The interplay of central and peripheral factors in irreversible hemorrhagic shock

Zweifach, Benjamin W.; Froněk, Arnošt

doi:10.1016/0033-0620(75)90003-1

Cited by 56 publications

(9 citation statements)

References 175 publications

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“…Similar phenomena can occur in other forms of shock. In animal models of hemorrhagic shock, for example, shock and organ dysfunction persist after return of shed blood, again implicating secondary mechanisms (6). Evidence is accumulating that inflammatory cascades play a role in the pathophysiology of decompensation of hemorrhagic shock as well (7).…”

Section: Introductionmentioning

confidence: 99%

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Mouse Models of Resuscitated Shock

Hollenberg

2005

Shock

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Studies of sepsis in humans are difficult because the seriousness of the disease mandates immediate intervention and because the heterogeneity of patient presentations imposes substantial limitations on clinical trials. Thus, animal models have been used extensively to explore the pathogenesis of sepsis and to generate preclinical data for therapeutic interventions. Translation of findings in these models into therapeutic strategies has been difficult, in part because of limitations in preclinical models and in part to imperfect understanding of the pathophysiology of sepsis. It is important to use an animal model that reproduces the relevant physiologic parameters present in patients with septic shock. Mouse models are particularly useful for the dissection of molecular mechanisms of disease because of the proliferation of transgenic strains. We have developed a murine model of sepsis with fluid resuscitation and antibiotic treatment that reproduces the timing and degree of mortality seen in patients with septic shock. Using continuous micromanometric pressure monitoring and assessment of hemodynamics by echocardiography, we have shown that this model reproduces the hyperdynamic state with hypotension seen in clinical sepsis. The use of transgenic technology in appropriate murine models is exciting because of its potential to permit significant strides in our understanding of the molecular mechanisms of sepsis, multiple organ system failure, and other diseases. The use of reproducible and clinically relevant mouse models of shock is essential for delineation of pathogenetic mechanisms and for initial testing of potential therapeutic strategies.

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Section: Introductionmentioning

confidence: 99%

“…Circulating catecholamines and the sympathetic and parasympathetic nervous systems are known to play crucial roles in modulating the compensatory responses to shock (6,9), and dysregulation of these compensatory responses is likely to be important in the transition to irreversibility.…”

Section: Introductionmentioning

confidence: 99%

Mouse Models of Resuscitated Shock

Hollenberg

2005

Shock

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“…The blood flow reduction in peripheral tissues following a large, acute hemorrhage, produces local disturbances in tissue metabolism and function, if the transport of oxygen and nutrients becomes insufficient to meet the tissue demands. These cellular changes, rather than hemodynamic events, will constitute the pivotal factors in an ensuing circulatory shock condition (Zweifach & Fronek 1975, Messmer & Sunder-Plassman 1975. To gain further understanding of the pathophysiology of shock at the cell level in peripheral tissues, it thus seems pertinent to establish the precise characteristics of nutritive flow deficiencies and how fast and to what extent these affect tissue metabolism and function.…”

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confidence: 99%

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Amundson¹,

Jennische²,

Haljamäe

1980

Acta Physiologica Scandinavica

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Skeletal muscle reactions to hemorrhagic shock were investigated in anesthetized cats (n = 23). The tenuissimus muscle was exposed for vital microscopy and shock was induced by single-withdrawal of 45% of the blood volume. Muscle microcirculation, energy metabolism and cell membrane potentials were followed over a 2 h period along with blood pressure, hematocrit and blood leukocyte, platelet, glucose, pyruvate and lactate contents. Bleeding usually caused complete cessation of muscle blood flow for 5--20 min, while the animal compensated the blood pressure. Reflex constriction occurred in medium-sized but not in terminal arterioles. When flow reappeared a marked maldistribution was evident in the capillary bed. Flow remained in 30--50% of the capillaries, permanently or intermittedly. Leukocytes could be found lodged in many arrested capillaries and also adhering to venules in large numbers. Erythrocyte or platelet plugs were not seen in the muscle microvasculature. Glucose and G6-P contents doubled and lactate increased 5-fold in muscle tissue during shock. CP was reduced by about 25% while the ATP-level remained unchanged. Membrane potentials declined 12% in shock and the spread in potentials from adjacent fibers increased.

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“…As reviewed recently by Zweifach and Fronek [3], two main experimental procedures have been used to induce shock, these are: [4][5][6][7][8] The following three variables can be studied with this procedure: (a) the amount of blood withdrawn in one or several steps, (b) the effect of the duration of the hypotensive period on mortality, and (c) the effects of retransfusion of the blood shed from the reservoir at the end of the experimental period or the influence of blood volume restitution by means of electrolyte solutions, plasma expanders, or blood substitutes.…”

Section: Introductionmentioning

confidence: 96%

Experimental hemorrhagic shock in dogs: Standardization

1983

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The purpose of the present study was to design a standardized model of hemorrhagic shock in dogs as a prerequisite for future studies on the pathogenesis of this syndrome. Hemorrhagic shock was induced in 86 mongrel dogs submitted to a systemic hypotension of 45 mm Hg by means of a constant pressure reservoir procedure. The following blood volumes (ml/kg) were measured during the evolution of shock: (1) initial bleeding volume, (2) secondary bleeding volume, (3) maximum bleeding volume, (4) automatic reinfusion volume, and (5) duration of the hypotensive period (min). The corresponding mortalities were submitted to a statistical analysis which yielded the following conclusions: (a) the initial, secondary, and maximum bleeding volumes do not correlate with mortality, (b) the duration of the hypotensive period is of only relative importance, and (c) the automatic reinfusion volumes shows a high degree correlation with the fatal outcome.

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The interplay of central and peripheral factors in irreversible hemorrhagic shock

Cited by 56 publications

References 175 publications

Mouse Models of Resuscitated Shock

Mouse Models of Resuscitated Shock

Correlative analysis of microcirculatory and cellular metabolic events in skeletal muscle during hemorrhagic shock

Experimental hemorrhagic shock in dogs: Standardization

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