Colloid-induced changes in bleeding following liver resection in the rat

Zoucas, Evita; Göransson, Göran; Bengmark, S

doi:10.1007/bf01852384

Cited by 6 publications

(6 citation statements)

References 28 publications

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“…Blood loss in the liver injury model with no treatment was 357.57 ± 267.31 µL and lasted the entire experimental period. These findings are similar to those in the literature when 2.5% to 4% of the liver was resected and bleeding lasted between 5–9 minutes with 1.0 to 3.4 mL of blood lost (Alwmark et al, 1986; Bengmark et al, 1980; Bengmark et al, 1981; Holcomb et al, 2000; Kullendorff et al, 1984; Lindfeldt et al, 1987; Tanaka et al, 1985; Zoucas et al, 1982; Zoucas et al, 1984a; Zoucas et al, 1984b;). Additionally, Holcomb et al (2000) demonstrated a reduction in blood loss by 52% using fibrin glue in a model of median hepatic lobe injury in rats.…”

Section: Discussionsupporting

confidence: 89%

“…When the concentration of Q8009 was increased to 250 µg/mL, the overall blood loss was reduced by 75% (Spleen 56%, Liver 90% and Kidney 77%) from internal organ wounds. Zoucas et al (1984a) demonstrated in a rat liver injury model, a reduced blood loss of between 50%–75% with the application of gelatin foam, oxidized cellulose, collagen fleece or microcrystalline collagen. At a concentration of Q8009 at 1,000 µg/mL plus collagen matrix the overall blood loss was reduced by 65% (Spleen 42%, Liver 85% and Kidney 68%) from wounds on internal organs.…”

Section: Discussionmentioning

confidence: 99%

“…Evaluations of existing techniques for determining blood loss were imprecise and highly variable. Historically, blood loss determinations in models of liver, spleen or kidney wound were performed using a preweighed aluminum cup (Bengmark et al, 1980; Kullendorff et al, 1984; Kullendorff and Zoucas, 1985; Lindblom et al, 1990; Lindfeldt et al, 1987; Vagianos et al, 1987; Zoucas et al, 1984a; Zoucas et al, 1984b;) or a stack of gauze pads (Holcomb et al, 2000; Tuthill et al, 2001) and determining final blood loss by weight. A more extensive search of the literature provided a protocol for hematin determination (Masci et al, 1988) and coupled with the use of Whatman filter paper “chads” this provided the desired accuracy.…”

Section: Discussionmentioning

confidence: 99%

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Hemostatic properties of a venomic protein in rat organ trauma

Warner¹,

McClintock²,

Barron³

et al. 2009

Experimental and Molecular Pathology

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Previous in vitro work characterized the protease Q8009 isolated from the venom of the Australian brown snake Pseudonaja textilis textilis with Factor Xa-like activity and hemostatic properties. The purpose of the work described here characterizes the in vivo hemostatic properties in a rat model of parenchymatous organ injury. The key parameters of activity included reduction in time-tohemostasis and total volume of blood loss in spleen, liver and kidney wound models in rats. The surgical protocols involved exposure of the organs via a midline abdominal laparotomy. Using a clean metal template with 6, 6.5 9 mm holes for spleen, liver and kidney, respectively, a predetermined volume of the organ was gently extruded through the template hole and excised with a razor blade. About 50 to 75 µL of collagen matrix with the different test solutions was applied to the wounds. Blood was collected and at the end of the procedure animals were humanely sacrificed with an anesthetic overdose. Determination of blood was performed using the hematin assay using a standard curve. Blood loss per minute and total blood loss were calculated. Results from the studies demonstrated that the application of Q8009 and collagen matrix to surgical wounds significantly reduced the total amount of blood loss and the time-to-hemostasis. In the spleen wound model, Q8009 at 100, 250 and 1000 µg/ml) significantly reduced (p<0.001) the total volume of blood lost relative to thrombin and reduced the time-to-hemostasis by 25-50%, as compared to 7% by thrombin. In the liver wound model, Q8009 at 250 and 1000 µg/ml significantly reduced (p<0.001) the total volume of blood lost relative to thrombin and reduced the time-to-hemostasis from 10.5 minutes by thrombin to 5.6 minutes with Q8009. In the kidney wound model, Q8009 at 250 µg/ml significantly reduced (p<0.05) the total volume of blood lost and reduced the time-to-hemostasis by 25% when compared to thrombin. The hemostasis levels were consistent with previous findings in skin wound rat models where Q8009 consistently reduced the total volume of blood lost and shortened time-to-hemostasis. Application of Q8009 plus collagen matrix significantly reduced the volume of total blood loss and time-to-hemostasis in rat surgical organ wound models induced bleeding, as compared to a commercially available hemostat device. The protein Q8009 has greater capacity to reduce blood

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hemostatic properties of a venomic protein in rat organ trauma

Warner¹,

McClintock²,

Barron³

et al. 2009

Experimental and Molecular Pathology

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“…In a previous study it was noticed that Haemaccel infusion to traumatized patients was associated with an increased bleeding time and pronounced blood loss. 3 An increased bleeding time in animals receiving Haemaccel has been documented, 4 and this was associated with significantly reduced adenosine-diphosphate-induced platelet aggregation in platelet-rich plasma derived from these animals. Haemaccel infusion to trauma patients can lead to hypercalcaemia, because of its high Ca 2; content.…”

mentioning

confidence: 99%

Effects of gelatin-based resuscitation fluids on platelet aggregation

Evans¹,

Glenn²,

Heptinstall³

et al. 1998

British Journal of Anaesthesia

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Fluid resuscitation aims to maintain intravenous volume without significant effects on haemostasis. Several different types of i.v. fluid are available for use in a patient who has suffered trauma, but there is evidence that some resuscitation fluids may affect primary haemostasis. We have compared the effects of two resuscitation fluids, Haemaccel and Gelofusin, on platelet aggregation in vitro. These resuscitation fluids are both based on gelatin but Haemaccel contains a high concentration of Ca2+ whereas Gelofusin does not. Their effects on platelet aggregation in whole blood, induced by a range of different agents, were determined using a platelet-counting technique. Both Haemaccel and Gelofusin prevented platelet aggregation induced by ristocetin (P < 0.05, Mann-Whitney). In addition, Haemaccel proved to be a potent inhibitor of the platelet aggregation that occurred in response to all of the other agonists investigated: adenosine diphosphate, platelet-activating factor, collagen, a thromboxane A2 mimetic (U46619) and epinephrine. The additional inhibitory effects of Haemaccel were largely, but not completely, attributable to its high Ca2+ content. Inhibition of platelet aggregation by ristocetin may indicate a mechanism by which Haemaccel or Gelofusin may contribute to impaired haemostasis. The presence in Haemaccel of high concentrations of Ca2+, which is largely responsible for inhibition of the aggregation induced by other agents, may provide an additional means by which haemostasis could be impaired.

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“…Our subsequent studies demonstrated that dextrans, degraded gelatin and hydroxyethyl starch all increased APT time, impaired ADP- and collagen-induced aggregation, and induced a significantly increased bleeding time and blood loss after experimental liver resection [40]. Another study of ours at that time demonstrated that dextrans significantly increased mortality in experimental pneumococcal infections (59%) and numbers of abscesses compared to animals treated with only saline (23%) ( p < 0.05) [41].…”

Section: Colloid-associated Morbidity Often Neglectedmentioning

confidence: 99%

Nutrition of the Critically Ill — A 21st-Century Perspective

Bengmark

2013

Nutrients

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Health care-induced diseases constitute a fast-increasing problem. Just one type of these health care-associated infections (HCAI) constitutes the fourth leading cause of death in Western countries. About 25 million individuals worldwide are estimated each year to undergo major surgery, of which approximately 3 million will never return home from the hospital. Furthermore, the quality of life is reported to be significantly impaired for the rest of the lives of those who, during their hospital stay, suffered life-threatening infections/sepsis. Severe infections are strongly associated with a high degree of systemic inflammation in the body, and intimately associated with significantly reduced and malfunctioning GI microbiota, a condition called dysbiosis. Deranged composition and function of the gastrointestinal microbiota, occurring from the mouth to the anus, has been found to cause impaired ability to maintain intact mucosal membrane functions and prevent leakage of toxins—bacterial endotoxins, as well as whole bacteria or debris of bacteria, the DNA of which are commonly found in most cells of the body, often in adipocytes of obese individuals or in arteriosclerotic plaques. Foods rich in proteotoxins such as gluten, casein and zein, and proteins, have been observed to have endotoxin-like effects that can contribute to dysbiosis. About 75% of the food in the Western diet is of limited or no benefit to the microbiota in the lower gut. Most of it, comprised specifically of refined carbohydrates, is already absorbed in the upper part of the GI tract, and what eventually reaches the large intestine is of limited value, as it contains only small amounts of the minerals, vitamins and other nutrients necessary for maintenance of the microbiota. The consequence is that the microbiota of modern humans is greatly reduced, both in terms of numbers and diversity when compared to the diets of our paleolithic forebears and the individuals living a rural lifestyle today. It is the artificial treatment provided in modern medical care—unfortunately often the only alternative provided—which constitute the main contributors to a poor outcome. These treatments include artificial ventilation, artificial nutrition, hygienic measures, use of skin-penetrating devices, tubes and catheters, frequent use of pharmaceuticals; they are all known to severely impair the microbiomes in various locations of the body, which, to a large extent, are ultimately responsible for a poor outcome. Attempts to reconstitute a normal microbiome by supply of probiotics have often failed as they are almost always undertaken as a complement to—and not as an alternative to—existing treatment schemes, especially those based on antibiotics, but also other pharmaceuticals.

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Colloid-induced changes in bleeding following liver resection in the rat

Cited by 6 publications

References 28 publications

Hemostatic properties of a venomic protein in rat organ trauma

Hemostatic properties of a venomic protein in rat organ trauma

Effects of gelatin-based resuscitation fluids on platelet aggregation

Nutrition of the Critically Ill — A 21st-Century Perspective

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