Effects Of Septic Shock Research Articles

Alterations in systemic arterial mechanical properties during septic shock: role of fluid resuscitation

The effects of septic shock (endotoxin; EDTX) on arterial mechanical properties were studied in anesthetized rabbits, both in the absence (EDTX alone) and presence (EDTX + fluids) of fluid resuscitation. Aortic pressure-flow (n = 20) and pressure-diameter (n = 10) measurements were used to calculate systemic arterial and regional aortic mechanical properties. At 3 h of EDTX shock, EDTX-alone rabbits had elevated total peripheral resistance (TPR, + 30%, P < 0.05), reduced cardiac output (CO, -40%, P < 0.05), and increased aortic characteristic impedance (Zc, +78%, P < 0.05). In contrast, the EDTX + fluids group responded with decreased TPR (-30%, P < 0.05), a tendency to increase CO (+23%), and elevated Zc (+46%, P < 0.05). A reduction in aortic diameter (-20%, P < 0.05) and an increase in elastic modulus (+50%, P < 0.05) and water content (+23%, P < 0.02) of the aortic wall were observed following endotoxemia. Thus following EDTX 1) "hyperdynamic" septic shock profile (i.e., low TPR, high CO) was observed only when concomitant fluid replacement was provided, 2) aortic wall stiffening was present due to both increased smooth muscle tone and vessel wall edema, and 3) fluid resuscitation resulted in discordant changes in TPR and Zc, suggesting differential flow-induced vasodilation between arteriolar and aortic smooth muscle.

Effects of L-arginine and L-nitro-arginine treatment on blood pressure and cardiac output in a rabbit endotoxin shock model

To verify the effect of nitric oxide system modification during sepsis, not only in terms of pressure but also in terms of perfusion flow. Experimental, comparative study. Laboratory of a university hospital. Twenty-six New Zealand male rabbits (2 to 2.5 kg body weight) were studied under anesthesia. Nitric oxide pathways were modified during shock-induced hypotension, using L-arginine (600 mg/kg) and L-nitro-arginine (7.5 mg/kg), which were infused 75 mins after endotoxin injection. Mean arterial pressure (MAP) and cardiac output, as well as ascending aortic velocity, were measured and aortic conductance (aortic velocity/MAP in cm/sec/mm Hg) was calculated. Both L-arginine and L-nitro-arginine increased MAP to the pre-endotoxin level, but only L-arginine increased aortic velocity in association with a marked increase in aortic conductance (p < .001). L-nitro-arginine significantly (p < .05) decreased aortic velocity as compared with the control endotoxin group, with an intense vasoconstriction as shown by a significant (p < .001) decrease in aortic conductance. These results, along with the high mortality rate in the L-nitro-arginine treated group, challenge the hypothesis that nitric oxide release inhibition has a beneficial effect in septic shock.

Adrenaline in treatment of septic shock: Effects on haemodynamics and oxygen transport

The effects of adrenaline on haemodynamics and oxygen transport were studied in 13 patients with septic shock persisting after optimal fluid loading. Adrenaline was administered by intravenous infusion at an increasing dose until no further benefit was seen. There were significant increases in mean arterial pressure, cardiac index, left ventricular stroke work index and oxygen delivery index. There was no significant change in oxygen consumption although the trend was towards an increase. There was a significant reduction in oxygen extraction ratio, but no change in shunt fraction. Adrenaline would appear to have beneficial haemodynamic effects in septic shock.

Dobutamine administration in septic shock

Dobutamine administration has been shown to increase oxygen delivery in various conditions, but there are little data to document its effects in septic shock. We investigated the effects of dobutamine infusion at a rate of 5 micrograms/kg.min in 18 patients (mean 60 +/- 16 yr) with septic shock initially characterized by hypotension, oliguria, and hyperlactatemia in the presence of a documented source of sepsis. Early resuscitation had consisted of fluid administration and vasopressors when required. When added to this standard regimen, dobutamine had no significant effect on mean arterial pressure (MAP) (from 71 +/- 12 to 73 +/- 13 mm Hg), but markedly increased cardiac index (from 3.0 +/- 0.7 to 3.9 +/- 1.0 L/min.m2, p less than .001), stroke index (from 32 +/- 8 to 37 +/- 9 ml/m2, p less than .001) and oxygen transport (from 410 +/- 105 to 530 +/- 146 ml/min.m2, p less than .001). Oxygen consumption (VO2) increased concurrently (from 137 +/- 42 to 162 +/- 66 ml/min.m2, p less than .002). MAP increased (from 68 +/- 9 to 76 +/- 11 mm Hg) in 12 patients and decreased moderately (from 76 +/- 18 to 69 +/- 17 mm Hg) in six patients. The two subgroups of patients had similar hemodynamic profiles before the dobutamine infusion, but vasopressor therapy was already used in one of the 12 patients in the first subgroup and in three of the six patients in the second subgroup (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Tumor necrosis factor suppresses transcription of the thrombomodulin gene in endothelial cells.

Tumor necrosis factor (TNF) dramatically alters the levels of various surface components of the blood vessel wall, such as blood coagulation enzyme receptors, leukocyte-adhesive receptors, and class 1 major histocompatibility complex antigens, which may have relevance to its effects in septic shock, angiogenesis, and tumor growth. However, the precise mechanism by which the cytokine is able to accomplish this remodeling of the endothelial cell surface has not been defined. We have demonstrated that exposure of bovine and human endothelial cells to TNF leads to suppression of the functional cell surface thrombin receptor, thrombomodulin (TM), and TM mRNA of virtually identical magnitude. The cytokine has no significant effect on the stability of TM mRNA or endothelial receptor turnover. Nuclear run-on studies reveal that the treatment of endothelial cells with TNF for short periods reduces TM gene transcription to as little as 3% of control values and that this inhibition does not require new protein synthesis.

Tumor necrosis factor suppresses transcription of the thrombomodulin gene in endothelial cells.

Tumor necrosis factor (TNF) dramatically alters the levels of various surface components of the blood vessel wall, such as blood coagulation enzyme receptors, leukocyte-adhesive receptors, and class 1 major histocompatibility complex antigens, which may have relevance to its effects in septic shock, angiogenesis, and tumor growth. However, the precise mechanism by which the cytokine is able to accomplish this remodeling of the endothelial cell surface has not been defined. We have demonstrated that exposure of bovine and human endothelial cells to TNF leads to suppression of the functional cell surface thrombin receptor, thrombomodulin (TM), and TM mRNA of virtually identical magnitude. The cytokine has no significant effect on the stability of TM mRNA or endothelial receptor turnover. Nuclear run-on studies reveal that the treatment of endothelial cells with TNF for short periods reduces TM gene transcription to as little as 3% of control values and that this inhibition does not require new protein synthesis.

Lipoid A antibody titer in humans

Lipid A is the toxic component of endotoxin in gram-negative bacteria. Antibodies to lipid A are not usually found in healthy persons (or only at a low titer) without a corresponding history of infection. Even gram-negative septicemia is found to be accompanied by only low titers. A completely different situation is seen in patients with chronic or recurrent infections due to Enterobacteriaceae and other gram-negative bacteria. Here it is notable that the antibody titer varies with the type of disorder (e. g. cystitis and pyelonephritis). A severe would infection, e. g. due to Pseudomonas aeruginosa, also leads to measurable lipid A antibody titers. Varying antibody titers can be observed in cystic fibrosis, Crohn's disease, and severe surgical infections. One can conclude that a significantly elevated antibody titer develops during an extensive tissue involvement of long duration and indeed is caused by tissue inhibition by endotoxin. Based on clinical experience, it can be assumed that lipid A antibodies present in the body have a protective effect in septic shock.

Lipoid A antibody titer in the human

Lipid A is the toxic component of endotoxin in gram-negative bacteria. Antibodies to lipid A are not usually found in healthy persons (or only at a low titer) without a corresponding history of infection. Even gram-negative septicemia is found to be accompanied by only low titers. A completely different situation is seen in patients with chronic or recurrent infections due to Enterobacteriaceae and other gram-negative bacteria. Here it is notable that the antibody titer varies with the type of disorder (e.g. cystitis and pyelonephritis). A severe wound infection, e.g. due to Pseudomonas aeruginosa, also leads to measurable lipid A antibody titers. Varying antibody titers can be observed in cystic fibrosis, Crohn's disease, and severe surgical infections. One can conclude that a significantly elevated antibody titer develops during an extensive tissue involvement of long duration and indeed is caused by tissue inhibition by endotoxin. Based on clinical experience, it can be assumed that lipid A antibodies present in the body have a protective effect in septic shock.

ANTIBODY TITRES TO A ROUGH-MUTANT STRAIN OF ESCHERICHIA COLI IN PATIENTS UNDERGOING ALLOGENEIC BONE-MARROW TRANSPLANTATION: Evidence of a Protective Effect Against Graft-versus-host Disease

Much clinical and experimental evidence suggests that infection and graft-versus-host disease (GvHD) are commonly associated as complications of bone-marrow transplantation (BMT). A likely basis for this association is the gram-negative faecal flora, the origin of many septicaemias and a source of bacterial endotoxin, which has potent immunostimulatory effects. A rough-mutant strain, Escherichia coli J5, has only core determinants in its endotoxin, and antibodies to E coli J5 protect animals and human beings from the consequences of septic shock. Naturally occurring antibodies to E coli J5 ("anti-endotoxin") were assayed in serum from patients undergoing BMT, healthy controls, and patients with obstructive jaundice. BMT recipients had significantly lower titres than the other two groups. Furthermore, the titre of IgM class anti-J5 antibody was significantly associated with protection from GvHD.

Ultrastructural modifications of the cavities formed by folliculo-stellate cells in chicken adenohypophysis under septic shock conditions.

Effects of septic shock by repeated inoculations with Escherichia coli on the ultrastructure of the folliculo-stellate cells and cavities of the adenohypophysis of the chicken were investigated in order to determine the function of these cavities. The principal morphological modifications were dilation of the Golgi apparatus, endoplasmic reticulum and autophagic vacuoles, and necrosis phenomena in the stellate cells. The follicular cavities showed dilation, and there was heterogeneous dense material and granular elements in the follicular lumen. Based on results reported in the literature, the observations reported here are evidence of a "cleaning-role", for the removal of cell debris, when there is endocrine disfunction.

Gastritis Necroticans in Children

The authors discuss two cases in which following abdominal operations in consequence of septic shock, infection and hypoxia, necrosis of the gastric wall developed requiring further operations, subtotal resection of the stomach included. Attention is paid to the factors responsible for full recovery.

The effect of septic shock on skeletal muscle action potentials in the primate

The effect of septic shock on skeletal muscle action potentials in the primate

The effect of septic shock on skeletal muscle action potentials in the primate.

Techniques developed for the in vivo study of cellular physiology have been applied to septic shock in primates. Measurements of skeletal muscle transmembrane resting and action potentials were correlated with an analysis of fluid and electrolyte changes in the intracellular and extracellular compartments of skeletal muscle. The data obtained indicated a marked depletion of muscle extracellular water and an increase in intracellular sodium chloride and water content during shock. The significant decrease of resting membrane potential was associated with a decrease in amplitude of the action potential and prolongation of both the repolarization and depolarization time. In addition, there was a decrease of muscle intracellular potassium concentration during shock. This study demonstrates that the alterations in cellular membranes in hemorrhagic shock and septic shock are similar.

Ionized calcium: The effect of septic shock in the human

Ionized calcium: The effect of septic shock in the human

Ionized Calcium and Magnesium

Ionized calcium (Ca2+) and ionized magnesium (Mg2+) are important intracellular "second messengers" and control exictation-contraction coupling, excitation-secretion, oxidative phosphorylation, and mitochondrial acid-base balance. The present study examines the effect of septic shock on serum (Ca2+) and (Mg2+). Five adult female baboons were subjected to live E. coli septic shock and then resuscitated. Three baboons served as controls. Ca2+ was measured by the Orion SS-20 flow-through calcium electrode and Mg2+ calculated by the method of Killen. Other measurements included: total calcium, bound calcium, total magnesium, bound magnesium, phosphate, albumin, globulin, hemotocrit, and total protein. This study shows that there are significant disturbances of Ca2+ and Mg2+ during septic shock in the baboon. These disturbances may in part explain cellular dysfunction during shock including: decreased myocardial contractility, inappropriate secretion of endocrine cells, decrease in oxidative phosphorylation, and mitochondrial acidosis.

Effects of septic shock on renal function in humans

Effects of septic shock on renal function in humans

Effects of septic shock on renal function in humans.

Effects of septic shock on renal function in humans.