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PubMed1985

Dextran as a modulator of immune and coagulation activities in trauma patients.

Low Mr dextran has been utilized as a prophylactic therapy in treatment of coagulopathy. There is evidence that monocyte dysfunctions are important contributors to hypercoagulability episodes, as well as to immunoincompetence post-trauma. Dextran is a known monocyte modulator. Consequently, we evaluated the efficacy of dextran infusion in moderating immune dysfunction, monocyte aberrations, and hypercoagulability episodes. Twenty-eight trauma patients were randomly divided into two groups. One group of 15 received dextran at 1 g/kg wt/24 hr for 5 days in addition to standard resuscitation and treatment. The control or nontreated patient group received only standard treatment. Trauma patients in the two groups were retrospectively matched by injury severity score (ISS) to ensure comparability. Blood samples were collected daily for some studies and at 3-day intervals for other assays. In vivo coagulation status was evaluated by assessing the changes in intravascular fibrinopeptide A (FPA). Immune reactivity to the mitogen phytohemagglutinin (PHA) was also evaluated. Both monocyte production of plasminogen activator (PA) and monocyte production of procoagulant activity (PCA) have been shown to correspond to and be augmented by monocyte-T lymphocyte interactions. Consequently, monocyte production of plasminogen activator and procoagulant activity were assessed as measures of monocyte immune activity as well as indicators of monocyte function in controlling the balance between fibrinolysis and coagulation. Only patients with ISS of greater than 25 experienced significant immune, coagulation, or monocyte aberrations. Of those having an injury severity score (ISS) score of 25-35, all of the control and two of the dextran patients had significant perturbations in their immune and monocyte functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation↗

PubMed1975

Effect of intravascular cellular aggregate dissolution in postoperative patients.

It was the purpose of this study to confirm whether the increase in packed cell (PC) viscosity that occurs in humans after elective surgery is accompanied by a decrease in total body O2 consumption as previously noted in animals, and further to define the effect of resolution of intravascular cellular aggregates (ICA) on these parameters. Thirty nine patients were studied. Total body O2 consumption was 76% of normal 6 hours postop, 81% of normal 24 hours postop and 87% of normal 48 hours postop. Twenty four hours after operation PC viscosity and increased markedly. Saline infusion had no significant effect on total body O2 consumption or PC viscosity, either pre- or postop, but WB viscosity decreased linearly in proportion in the drop in hematocrit. Resolution of ICA by dextran-40 infusion was associated with return of total body O2 consumption and PC viscosity to normal; a decrease in WB viscosity was disproportionately greater than would have been seen had the decrease been due solely to the drop in hematocrit. It is concluded that in humans surgical trauma causes an increase in PC viscosity and microcirculatory impairment as evidenced by a decrease in total body O2 consumption. Resolution of ICA by dextran-40 infusion reverses that detrimental changes.

Animals↗

PubMed1988

Fahraeus-effect-reversal (FER) in compaction stasis (CS): microrheological and haemodynamic consequences of intravascular sedimentation of red cell aggregates.

Red cell aggregate sedimentation under gravitation produces pronounced and rapid "phase separation effects" culminating in "compaction stasis" (CS), i.e. almost complete stuffing of microvessels by RBC. This can be readily observed and monitored in microvessels of vertically placed mesentery preparations by a horizontally aimed intravital microscope as shown by (GOBEL et al. VIRCHOW's Arch., 1988,). "Layered flow", floatational plasma skimming and progressive increase in local tube hematocrit (HT) up to 100% ("compaction stasis") occurs during induced low flow states in vivo (here preferentially in postcapillary venules), as well as in vitro (non-permeable artificial micro tube networks). Quantitative densitometry and velocimetry in vertically placed microvessels demonstrates that the process of RCA sedimentation results in progressive vertical skewing of the velocity profile, culminating in standstill of the RBC-sediment in the dependent vessel half, with superfluent plasma and small aggregates in the upper vessel half. The theory of compaction stasis is developed: in striking contrast to the situation under high shear conditions, red cells travel on slower trajectories than plasma: due to "red cell undervelocity" the average residence times of RBC in a venule is much higher than that of plasma. Consequently, CS can be explained as the result of a FAHRAEUS effect reversal since the principle of mass conservation requires that HT much greater than HD. Network aspects and hemodynamic consequences are also incorporated into the theory.

Animals↗

PubMed2004

Effects of aggregation of red cells and linear velocity gradients on the correlation-based method for quantitative IVUS blood flow at 20 MHz.

Recent computer simulations suggest that the presence of aggregates of red blood cells (RBCs), at random angles and lengths, does not affect the measurements of blood flow transverse to the ultrasound (US) beam direction using a correlation-based method and an intravascular (IV) US array catheter. However, in case of aggregates of RBCs aligned with the flow, measurements of simulated blood velocity are affected. Blood velocity gradients were also shown not to influence the correlation-based method for blood velocity estimation. The objective of this study was to quantify the influence of aggregates of RBCs and blood velocity gradients on the correlation-based method during in vitro experiments. For this purpose, measurements were performed on washed RBCs (no aggregation), normal human blood, and two types of diseased blood in which a lower or a higher level of aggregation was present. The decorrelation pattern of a circular US transducer as a function of transverse blood flow was studied using a Couette system. Changing the shear rate of the Couette system modified the aggregation level of RBCs and the velocity gradient. With the exception of the results at low shear rates and abnormally high aggregation levels, agreements were found between the autoconvolution of the acoustical beam (reference curve) and the radiofrequency (RF) decorrelation patterns. For the high shear rate present in coronary arteries, the correlation-based method for blood flow estimation should not be influenced by these phenomena.

Adult↗

PubMed1994

Comparison of the effects of aprotinin and tranexamic acid on blood loss and related variables after cardiopulmonary bypass.

Aprotinin reduces blood loss after cardiopulmonary bypass, but may sensitize recipients and is expensive. Tranexamic acid, a synthetic antifibrinolytic, has less disadvantages, but opinions differ regarding its efficacy. We studied three groups of patients undergoing cardiopulmonary bypass for coronary disease: recipients of aprotinin (total dose 4.2 x 10(6) kallikrein inhibiting units, n = 14), recipients of tranexamic acid (total dose 20 mg/kg body weight, n = 15), and nonmedicated controls (n = 14) during 24 hours after cardiopulmonary bypass. Compared with controls, aprotinin reduced blood loss, the number of patients requiring transfusions, and the mean number of transfused red cell units (all with p < 0.05), whereas the recipients of tranexamic acid did not differ either from aprotinin recipients or from controls. Aprotinin and tranexamic acid both mitigated the early postoperative reduction of adenosine diphosphate-induced platelet aggregation seen in the controls (p < 0.05). Postoperative increases of plasma concentrations of the prothrombin activation fragment F1 + 2 and the thrombin-antithrombin III complex showed an activation of intravascular coagulation, without any intergroup differences. The balance between concentrations of tissue plasminogen activator and the type 1 plasminogen activator inhibitor disclosed an activation of fibrinolysis, without differences between the groups. The concentrations of D-dimer, a breakdown product of cross-linked fibrin, remained at baseline in the recipients of aprotinin and tranexamic acid but tripled in the controls (p < 0.05). By contrast, the plasma antiplasmin activity was equally depressed in the tranexamic acid and the control groups but decreased less in the recipients of aprotinin (p < 0.05). This discrepancy may reflect the different modes of action of the two agents, which may make aprotinin more efficacious than tranexamic acid in the "nonfibrinolytic" act of protecting platelet function against attack by plasmin during cardiopulmonary bypass.

Aged↗

PubMed1993

Effect of intensified red blood cell aggregability on arterial pressure and mesenteric microcirculation.

Intensified aggregability of red blood cells (RBC) was produced in adult white rats by the step-by-step intravascular administration of a high-molecular-weight dextran, with a molecular weight approximating that of blood fibrinogen. As a result, the systemic arterial pressure was elevated by more than one-third of the initial level, whereas the diameter of arterioles in the intestinal mesentery remained practically unchanged. This provided sufficient grounds for the conclusion that the increase in the total peripheral resistance was due to disturbances in blood rheological properties. Despite the elevated arterial pressure, the blood flow velocity in mesenteric arterioles displayed a clear-cut tendency to slow down. Simultaneously, a large number of RBC aggregates appeared in the mesenteric microvessels. In patients with a stable form of arterial hypertension the RBC aggregability index was found to be significantly increased as compared with that of the healthy control group. Following treatment with Ca(2+)- and beta-adrenergic blockers the index decreased significantly in parallel with the lowering of arterial pressure. The obtained results suggest that the intensified RBC aggregation in microvessels causing a disturbance of normal blood flow structure, and hence of blood rheological properties, might be an important factor responsible for the elevation of systemic arterial pressure in humans with arterial hypertension.

Animals↗

PubMed1975

[Activation of the blood coagulation system during gram-negative infections and endotoxemias].

Blood coagulation may be activated by the extrinsic or intrinsic pathways. The extrinsic clotting system is put into action by tissue thromboplastin, originating from injured tissue cells, but also from damaged leukocytes and erythrocytes. Tissue thromboplastin is a phospholipoprotein with an enzymatic component, capable of converting the clotting factor VII to its activated form, factor VIIa, which in turn activates factor X. The factor Xa-complex (containing also factor Va, phospholipid, and calcium) is the prothrombinconverting principle. The intrinsic clotting system is based on factors which are contained in the circulating blood. Its activation requires the availability of phospholipid and of activated factor XII (factor XIIa), or factor XIa. Factor XII is activated by collagen, i.e., whenever the vascular endothelium is injured, and to a lesser extent also by "activated" blood platelets. Platelets in turn are activated primarily by thrombin, collagen, and, in a self-perpetuating process, since all these materials are released from activated platelets, also by adenosine-5-diphosphate, adrenaline, and serotonin. The activation of platelets leads to a variety of morphological and biochemical alterations, culminating in their aggregation and in the selective release from storage organelles of different substances, among them those mentioned above. Of particular importance is the fact that in the course of platelet alterations, procoagulant phospholipid also becomes available on the platelet surface. The significance of the activation of the intrinsic system is seen in the possibility of the initiation of a self-sustained process which, after a primary event, e.g. vascular or cellular injury, will continue to convert prothrombin into thrombin. The effects of endotoxin on the blood clotting system show striking species differences. In the rabbit, endotoxin, with the involvement of factors of the complement system, will directly act upon blood platelets and thus initiate intravascular, intrinsic coagulation. In man, endotoxin remains without a direct effect on platelets and alternative possibilities of initiating thrombin formation must be considered. One possibility is extrinsic activation via tissue thromboplastin from injured leukocytes. Another pathway, which is supported by several experimental findings, starts out with endotoxin-mediated endothelial damage. Endothelial cells are in fact severely affected by endotoxin and may even be removed from the vascular wall, thus making accessible the subendothelial activator of factor XII. Thrombin in turn affects the vascular endothelium: therefore, one initiated, the process of intravascular activation of coagulation will perpetuate, this the more as platelets in turn will be stimulated into activity. The possible intervention of other vasoactive factors must also be considered...

Animals↗

PubMed2003

2-Butoxyethanol enhances the adherence of red blood cells.

We recently presented a unique, chemically-induced rat model of hemolytic anemia and disseminated thrombosis. In this 2-butoxyethanol (BE)-induced model the organs developing infarction are comparable to those seen in human diseases, characterized by hemolysis and thrombosis (e.g., thalassemia, sickle-cell disease, paroxysmal nocturnal hemoglobinuria, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome). Red blood cells (RBCs) have special flow properties, namely, self-aggregability, deformability, and potential adherence to endothelial cells (ECs) of the blood vessel wall, which are essential for adequate blood flow and tissue perfusion; their alteration facilitates circulatory disorders. To examine the possible contribution of alterations in RBC flow properties to the observed thrombosis in the present investigation we determined the BE-induced changes in adherence, aggregability, and deformability of RBCs from male and female Fischer F344 rats exposed to two, three, or four daily doses of BE at 250 mg BE/kg body weight. Control animals were treated with the vehicle alone. Blood was taken on days 2, 3, 4, and 29. The administration of BE did not affect the RBCs aggregability but markedly enhanced their adherence to extracellular matrix; such enhancement was correlated with adherence to cultured ECs. RBC/EC interaction has been shown to be a potent catalyst of vascular occlusion in hemolytic hemoglobinopathies; thus the enhanced RBC adherence to EC is a likely mechanism by which thrombosis and organ infarct are induced in BE-treated rats.

Administration, Oral↗

PubMed2001

Decorrelation characteristics of transverse blood flow along an intravascular array catheter: effects of aggregation of red blood cells.

A method to measure transverse blood flow, based on the correlation between consecutive radiofrequency (RF) signals, has been introduced. This method was validated for an intravascular (IVUS) rotating single element catheter. Currently, we are implementing the method for an IVUS array transducer catheter. The decorrelation characteristics during transverse blood flow using the IVUS array catheter were investigated using computer modeling. Before this, blood was simulated as a collection of randomly located point scatterers and, by moving this scattering medium transversely across the acoustical beam, blood flow was simulated. This paper presents a more realistic scattering media by simulating aggregates of red blood cells (RBCs) as strings of point scatterers. Three configurations of aggregates of RBCs were simulated. First, aggregates of RBCs were strings with different lengths and parallel to the catheter axis. Second, the strings were with a fixed length and angles of plus or minus 45 degrees with respect to the catheter axis. Third, the strings were with different lengths and random angles ranging from -45 degrees to + 45 degrees. The decorrelation characteristics for these configurations of aggregates of RBCs were investigated and compared with point scatterers. For the aggregates of RBCs parallel to the catheter axis, the decorrelation rate became slower when the aggregate length was increased. RBC aggregations with fixed and random lengths and angles resulted in a decorrelation rate that approaches the decorrelation pattern from point scatterers. Results suggests that the presence of aggregates of RBCs will probably not affect the measurements of transverse blood flow using a decorrelation-based method and an IVUS array catheter.

Blood Flow Velocity↗

PubMedDate not supplied

The significance of red cell surface area to the permeability of fibrin network.

Thrombus formed under low shear conditions in the intravascular compartment consists of red cells enmeshed within a fibrin network framework. The permeability of the network determines the rate of molecular transport by convection. The effect of red cells on the permeability of the fibrin network was examined in networks developed from red cell suspensions in platelet-rich (PRP) and platelet-poor plasma (PPP). Red cell-rich networks developed in PRP were significantly more permeable than those developed in PPP. Network permeability decreased linearly with increase in hematocrit due to volume exclusion and cell surface hydraulic drag. The hydraulic resistance of the red cells was similar in order of magnitude to that of the fibrin fibers. The hydraulic resistance was calculated to be dependent on the surface area of the red cells, as well as on red cell concentration. Calculation of red cell surface area from permeability (45-90 microns2) was found to be lower than the known surface area (145 microns2). From these studies, it is suggested that red cells entrapped within the network are aggregated. Aggregation is promoted by low shear plasma conditions during fibrin polymerization and by fibrin polymerization intermediaries. The degree of red cell aggregation regulates the hydraulic resistivity of the red cells, and the fibrin fiber structure regulates the hydraulic resistivity of the fibrin network. Both are significant determinants of the network permeability and, therefore, of molecular transport in thrombi.

Blood Platelets↗

PubMed1987

Renal capillary permeability and intravascular red cell aggregation after ischaemia. I. Effects of xanthine oxidase activity.

The macromolecular permeability of renal capillaries and the intravascular red cell aggregation resulting from 45 min of warm ischaemia were investigated. The effects of the xanthine oxidase inhibitor Allopurinol on these factors and also on the post-ischaemic nephron function were also studied. Following ischaemia there was a more than 10-fold increase in the transport from plasma to renal hilar lymph both of plasma proteins and of two isomers of lactate dehydrogenase (LDH)-the nearly neutral LDH-M4 and the negatively charged LDH-H4. The ischaemia also resulted in massive intravascular red cell aggregation, especially in the renal medulla. Through reduction of plasma xanthine oxidase activity from 13.1 +/- 1.1 microU microliter-1 (mean +/- SEM) to essentially zero by Allopurinol, the capillary leakiness was substantially diminished with almost complete normalization after 120 min. At the same time the relative volume of trapped red cells was reduced; in the inner stripe of the outer medulla, for example, it decreased from 11.3 +/- 1.7% in untreated animals to 4.0 +/- 1.1% after treatment with 20 mg of Allopurinol given intravenously 3 h before the ischaemia. Oral feeding with 4 mg of Allopurinol day-1 for one week gave essentially the same result. The net driving force for filtration after treatment with this drug was thus 19 mmHg, as against 26 mmHg in the normal kidney and the resulting SNGFR was half the normal. The total filtration rate was proportionally more reduced to less than 1/3 of the normal. Tubular obstruction was still present but was not as severe as in untreated kidneys (Karlberg et al., 1982b) where the tubular fluid flow and thereby the filtration are essentially zero. It is suggested that oxygen free radicals increased the macromolecular permeability and the adhesiveness of white blood cells and that these two factors combined underlie the aggregation of red blood cells in the medullary vasa recta with consequent persistence of medullary ischaemia.

Allopurinol↗

PubMed2001

Radioisotope albumin flux measurement of microvascular lung permeability: an independent parameter in acute respiratory failure?

AIM: To evaluate the extent to which single measurements of microvascular lung permeability may be relevant as an additional parameter in a heterogenous clinical patient collective with Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS). METHODS: In 36 patients with pneumonia (13), non pneumogenic sepsis (9) or trauma (14) meeting the consensus conference criteria of ALI or ARDS double-isotope protein flux measurements (51Cr erythrocytes as intravascular tracer, Tc-99m human albumin as diffusible tracer) of microvascular lung permeability were performed using the Normalized Slope Index (NSI). The examination was to determine whether there is a relationship between the clinical diagnosis of ALI/ARDS, impaired permeability and clinical parameters, that is the underlying disease, oxygenation, duration of mechanical ventilation and mean pulmonary-artery pressure (PAP). RESULTS: At the time of study, 25 patients presented with increased permeability (NSI > 1 x 10(-3) min-1) indicating on exudative stage of disease, and 11 patients with normal permeability. The permeability impairment correlated with the underlying disease (p > 0.05). With respect to survival, there was a negative correlation to PAP (p < 0.01). Apart from that no correlations between the individual parameters were found. Especially no correlation was found between permeability impairment and oxygenation, duration of disease or PAP. CONCLUSION: In ALI and ARDS, pulmonary capillary permeability is a diagnostic parameter which is independent from clinical variables. Permeability measurement makes a stage classification (exudative versus non exudative phase) of ALI/ARDS possible based on a measurable pathophysiological correlate.

Adult↗

PubMed1975

Comparison of several activated partial thromboplastin time methods.

Activated partial thromboplastin times (APTT's) performed with a semi-automated electrical-conductivity type of clot timer on plasmas from patients with hepatic disease and intravascular coagulation, and on warfarin or heparin therapy, were significantly lower than when done on the same plasmas with either a manual optical method or an automated optical-endpoint instrument. Results of APTT's done on normal plasmas by the three methods were not significantly different. Substitution of different activator-phospholipid reagents resulted in some variability in results, but these differences were less than those between the different done with both the electrical clot timer and the automated optical instrument on prepared plasmas containing 5.0 or 1.0% of factor II, V, VIII, IX, OR X revealed shorter times with the electrical clot timer only in the case of factor II- and factor V-deficient plasmas. APTT's done on normal plasmas to which 0.1 or 0.3 units per ml. of heparin had been added vitro also were shorter with the electrical clot itmer than the automatic optical instrument. Prothrombin times done on normal and abnormal control plasmas and on a series of plasmas from patients on warfarin therapy showed no significant difference between the two methods.

Autoanalysis↗

PubMed1990

Peritubular capillary permeability and intravascular RBC aggregation after ischemia: effects of neutrophils.

The influence of neutrophils on peritubular capillary permeability and intravascular red blood cell (RBC) aggregation after renal ischemia was studied in anesthetized Sprague-Dawley rats. Intraperitoneal administration of antineutrophil serum (ANS) reduced the number of neutrophils in the blood to 3% of normal. The control group received an equal volume of inactive serum. Renal macromolecular capillary permeability was studied from 1) extravasation of albumin and 2) plasma to lymph transport of plasma proteins and of neutral and negatively charged lactate dehydrogenase (LDH). The net driving force (NDF) for fluid transfer over the peritubular capillary membrane was determined by the micropuncture technique. The intrarenal distributions of neutrophils and RBC were measured by a histochemical method and 51Cr-labeled RBC, respectively. Under preischemic control conditions neither macromolecular permeability nor renal clearance of inulin was affected by ANS. However, the steep increase in the macromolecular transport from plasma to lymph resulting from 45 min of ischemia and reperfusion was blunted by ANS, and preischemic control values were restored after 1 h of recirculation. In the control group the mass transport of plasma proteins increased twofold and that of both neutral and negatively charged LDH fourfold. NDF was equal in the two groups. In the ANS-treated animals the intrarenal neutrophil content was only 2% of the control. Neutrophils were found mainly in the cortex, whereas RBC aggregation was observed only in the renal medulla. It is concluded that neutrophils mediate postischemic capillary leakage. It is suggested that this leakage underlies RBC aggregation and incomplete return of blood flow in the renal medulla after ischemia.

Animals↗

PubMed1989

Fibronectin fragments in lung lymph after thrombin-induced lung vascular injury.

Fibronectin is an adhesive glycoprotein found in plasma and lymph as well as between lung endothelial cells and their collagenous basement membranes. Fibronectin is highly sensitive to proteolytic cleavage. We determined if fragments of fibronectin appear in lung lymph in association with increased lung protein clearance after thrombin-induced intravascular coagulation. Thrombin was infused intravenously, (80 units/kg for 30 minutes) into sheep (n = 8) surgically prepared with chronic lung lymph fistulas. Plasma and lymph fibronectin was assayed by electroimmunoassay. Fibronectin fragments were detected using Western blot analysis. After thrombin infusion, lymph flow increased 650% above baseline within 1-2 hours in association with a 35% decline in lymph-to-plasma total protein concentration ratio. This was followed by a second phase (3.5-6 hours) of normalized lymph-to-plasma ratios coupled with sustained elevation of lymph flow. Lung protein clearance remained elevated (p less than 0.10) for 5.5 hours. Plasma fibronectin levels declined slightly over 1-5 hours (zero time = 597 +/- 64 micrograms/ml; 1.5 hours = 478 +/- 59 micrograms/ml) and then increased significantly (p less than 0.05) over 24-48 hours (760 +/- 85 micrograms/ml). The amount of low molecular weight fibronectin fragments in lung lymph increased over the 1.5-6 hours post-thrombin and then declined over 12-48 hours. Thus after thrombin infusion, fragments of fibronectin were usually detected in increased amounts of lung lymph in association with an elevation of lung protein clearance.

Animals↗

PubMed2006

Clinical and laboratory patterns of the haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura in southern Iran.

OBJECTIVE: The haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are rare disorders characterised by intravascular platelet aggregation and widespread thrombus formation in the microcirculation resulting in tissue ischaemia. A retrospective analysis was carried out in 136 patients with HUS or TTP hospitalized from April 1991 through March 2004 in three tertiary referral hospitals of Shiraz (the largest city in southern Iran) to evaluate the epidemiological aspects, clinical characteristics and laboratory findings of the two diseases. METHODS: One hundred and one cases of HUS (49 females and 52 males) and 35 cases of TTP (21 females and 14 males) were identified. The mean age was 3.5 years for HUS, 30.8 years for TTP. RESULTS: The mean annual incidence rate of HUS decreased approximately 30-fold throughout the observed period, while the incidence rate of TTP increased approximately 6-fold. A seasonal pattern was noted for both TTP and HUS, with the highest incidence during the summer months. Twenty patients with HUS and 16 patients with TTP died, resulting in case fatality rates of 19.8% and 45.7%, respectively. No prognostic factor was identified for TTP, whereas signs of neurological impairment and high leucocyte counts had an adverse effect on the prognosis of HUS patients. CONCLUSIONS: This study shows that, in contrast to other countries, the incidence rate of HUS shows a decreasing trend in southern Iran, probably related to the prevention of gastrointestinal diarrhoeal infections (especially Escherichia coli 0157:H7) and to their improved management. The incidence of TTP is increasing in Iran as in other countries.

Adolescent↗

PubMed1975

Endotoxin-induced liver necrosis and intravascular coagulation in rats enhanced by portacaval collateral circulation.

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.

Alanine Transaminase↗

PubMed1995

Ultrasound backscatter at 30 MHz from human blood: influence of rouleau size affected by blood modification and shear rate.

High frequency intravascular ultrasound may show a high intensity backscatter from blood which hampers the discrimination between lumen and arterial wall. In this study, the acoustic behaviour of blood at 30 MHz in relation to rouleau size was analyzed. In a Couette viscometer, high frequency (20-40 MHz) backscatter data from normal and modified blood samples from eight volunteers were obtained at shear rates from 0 to 1000 s-1. The acoustic behaviour of blood was quantified by the integrated backscatter power and the spectral slope of the backscatter coefficient. Backscatter from blood depended on rouleau size. At a shear rate of zero, both whole blood and rouleau-enhanced blood showed a 11-dB-higher integrated backscatter power than rouleau-suppressed blood, which itself was 10 dB higher than that of hemolysed blood, the latter showing a 6-dB-higher backscatter than saline. Platelets did not contribute to the backscatter power. Plasma and saline produced no detectable integrated backscatter power other than noise. The spectral slope of whole and rouleau-enhanced blood was small (1 and 0.5, respectively), whereas rouleau-suppressed blood and hemolysed blood (both with a slope of 3.3) behaved almost like a Rayleigh scattering medium (slope = 4). The backscatter from rouleau-suppressed blood showed no shear rate dependence. At low shear rates ( < 0.8 s-1 for integrated backscatter power and < 0.2 s-1 for the spectral slope), whole blood and rouleau-enhanced blood tended to the results from the static situation (no shear). At high shear rates ( > 80 s-1 for integrated backscatter power and >11 s-1 for spectral slope), these samples tended to the results of rouleau-suppressed blood. Ultrasound backscatter at 30 MHz from human blood is only caused by red blood cells. With increasing aggregate (rouleau) size, the integrated backscatter power increased by 11 dB, and the spectral slope decreased from 3.3 to 1.

Blood↗