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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During sepsis vasoactive arachidonic acid metabolites of the cyclo-oxygenase pathway and the endothelium-derived vasoconstrictor endothelin-1 (ET-1) are released. The effects of cyclo-oxygenase pathway inhibition by diclofenac on the endotoxin shock response and ET-1 turnover, were investigated in five groups of pigs. In the first group (n = 7; controls) endotoxin (15 micrograms.kg-1.h-1 i.v.) was infused for two hours. In a second endotoxin group (n = 7), the animals were pretreated with diclofenac (3 mg.kg-1 i.v.). In a third group (n = 7), high-dose ET-1 was infused (20 pmol.kg-1.min-1 i.v.) and in a fourth group (n = 7), the ET-1 infusion was preceded by diclofenac. In a fifth group (n = 4), a low and intermediate dose of ET-1 (0.2 and 4 pmol.kg-1.min-1) was infused. A significant increase in ET-1-like immunoreactivity (LI) plasma levels was observed in both endotoxin groups, but in the diclofenac group the increase was comparatively delayed. Furthermore, this group showed a more stable haemodynamic course and in the biphasic increase of pulmonary vascular resistance seen in endotoxin controls, the initial peak was abolished by diclofenac. Exogenous ET-1 infusion indicated that not only locally released but possibly also circulating ET-1 could be a mediator of vascular responses to endotoxin. Indications of release from the lungs were seen during endotoxin infusion. Diclofenac had no effect on basal ET-1-LI plasma levels or on the disappearance rate from plasma of ET-1-LI and the haemodynamic changes seen on ET-1 infusion. The inhibition of cyclo-oxygenase pathway by diclofenac resulted in prevention of the initial pulmonary hypertension and a delayed increase in plasma ET-1-LI levels in porcine endotoxin shock and this latter effect is not due to an increased rate of disappearance from plasma but rather to a decreased release of ET-1.
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PMID:Inhibitory effects of diclofenac on the endotoxin shock response in relation to endothelin turnover in the pig. 772 84

The peripheral vascular response to sepsis is characterized by a vasodilatation of the systemic arterial vessels. Pulmonary hypertension with an increase in resistance and back pressure to flow defined by pressure-flow (P-Q) relationships has been reported in experimental sepsis. We hypothesized that endotoxin can induce differential alterations in resistance and back pressure to flow in the liver venous and arterial beds. Ninety minutes after endotoxin administration in intact anesthetized pigs (n = 8), the liver was vascularly isolated and perfused. Steady-state P-Q relationships in both the portal vein (PV) and hepatic artery (HA) were generated at multiple outflow pressures (Pout; 0, 5, 10, and 15 mmHg) and compared with those obtained in control livers (n = 6). Extrapolated zero-flow pressure intercepts (Pback) and slopes of the P-Q relationships were obtained by least squares linear regression analysis. Endotoxemia increased PV Pback (P < 0.05), and Pback always exceeded Pout (P < 0.05) when the latter was raised. In contrast, in controls, no difference was observed between Pback and Pout when the latter was raised. Endotoxemia also increased the PV slope compared with control. Raising Pout from 0 to 15 mmHg decreased PV slope in the endotoxin group to a greater degree than in controls (P < 0.05). In the HA, endotoxin caused a decrease in slope but did not alter Pback. The simultaneous increase in the PV Pback and slope that occurs with endotoxemia decreases splanchnic venous return, pooling blood in the splanchnic compartment for a given total blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of endotoxin on isolated porcine liver: pressure-flow analysis. 777 19

Paediatric cardiac transplantation (pHTX) has gained widespread acceptance as a therapy in end-stage myocardial failure and some forms of congenital heart disease, particularly hypoplastic left heart syndrome (HLHS). The major problems to the anaesthesiologist in these patients are induction of anaesthesia in infants with HLHS and treatment of pulmonary hypertension in the early post-bypass period. PATIENTS AND METHODS. Anaesthesia for pHTX was performed in 15 children < 1 year of age (4-237 days); 12 suffered from HLHS, 2 from endocardial fibroelastosis, and 1 from dilatative cardiomyopathy. Induction of anaesthesia in patients with HLHS IS a challenge to the anaesthesiologist, as he has to maintain the delicate balance between pulmonary and systemic blood flow. Anaesthesia was induced with fentanyl (10-15 micrograms/kg) and pancuronium (0.2-0.4 mg/kg) and maintained with fentanyl (total dosage 70-100 micrograms/kg). Modification of ventilatory parameters such as FiO2, PaCO2, and airway pressure (PEEP, I:E ratio) was used to influence systemic and pulmonary blood distribution in the pre-bypass period according to changes in haemodynamics (target: O2 saturation approximately 75%-80%, PaCO2 45-50 mmHg). Treatment of pulmonary hypertension in the weaning and early post-bypass period consisted of respiratory (PaCO2 < 30 mmHg) and metabolic alkalinisation (pH 7.45-7.55, BE > +3 mmol/l), the use of prostaglandin E1 (3-6-12 micrograms/kg.h), and the phosphodiesterase inhibitor enoximone (10-15 micrograms/kg.min). Additional positive inotropic support was achieved with dobutamine (5-10 micrograms/kg.min), adrenaline (0.1-0.5 micrograms/kg.min), and/or orciprenaline (0.1-0.2 micrograms/kg.min) and calcium chloride (25-100 mg/kg). RESULTS. Two children died intraoperatively and 1 on the 1st postoperative day from overwhelming pulmonary vascular resistance and right ventricular failure. Three children died between 3 and 4 weeks postoperatively, 1 from cytomegalovirus infection, 1 from sepsis, and 1 from acute rejection. Nine patients survived and are well up to 5.5 years after transplantation. CONCLUSION. Pulmonary hypertension in the weaning and early post-bypass period is the main anaesthesiological problem of pHTX, particularly in children with HLHS. A polypragmatic approach to this problem consisting of alkalinisation, pulmonary vasodilatation, and inotropic support is presented and seems to be effective. Further improvements in concepts of pHTX are limited by the lack of donor organs. Though the experience with pHTX in neonates and infants is growing slowly, it might be a routine procedure from the anaesthesiological point of view within a few years in some selected centres.
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PMID:[Anesthesia for heart transplantation in newborn and suckling infants. Special aspects of the hypoplastic left heart syndrome]. 778 53

Non-resolved chronic pulmonary thromboembolism is a frequent cause of pulmonary hypertension. In long-standing disease hypertension is progressive due to intimal and medial changes in the perfused vessels. Non-resolution of thromboemboli is often associated with underlying coagulopathies; the presence of a lupus anticoagulant may pose a significant problem in the peri-operative management of these patients. Pulmonary thrombendarterectomy presents an efficient option of treatment which is feasible in the majority of patients. By means of pulmonary angiography and computed tomography operability is verified by the often difficult recognition of thromboembolic changes in the central pulmonary arteries. Patients with solely peripheral thromboembolic changes or primary pulmonary hypertension must be excluded. In presence of significant exertional dyspnea and/or pulmonary pressure elevation surgery is indicated. Mortality is high and mainly related to unrelieved pulmonary hypertension or pulmonary complications; pulmonary reperfusion edema, respiratory failure or pneumonia and sepsis. In all survivors the reduction of pulmonary hypertension is highly significant and persistent. Thromboembolic pulmonary hypertension may be treated curatively in most patients by thrombendarterectomy. Correct selection of surgical candidates is mandatory, and the patients should preferably be diagnosed and undergo surgery in an early stage of their disease.
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PMID:[Surgical treatment of thromboembolism-induced pulmonary hypertension]. 786 94

Both tumor necrosis factor (TNF) and platelet-activating factor (PAF) are released during sepsis and are important mediators of septic lung injury. I investigated the interactions of TNF and PAF on vasoactive responses in the pulmonary circulation. In isolated rat lungs perfused with a cell- and plasma-free physiological salt solution, PAF (0.01- and 0.1-micrograms boluses) caused transient dose-dependent pulmonary arterial and venous constrictions. In vivo pretreatment of the rats with TNF (0.02 or 0.2 mg/kg i.v.) 1 h before lung isolation increased lung myeloperoxidase activity and markedly enhanced PAF-induced pulmonary vasoconstriction without affecting the pressor responses to angiotensin II or hypoxia. In contrast, pretreatment with lipopolysaccharide (10 mg/kg), which increased lung myeloperoxidase to the same extent as TNF, caused only a modest enhancement of PAF-induced vasoconstriction associated with reduced pressor responses to angiotensin II and hypoxia. Ex vivo perfusion of isolated lungs with TNF for 1 h did not affect PAF vasoconstriction. The TNF-induced potentiation of PAF vasoconstriction was not altered by depletion of circulating neutrophils with vinblastine but was blocked by Dazmegrel, a thromboxane synthase inhibitor. Thus, TNF potentiates PAF-induced pulmonary vasoconstriction by an in vivo mechanism that is neutrophil independent but thromboxane dependent. This TNF-PAF interaction likely contributes to the development of pulmonary hypertension during sepsis.
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PMID:TNF potentiates PAF-induced pulmonary vasoconstriction in the rat: role of neutrophils and thromboxane A2. 789 27

In this review, the second of a two part series, the analytic techniques introduced in the first part are applied to a broad range of pulmonary pathophysiologic conditions. The contributions of hypoxic pulmonary vasoconstriction to both homeostasis and pathophysiology are quantitated for atelectasis, pneumonia, sepsis, pulmonary embolism, chronic obstructive pulmonary disease and adult respiratory distress syndrome. For each disease state the influence of principle variables, including inspired oxygen concentration, cardiac output and severity of pathology are explored and the actions of selected drugs including inhaled nitric oxide and infused vasodilators are illustrated. It is concluded that hypoxic pulmonary vasoconstriction is often a critical determinant of hypoxemia and/or pulmonary hypertension. Furthermore this analysis demonstrates the value of computer simulation to reveal which of the many variables are most responsible for pathophysiologic results.
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PMID:Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. 2. Pathophysiology. 793 36

Case records of 68 newborns who required assisted ventilation over a 24 month period were reviewed. Fortyfour (64.7%) received intermittent mandatory ventilation, 10 (14.7%) received nasal CPAP and the remaining 14 (20.58%) received a combination of the above. Some of the indications for ventilation were infections (21), hyaline membrane disease (16), problems related to asphyxia (11), apnea of prematurity (10) and persistent pulmonary hypertension of newborn (5). The overall survival rate was 41.17%. In the CPAP group 90% (9/10) survived, while in the remaining survival was 32.7% (19/58). The best outcome was observed in persistent pulmonary hypertension of newborn (80%) followed by apnea of prematurity (70%) and hyaline membrane disease (43.75). Outcome was poor in conditions related to birth asphyxia (27.2%) and infections (19.05%). Survival rates were higher (44.4%) in babies weighing > 1500g at birth as compared to 40.9% in babies < 1500g. Babies less than 32 weeks gestation had a survival rate of 32% as compared to 46.5% in those over 32 weeks. This difference was not statistically significant. Complications were seen in 12/68 patients (17.6%). Pneumothorax was the commonest followed by sepsis, intraventricular hemorrhage and blocked endotracheal tubes. Babies with hyaline membrane disease had the highest incidence of complications. Analysis of the data with regard to the indications, outcome and complications is presented.
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PMID:Assisted ventilation in neonates: the Manipal experience. 800 67

We investigated whether hypermagnesemia alleviates hypoxic or group B streptococcal (GBS) pulmonary hypertension (PH). Hypoxic PH was induced and maintained in 14 lambs by continuous ventilation with 12% oxygen. GBS PH was induced and maintained in 16 lambs by the continuous infusion of 5-10 x 10(8) colony-forming units.kg-1.h-1 of GBS. After the onset of PH, lambs were randomized to receive either magnesium sulfate (MgSO4, intermittent boluses of 0.38 mmol/kg, with a continuous infusion of 0.15 mmol.kg-1.h-1) or a similar volume of normal saline. Hypermagnesemia lowered pulmonary arterial pressure (PAP) and delayed the fall in systemic arterial pressure and stroke volume index seen in the control animals (each P < 0.05). At a serum magnesium concentration ([Mg]) of 2.75 +/- 0.25 mmol/l, PAP was 27 +/- 3 compared with 40 +/- 4 Torr in the control animals ([Mg] = 0.87 +/- 0.06 mmol/l; P < 0.05). In the GBS PH trial, hypermagnesemia prevented the continued increase in PAP seen in the control animals. At [Mg] = 2.15 +/- 0.07 mmol/l, PAP fell 2 +/- 1 Torr from prerandomization values, whereas it rose 4 +/- 2 Torr in the control animals ([Mg] = 0.59 +/- 0.07 mmol/l; P < 0.05). However, during the same time the systemic arterial pressure fell further in the magnesium-treated animals (-19 +/- 1 vs. -2 +/- 5 Torr). MgSO4 attenuates PH in both models but may cause systemic hypotension in sepsis.
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PMID:Magnesium attenuates pulmonary hypertension due to hypoxia and group B streptococci. 800 24

Fourteen patients with scimitar syndrome, aged from 4 days to 20 years, underwent surgical treatment between September 1980 and August 1988. Patients were separated into two groups. Group A comprised four neonates with heart failure and severe pulmonary hypertension; part of the right lung was supplied by large aberrant systemic subphrenic arteries (ASSAs) in each. Group B included ten patients (nine children and one adult) with mild to moderate symptoms, normal pulmonary artery pressures; only two had ASSAs. In group A, one neonate with multiple ventricular septal defects underwent pulmonary artery banding but later required a lobectomy because of a lung abscess. The other three neonates underwent ligation of ASSAs; two improved rapidly, and one died of sepsis. In group B, all patients survived intracardiac repair and remain asymptomatic during a follow-up of 24 to 108 (mean 54.9) months. In summary, prognosis after intracardiac repair is excellent in patients without pulmonary hypertension. Neonates with heart failure usually improve after ligation of ASSAs, and pulmonary resection is only indicated in patients with intractable pulmonary sequestrations.
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PMID:Surgical management of the scimitar syndrome: an age-dependent spectrum. 807 75

During January 1989-September 1991, in India, neonatologists prescribed assisted ventilation (intermittent positive pressure ventilation [IPPV] and continuous positive airway pressure [CPAP]) for 90 neonates born and treated at a tertiary hospital in Delhi. All neonates requiring more than 168 hours of ventilation received IPPV. The smallest surviving neonate weighed 830 g at birth and was born at 26 weeks' gestation. This neonate received 510 hours of ventilation. One neonate received 48 days of ventilation (gestational age at birth, 28 weeks; birth weight, 800 g). This neonate eventually died due to necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), and sepsis. This infant was the only infant to develop NEC. A total of two newborns developed BPD. One infant developed retinopathy of prematurity (ROP). Indications for ventilation were hyaline membrane disease (HMD) (45/90), apnea (13/90), and transient tachypnea of the newborn (TTNB) (11/90). Almost all HMD cases who weighed more than 1.5 kg at birth on CPAP survived. CPAP successfully treated all TTNB cases. Nine neonates developed pneumothorax. Three of them survived. 34 neonates developed sepsis, the most common complication. 20 sepsis cases also had underlying pneumonia. Sepsis was responsible for 35% of deaths (14/40). Five infants on IPPV developed persistent pulmonary hypertension (persistent fetal circulation). 35 infants developed infection during ventilation, 34 of whom had a nosocomial infection. The nosocomial infection rate was 37.7%. Nosocomial infection was responsible for 35% of deaths. 12 babies (13%) developed pulmonary air leaks, 50% of whom died. 25 of the 33 infants on CPAP survived. Few CPAP cases developed pulmonary air leak, BPD, and ROP. Six of 22 very low birth weight (VLBW) infants (1 kg) survived. These findings led the researchers to recommend that medical centers with basic facilities for level II care should provide neonatal ventilation. They proposed that ventilation may not be cost effective for VLBW newborns, however.
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PMID:Three-year experience with neonatal ventilation from a tertiary care hospital in Delhi. 788 27


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