING SHOCK

Shock was produced in the albino rat by means of a standardized method of blood removal. Coenzyme A (CoA) was extracted from the liver and estimated during the reversible and the irreversible phases of shock. The assay procedure was designed so that each animal served as its own "control".The CoA concentration in the liver fell rapidly during the first half hour of shock and thereafter at a progressively slower rate as the state of shock became more severe. Escape of the coenzyme from the mitochondria and the nucleus into the cytoplasm of the liver cells became evident during the reversible phase, and its breakdown in the cytoplasm began with the onset of the irreversible phase. Even at death, however, the CoA concentration of the liver was rarely lower than 35% of the original concentration. It is unlikely, therefore, that the decrease in the CoA content of the liver is a key factor in the initiation of the state of irreversibility in hemorrhagic shock.

実験的不可逆性出血ショック時における炭酸脱水酵素の変動

Irreversible shock was produced in dogs by massive bleeding from femoral artery into Lamson's bottle and maintaining mean arterial pressure at 50mmHg. Carbonic anhydrase activity of blood, liver and kidney tissues was measured by Warburg manometer during each of the three stadiums of hemorrhagic shock, namely that of the bleeding, equilibrium and back-flow stadium. Special attention was directed to the transition phase into irreversibility of shock. The effects of administration of Diamox and Chlorpromazine were compared. The results were summarized as follow.1) Carbonic anhydrase activity did not change appreciably in blood, liver or kidney tissues during the bleeding and equilibrium stadiums of hemorragic shock.2) During the back-flow stadium, carbonic anhydrase activity in arterial blood rose remarkably at the time of transition into irreversibility of hemorrhagic shock. The rise of the enzyme activity in venous blood preceded that in arterial blood. It also rose to a lesser degree in venous blood draining from the kidney and in the portal vein at transition into irreversibility of the shock, as well as in the liver and kidney tissues.3) The rise in carbonic anhydrase activity in arterial blood occurred simultaneously with a fall in arterial CO2 content and a fall in pH and these changes paralleled each other.4) The administration of Diamox did not prevent the transition into the irreversible phase of hemorrhagic shock but did inhibit carbonic anhhydrase activity. The enzyme activity rose slightly after the shock had progressed well into irreversibility but did not return to the previous level. It can be concluded from above that the rise in carbonic anhydrase activity is the result rather than the cause of the transition of the shock into irreversibility.5) In cases in which Chlorpromazine prevented full development of shock, the rise in carbonic anhydrase activity was absent.

Hemorrhagic shock of germfree rats

Germfree and ordinary laboratory rats of the same strain, half of each sort treated with oral aureomycin for 3 days prior to shock, were subjected to hemorrhagic shock. At the level and duration of hypotension selected, the procedure was highly lethal for all four groups. The single survivor was not a germfree rat. No evidence was found for protection against fatal outcome by either germfree status or treatment with aureomycin, and the gross pathological changes seen at autopsy following death from shock were essentially similar in all groups. The volumes of blood shed, the times spontaneous uptake of blood began, and the volumes of uptake did not differ significantly among the groups. It is concluded that bacteria and bacterial products are not essential for the development of irreversibility in hemorrhagic shock as customarily produced in rats.

The physiologic basis for vasopressor therapy during shock.

Excerpt INTRODUCTION The therapeutic usefulness of vasopressor agents, although employed many years for correction of various shock syndromes, remains highly controversial. Some investigators disap...

Traumatic shock. XXII. Irreversibility of hemorrhagic shock and VDM hypothesis; failure of ferritin to affect arterial pressure and survival period of hepatectomized-nephrectomized dogs.

ArticleTraumatic ShockXXII. Irreversibility of Hemorrhagic Shock and VDM Hypothesis. Failure of Ferritin to Affect Arterial Pressure and Survival Period of Hepatectomized-Nephrectomized DogsHoward A. Frank, Stanley Jacob, Edward W. Friedman, Alexander M. Rutenburg, Philip Glotzer, and Jacob FineHoward A. FrankFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts, Stanley JacobFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts, Edward W. FriedmanFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts, Alexander M. RutenburgFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts, Philip GlotzerFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts, and Jacob FineFrom the Surgical Research Department, Beth Israel Hospital, and the Department of Surgery, Harvard Medical School, Boston, MassachusettsPublished Online:31 Dec 1951https://doi.org/10.1152/ajplegacy.1951.168.1.150MoreSectionsPDF (751 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 168Issue 1December 1951Pages 150-155 Copyright & PermissionsCopyright © 1951 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1951.168.1.150History Received 13 August 1951 Published online 31 December 1951 Published in print 31 December 1951 Metrics

The question of traumatic heart disease.

Excerpt In a socially enlightened age of compensation and disability insurance, the relation of trauma to disease requires careful analysis. Only too often the prospect of reimbursement induces the...