Intrinsic Myocardial Function in Hemorrhagic Shock

McDonough, Kathleen H.; Giaimo, Mary E.; Quinn, Marie; Miller, Heather G.

doi:10.1097/00024382-199903000-00009

Cited by 28 publications

(18 citation statements)

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“…Although alcohol-induced diuresis (Taivainen et al, 1995) could result in a decreased effective blood volume and thus decreased basal hypotension, no change in hematocrit was detected in alcohol-treated animals before initiating the TÂHem protocol. The greater decline in blood pressure in response to a given blood loss could be the result of vasodilation , decreased cardiac output (Malt and Baue, 1971), impaired vasoreactivity (Edgarian and Altura, 1976), or depressed myocardial contractility (Horton, 1992;McDonough et al, 1999;Thomas et al, 1989), all of which have been demonstrated to contribute to alcohol-induced changes in hemodynamics. Alternatively, it is likely that the alcohol-induced blunting of sympathetic and sympathoadrenal responses to blood loss could have played a major role in the decreased tolerance to blood loss seen in the alcohol-treated animals.…”

Section: Discussionmentioning

confidence: 99%

Alcohol Intoxication Impact on Outcome from Traumatic Injury

Molina¹

2007

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ABSTRACT-The incidence of traumatic injury, frequently associated with hemorrhagic shock, is higher in the alcoholintoxicated individual. The outcome, as it pertains to both morbidity and mortality of this population, is partly dependent on duration of alcohol exposure and levels of blood alcohol at time of injury. In previous studies, we demonstrated that prolonged alcohol intoxication (15-h duration) produces marked hemodynamic instability and exacerbated early lung proinflammatory cytokine expression after hemorrhagic shock. The present study examines whether a shorter and more modest period of alcohol intoxication is sufficient to alter hemodynamic and proinflammatory responses to hemorrhagic shock. Chronically instrumented, conscious male Sprague-Dawley rats (250Y300 g) received a single intragastric bolus of alcohol (1.75 g/kg) 30 min before the administration of fixed-volume (50%) hemorrhagic shock, followed by fluid resuscitation with Ringer lactate. Time-matched controls were administered on isocaloric dextrose bolus (3 g/kg). Alcohol (blood alcohol concentration, 152 T 10 mg/dL) produced a 14% decrease in basal mean arterial blood pressure and a more profound hypotensive response to equal blood loss. The 2-fold rise in circulating norepinephrine levels was similar in alcohol-and dextrose-treated hemorrhaged animals despite greater hypotension in alcohol-treated animals. Significant upregulation in lung and spleen interleukin (IL) 1, IL-6, IL-10, and tumor necrosis factor ! expression was observed immediately after hemorrhage and fluid resuscitation, as previously reported. Only the hemorrhage-induced rise in lung IL-6 and tumor necrosis factor ! was prevented by alcohol administration. In contrast, spleen cytokine responses to hemorrhage were not altered by alcohol administration. These results indicate that moderate acute alcohol intoxication results in significant modulation of hemodynamic and neuroendocrine responses to hemorrhagic shock.

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Section: Discussionmentioning

confidence: 99%

Alcohol Intoxication Impact on Outcome from Traumatic Injury

Molina¹

2007

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“…On the other hand, a longer observation period may demonstrate typical progression to MOF, including renal failure (18). The elevated ALT and increased mortality when the ACS was introduced at 2 h postshock may have been due to the combined adverse effects of the ACS on residual hemorrhageinduced redistributive shock (19) and myocardial stunning (20), independent of PMN priming.…”

Section: Discussionmentioning

confidence: 99%

The Abdominal Compartment Syndrome as a Second Insult During Systemic Neutrophil Priming Provokes Multiple Organ Injury

Rezende-Neto¹,

Moore

Masuno

et al. 2003

Shock

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In our recent clinical study of damage control laparotomy, the abdominal compartment syndrome (ACS) emerged as an independent risk factor for postinjury multiple organ failure (MOF). We and others have shown previously that the ACS promotes the systemic production of proinflammatory cytokines. Our study objective was to develop a clinically relevant two-event animal model of postinjury MOF using the ACS as a second insult during systemic neutrophil priming to provoke organ dysfunction. Male adult rats underwent hemorrhagic shock (30 mmHg x 45 min) and were resuscitated with crystalloids and shed blood. The timing of postshock systemic neutrophil (PMN) priming was determined by the surface expression of CD11b via flow cytometry. Finding maximal PMN priming at 8 h, but no priming at 2 h (early) and 18 h (late), the ACS (25 mmHg x 60 min) was introduced at these time points. At 24 h postshock, lung injury was assessed by lung elastase concentration and Evans blue dye extravasation in bronchoalveolar lavage. Liver and renal injuries were determined by serum alanine aminotransferase, serum creatinine, and blood urea nitrogen. The ACS during the time of maximal systemic PMN priming (8 h) provoked lung and liver injury, but did not if introduced at 2 or 18 h postshock when there was no evidence of systemic PMN priming. The 24-h mortality of this two-event model was 33%. These findings corroborate the potential for the ACS to promote multiple organ injury when occurring at the time of systemic PMN priming. This clinically relevant two-event animal model of PMN organ injury may be useful in elucidating therapy strategies to prevent postinjury MOF.

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“…Hypovolemia can lead to severe impairment in liver, kidney and lung function [28][29][30][31][32][33][34]. Li et al observed that haemorrhagic shock releases mediators resulting in lung inflammation [28].…”

Section: Impact Of Hypovolemia On the Liver Kidneys And Lungsmentioning

confidence: 99%

“…Li et al observed that haemorrhagic shock releases mediators resulting in lung inflammation [28]. Experimental models have also demonstrated that haemorrhage impairs endothelial cell function [29] and depresses intrinsic myocardial contractility [30], suggesting reduced perfusion. Histological alterations in the liver after autologous whole blood transfusion were attributed to hypoxic hepatocellular damage associated with the severity of the shock model rather than to the administration of fluid itself [31,32].…”

Section: Impact Of Hypovolemia On the Liver Kidneys And Lungsmentioning

confidence: 99%

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

Lima¹,

Silva²,

Capelozzi³

et al. 2017

Anaesthesiol Intensive Ther

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Background: Abdominal compartment syndrome (ACS) sometimes occurs in critically ill patients following damage control surgery. The purpose of the present study was to develop a model of ACS and to evaluate its pathologic impact on liver, kidney, and lung morphology. Methods: Twenty Wistar rats (mass 300-350 g) were randomly divided into four groups: 1) intra-abdominal hypertension (IAH): a laparotomy was performed and the abdomen packed with cotton until an intra-abdominal pressure (IAP) of 15 mm Hg was reached; 2) hypovolemia (HYPO): blood was withdrawn until a mean arterial pressure ~60 mm Hg was reached; 3) IAH + HYPO (to resemble clinical ACS); and 4) sham surgery. After 3 hours of protective mechanical ventilation, the animals were euthanized and the liver, kidney and lungs removed to examine the degree of tissue damage. Results: IAH resulted in the following: oedema and neutrophil infiltration in the kidney; necrosis, congestion, and microsteatosis in the liver; and alveolar collapse, haemorrhage, interstitial oedema, and neutrophil infiltration in the lungs. Furthermore, IAH was associated with greater cell apoptosis in the kidney, liver and lungs compared to sham surgery. HYPO led to oedema and neutrophil infiltration in the kidney. The combination of IAH and HYPO resulted in all the aforementioned changes in lung, kidney and liver tissue, as well as exacerbation of the inflammatory process in the kidney and liver and kidney cell necrosis and apoptosis. Conclusions: Intra-abdominal hypertension by itself is associated with kidney, liver and lung damage; when combined with hypovolemia, it leads to further impairment and organ damage.

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Intrinsic Myocardial Function in Hemorrhagic Shock

Cited by 28 publications

References 0 publications

Alcohol Intoxication Impact on Outcome from Traumatic Injury

Alcohol Intoxication Impact on Outcome from Traumatic Injury

The Abdominal Compartment Syndrome as a Second Insult During Systemic Neutrophil Priming Provokes Multiple Organ Injury

Early impact of abdominal compartment syndrome on liver, kidney and lung damage in a rodent model

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