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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine if concentration of plasma arginine vasopressin (AVP) is inappropriate for the plasma Na+ concentration in hyponatremic burned patients, we obtained 32 plasma samples from 20 patients with total burn size (TBS) 15 to 80% of body surface on or after postburn day (PBD) 4 in the morning following all-night recumbency. In the 25 samples (17 patients) with hyponatremia, AVP was elevated, 1.6 to 14.3 (normal less than 0.5) pg/ml. Most patients with normal serum Na+ had normal AVP values. Out of the total, nine patients (12 samples) without renal failure or sepsis, selected also for hyponatremia and urinary Na+ greater than or equal to 20 mEq/L, were considered separately. BUN of 11.7 +/- 1.8 mg/dl and plasma glucose of 130 +/- 5.6 mg/dl, Na+ of 130 +/- 1.1 mEq/L, calculated osmolality of 272 +/- 1.6 mosm/kg, and cortisol of 20.4 +/- 1.6 micrograms/dl were associated with a 24-hour fluid intake of 4.3 +/- 0.26 L and urinary output of 2.7 +/- 0.33 L, Na+ of 80 +/- 14 mEq/L, and osmolality of 520 +/- 73 mosm/kg (mean +/- SE). In all of the plasma samples, AVP was markedly elevated (6.9 +/- 1.1 pg/ml). In another study, four hyponatremic burned patients were given a standard water load. Excretion of the water was delayed, and further dilution of the initially hypotonic plasma resulted in a fall of urinary osmolality and plasma AVP. Cutaneous thermal injury can cause resetting of the mechanism linking plasma tonicity and AVP secretion resulting in dilutional hyponatremia. This syndrome occurs in the absence of gross physiologic perturbations such as volume depletion or adrenal insufficiency.
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PMID:Inappropriate vasopressin secretion (SIADH) in burned patients. 683 44

The aetiology of hyponatremia in tetraplegic patients is multifactorial and includes not only general factors such as the use of diuretics and the intravenous infusion of hypotonic fluids, but also certain mechanisms which operate in the spinal cord injured: decreased renal water excretion due to both intrarenal and arginine vasopressin dependent mechanisms (resetting of the osmostat), coupled with habitually increased fluid intake, and the ingestion of a low salt diet. Between 1984 and 1993 we treated 28 episodes of hyponatremia in 19 patients (males: 10; females: 9). Fourteen were tetraplegic and five paraplegic (thoracic lesion in four and lumbar lesion in one). Six patients were asymptomatic during seven episodes of hyponatremia which were detected during routine blood tests. Seven patients were suffering from an acute chest infection, three had an acute urinary tract infection, one had an infected ischial pressure sore and a 69 year old paraplegic patient had bronchopneumonia as well as sepsis from a gangrenous pressure sore in the supraanal region. The time interval between the onset of paralysis and occurrence of the first episode of hypnoatremia was less than a month in only four of the patients. The lowest plasma sodium level observed was less than 100 mmol/l in two, between 100 and 110 mmol/l in four, between 111 and 120 mmol/l in eight patients, and between 121 and 128 mmol/l in 14 cases. Six patients also had hypokalemia (K+ < 3 mmol/l). Only one patient had and elevated plasma creatinine (201 umol/l). Treatment of sepsis and fluid restriction were the mainstay of treatment with only two patients receiving hypertonic saline. All patients with underlying sepsis were treated with antibiotics, usually administered intravenously. The outcome was good in 26 of the 28 episodes. Two patients died: a 68 year old tetraplegic patient with consolidation of the left lung, cystadenocarcinoma of both ovaries and squamous cell carcinoma of the forehead who presented with generalised oedema, with a plasma sodium level of 118 mmol/l, and potassium of 2.4 mmol/l and who was treated with 2 N saline + potassium + frusemide; she died 1 day later. The only other death was that of a 78 year old female tetraplegic patient who 2 days after sustaining cervical trauma developed hyponatremia because of intravenous infusion of hypotonic fluids given at another hospital, presumably to correct hypotension. She recovered from hyponatremia with fluid restriction, but 3 days later she succumbed to bronchopneumonia and respiratory insufficiency. No patient developed central pontine myelinolysis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A retrospective study of hyponatremia in tetraplegic/paraplegic patients with a review of the literature. 799 39

Transfusion risks include the possibility of ABO/Rh incompatibility, sepsis, febrile reactions, immunosuppression, and viral transmission; incidences and consequences of these complications are reviewed. Predonation of autologous blood generally reduces the need for homologous blood by about 30% to 40%, but relatively few coronary artery bypass surgery (CABG) patients predonate blood. Drug products to decrease blood use include 1-deamino-8-D-arginine vasopressin (DDAVP), tranexamic acid, epsilon-aminocaproic acid, and aprotinin. A recent study suggests that a subgroup of patients with abnormal platelet function may benefit from a platelet therapy such as DDAVP. The prophylactic use of tranexamic acid reduces cardiac surgery postoperative blood loss, as measured by chest-tube output, by about 30%; unfortunately, data demonstrating a reduction in transfusion requirements are not available. Aprotinin use is associated with major reductions in blood transfusion requirements. Aprotinin provides platelet protection during cardiopulmonary bypass. Duration of stay in the intensive care unit was not increased by use of aprotinin, thus alleviating some concerns that aprotinin might promote coronary thrombosis. A recent report cites early graft closure as a major concern with aprotinin therapy, but data from other studies show no significant differences in rates of graft closure between patients receiving and those not receiving aprotinin. Routine use of a thromboelastogram with all cardiopulmonary bypass surgery at the University of Washington Hospital has reduced use of blood products by 30%.
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PMID:Cardiac anesthesia risk management. Hemorrhage, coagulation, and transfusion: a risk-benefit analysis. 816 99

Immune neuroendocrine interactions are vital for the individual's survival in certain physiopathological conditions, such as sepsis and tissular injury. It is known that several animal venoms, such as those from different snakes, are potent neurotoxic compounds and that their main component is a specific phospholipase A type 2 (PLA2). It has been described recently that the venom from Crotalus durissus terrificus [snake venom (SV), in the present study] possesses some cytotoxic effect in different in vitro and in vivo animal models. In the present study, we investigated whether SV and its main component, PLA2 (obtained from the same source), are able to stimulate both immune and neuroendocrine functions in mice, thus characterizing this type of neurotoxic shock. For this purpose, several in vivo and in vitro designs were used to further determine the sites of action of SV-PLA2 on the hypothalamo-pituitary-adrenal (HPA) axis function and on the release of the pathognomonic cytokine, tumor necrosis factor alpha (TNF alpha), of different types of inflammatory stress. Our results indicate that SV (25 microg/animal) and PLA2 (5 microg/animal), from the same origin, stimulate the HPA and immune axes when administered (i.p.) to adult mice; both preparations were able to enhance plasma glucose, ACTH, corticosterone (B), and TNF alpha plasma levels in a time-related fashion. SV was found to activate CRH- and arginine vasopressin-ergic functions in vivo and, in vitro, SV and PLA2 induced a concentration-related (0.05-10 microg/ml) effect on the release of both neuropeptides. SV also was effective in changing anterior pituitary ACTH and adrenal B contents, also in a time-dependent fashion. Direct effects of SV and PLA2 on anterior pituitary ACTH secretion also were found to function in a concentration-related fashion (0.001-1 microg/ml), and the direct corticotropin-releasing activity of PLA2 was additive to those of CRH and arginine vasopressin; the corticotropin-releasing activity of both SV and PLA2 were partially reversed by the specific PLA2 inhibitor, manoalide. On the other hand, neither preparation was able to directly modify spontaneous and ACTH-stimulated adrenal B output. The stimulatory effect of SV and PLA2 on in vivo TNF alpha release was confirmed by in vitro experiments on peripheral mononuclear cells; in fact, both PLA2 (0.001-1 microg/ml) and SV (0.1-10 microg/ml), as well as concavalin A (1-100 microg/ml), were able to stimulate TNF alpha output in the incubation medium. Our results clearly indicate that PLA2-dependent mechanisms are responsible for several symptoms of inflammatory stress induced during neurotoxemia. In fact, we found that this particular PLA2-related SV is able to stimulate both HPA axis and immune functions during the acute phase response of the inflammatory processes.
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PMID:A phospholipase A2-related snake venom (from Crotalus durissus terrificus) stimulates neuroendocrine and immune functions: determination of different sites of action. 944 33

Before de novo synthesized von Willebrand factor (vWF) leaves the endothelial cell, it undergoes endoproteolytic cleavage of its propeptide (vW antigen II). The processed vWF and propeptide are either released constitutively or, following activation of the endothelium, released through the regulated pathway. In a recent study (Borchiellini et al, Blood 88:2951, 1996), we showed that the half-life of mature vWF and of its propeptide differ fourfold to fivefold. We postulated that the molar ratio of the propeptide to mature vWF could serve as a tool to assess the extent of endothelial cell activation under physiologic and clinical conditions. To test this hypothesis, we measured mature vWF and propeptide in patients with documented acute and chronic vascular disease, including patients with thrombotic thrombocytopenic purpura (TTP), acute septicemia, and diabetes mellitus. These data were compared with experimental conditions in healthy subjects in which perturbation of the endothelium was simulated by physical exercise or by administration of 1-deamino-8-D-arginine vasopressin (DDAVP) or endotoxin. In all individuals of the latter study group, both vWF and propeptide levels were elevated during the acute phase of the experimentally induced vascular perturbation; at later time points after stimulation, only vWF levels remained elevated. In patients with sepsis and TTP, both vWF and propeptide were elevated several-fold. Thus, this pattern can readily be explained in terms of acute perturbation of the endothelium. In contrast, in patients with diabetes mellitus propeptide levels were only slightly elevated, whereas vWF levels were elevated twofold to threefold. This pattern is a typical feature of chronic, low-grade activation of the endothelium. These observations support our hypothesis that measurement of both propeptide and vWF levels allows to discriminate between chronic and acute phases of endothelial cell activation in vivo. Measurement of only vWF is less indicative in this respect.
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PMID:von Willebrand factor propeptide in vascular disorders: A tool to distinguish between acute and chronic endothelial cell perturbation. 1038 11

In the current issue of Critical Care, Friesenecker and colleagues present a well-designed comparative study on the microvascular effects of arginine vasopressin (AVP) and norepinephrine (NE) in a physiological, unanesthetized hamster model. The authors clearly demonstrate that AVP, but not NE, has marked vasoconstrictive effects on large arterioles, whereas the impact on small arterioles is comparable for both vasopressors. However, it remains unclear if these results, per se, reflect a stronger vasopressive potential of AVP versus NE, as macrohemodynamic variables were not different between study groups. Since the authors did not investigate the effects of AVP and NE in vasodilatory shock states, the microcirculatory response in sepsis or systemic inflammatory response syndrome remains inconclusive. The same authors previously reported that AVP infusion in patients suffering from vasodilatory shock carries the risk for ischemic skin lesions. This in turn raises the question whether the quality of vasopressors should be judged by their potency.
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PMID:Arginine vasopressin versus norepinephrine: will the stronger one win the race? 1669 66

Vasodilatory shock is the most common form of shock in the critically ill patient. As a consequence of overwhelming and prolonged mediator production, vasodilatory shock can be the common final pathway of primary non-vasodilatory shock (e.g. cardiogenic or hypovolemic shock). A supplementary infusion of arginine vasopressin (AVP) showed beneficial effects on hemodynamics and potentially on the outcome in patients with vasodilatory shock due to sepsis or after major surgery. In this case series, successful administration of AVP in three surgical patients with primary cardiogenic shock forms is reported. The hemodynamic effects of AVP were comparable to those AVP-induced alterations described in septic shock and seem to be predominantly mediated by potent vasoconstriction and the facilitated reduction of higher, potentially toxic catecholamine doses. Thus, an AVP-induced decrease in heart rate and pulmonary arterial pressures may be particularly beneficial in patients with impaired cardiac function.
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PMID:[Vasopressin as a rescue vasopressor agent. Treatment of selected cardiogenic shock states]. 1759 65

Recent studies revealed that vasopressinergic neurons have a high content of cys-leukotriene C(4) (LTC(4)) synthase, a critical enzyme in cys-leukotriene synthesis that may play a role in regulating vasopressin secretion. This study investigates the role of this enzyme in arginine vasopressin (AVP) release during experimentally induced sepsis. Male Wistar rats received an i.c.v. injection of 3-[1-(p-chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2, 2-dimethylpropanoic acid (MK-886) (1.0 microg/kg), a leukotrienes (LTs) synthesis inhibitor, or vehicle, 1 h before cecal ligation and puncture (CLP) or sham operation. In one group of animals the survival rate was monitored for 3 days. In another group, the animals were decapitated at 0, 4, 6, 18 and 24 h after CLP or sham operation, and blood was collected for hematocrit, serum sodium and nitrate, plasma osmolality, protein and AVP determination. A third group was used for blood pressure measurements. The neurohypophysis was removed for quantification of AVP content, and the hypothalamus was dissected for LTC(4) synthase analysis by Western blot. Mortality after CLP was reduced by the central administration of MK-886. The increase in plasma AVP levels and hypothalamus LTC(4) synthase content in the initial phase of sepsis was blocked, whereas the decrease in neurohypophyseal AVP content was partially reversed. Also the blood pressure drop was abolished in this phase. The increase of serum nitric oxide and hematocrit was reduced, and the decrease in plasma protein and osmolality was not affected by the LTs blocker. In the final phase of sepsis, the plasma AVP level and the hypothalamic LTC(4) synthase content were at basal levels. The central administration of MK-886 increased the hypothalamic LTC(4) synthase content but did not alter the plasma and neurohypophysis AVP levels observed, or the blood pressure during this phase. These results suggest that the central LTs are involved in the vasopressin release observed during sepsis.
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PMID:Blocking central leukotrienes synthesis affects vasopressin release during sepsis. 1928 13

The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.
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PMID:Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress. 2750 1

Impaired arginine vasopressin (AVP) synthesis and release by the neurohypophyseal system, which includes the neurohypophysis and magnocellular neurons of the paraventricular and supraoptic nuclei, have been postulated in septic shock, but changes in this system have never been assessed in human septic shock, and only partially experimentally. We investigated AVP synthesis and release by the neurohypophyseal system in 9 patients who died from septic shock and 10 controls, and in 20 rats with fecal peritonitis-induced sepsis and 8 sham-operation controls. Ten rats died spontaneously from septic shock, and the others were sacrificed. In patients with septic shock, as in rats that died spontaneously following sepsis induction, AVP immunohistochemical expression was decreased in the neurohypophysis and supraoptic magnocellular neurons, whereas it was increased in the paraventricular magnocellular neurons. No significant change was observed in AVP messenger RiboNucleic Acid (mRNA) expression assessed by in situ hybridization in either paraventricular or supraoptic magnocellular cells. This study shows that both in human and experimental septic shock, AVP posttranscriptional synthesis and transport are differently modified in the magnocellular neurons of the supraoptic and paraventricular nuclei. This may account for the inappropriate AVP release in septic shock and suggests that distinct pathogenic mechanisms operate in these nuclei.
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PMID:Vasopressin synthesis by the magnocellular neurons is different in the supraoptic nucleus and in the paraventricular nucleus in human and experimental septic shock. 2001 89


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