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

To examine the relative roles of passive factors (flow; filling pressures of left side of heart) and active factors (acidosis; arterial unsaturation) in the genesis of pulmonary hypertension when associated with sepsis, 37 patients with sepsis and 24 patients without sepsis were examined. Pulmonary hypertension was measured by the pulmonary arterial diastolic-pulmonary wedge pressure gradient (PAd-PWP gradient) and correlated reasonably with a standard formula for calculated resistance ([PA--PWP]/CI, where PA is mean pulmonary artery pressure and CI is cardiac index). In 22 of 37 patients, sepsis was associated with a significant degree of resistance to flow in the pulmonary circulation, as measured by the PAd-PWP gradient: and the higher the PAd--PWP gradient, the greater the likelihood of early death. None of the examined passive or active factors appeared to be adequate to explain pulmonary hypertension when present. By the use of previously derived formulae to estimate the compliance of the elastic pulmonary arteries, factors affecting this part of the pulmonary microcirculation could not be held accountable for apparent pulmonary hypertension. Therefore, the presence of pulmonary hypertension in sepis appears to be an active, rather than a passive, phenomenon and unrelated to arterial oxygen saturation or acid-base imbalance. Although the exact cause is unknown, pulmonary hypertension in sepis is associated with a high mortality and may be clinically followed by measurement of the PAd-PWP gradient.
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PMID:Pulmonary hypertension in sepsis: measurement by the pulmonary arterial diastolic-pulmonary wedge pressure gradient and the influence of passive and active factors. 64 8

Anisodamine, an anticholinergic drug, is widely used in China for treatment of infants with septic shock and has been reported to inhibit thromboxane synthesis in cultured cells. Thromboxane A2 plays an important role in the early pulmonary hypertension in sepsis; however, the role of thromboxane A2 later in sepsis is unclear. We tested the hypothesis that thromboxane A2 synthesis inhibition with dazmegrel, and cholinergic blockade with anisodamine, would attenuate the later phase of pulmonary hypertension induced by 4 h of group B streptococcus (GBS) infusion. 1 mg/kg of dazmegrel reversed the pulmonary hypertension and slightly increased cardiac output; these hemodynamic improvements persisted for 30-60 min. Plasma thromboxane B2 levels returned toward pre-GBS baseline values after dazmegrel treatment. Thus, thromboxane A2 is still a major mediator of pulmonary hypertension in piglets after 4 h of continuous GBS infusion. 0.5 mg/kg of anisodamine had no significant hemodynamic effect. 2 and 4 mg/kg of anisodamine each caused transient, dose-related decreases in systemic artery pressure; cardiac output also fell after the highest anisodamine dose. Pulmonary hypertension was not alleviated by anisodamine. All hemodynamic changes induced by anisodamine were short-lived and returned to preanisodamine values within 10 min. Anisodamine did not ameliorate thromboxane-mediated pulmonary hypertension in this animal model, and therefore may not inhibit thromboxane synthesis in vivo. The results of this study do not support the use of anticholinergic therapy to improve hemodynamics in GBS sepsis, but do suggest that thromboxane synthesis inhibition may be a clinically useful therapy in advanced GBS sepsis.
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PMID:Delayed thromboxane synthesis inhibition, but not cholinergic blockade, reverses group B streptococcus-induced pulmonary hypertension. 130 45

Group B beta-hemolytic streptococcus (GBS) infection is an important cause of neonatal pneumonia and sepsis. GBS infection is frequently associated with persistent pulmonary hypertension of the newborn. To better understand the early pulmonary hypertension phase of GBS-induced acute lung injury in a conscious animal, we characterized the pulmonary and systemic hemodynamic response of spontaneously breathing, chronically instrumented newborn lambs to injections of heat-killed type Ib GBS, 0.1-9.0 x 10(9) colony forming units. Heat-killed GBS caused marked dose-dependent increases in mean pulmonary arterial pressure and calculated pulmonary vascular resistance, 190 and 370% at the maximum dose, respectively. Similarly, GBS caused dose-dependent increases in mean systemic arterial pressure and systemic vascular resistance (28.5 and 108% at the maximum dose, respectively) and a decrease in cardiac output (33.5%). Arterial oxygen tension worsened at the higher doses. GBS-induced pulmonary hypertension was decreased by two structurally unrelated, putative leukotriene D4 receptor antagonists. Pretreatment with LY171883 blocked GBS-induced pulmonary hypertension by 95%, and WY48,252 attenuated this effect by 27%. Both drugs completely blocked the hemodynamic effects of exogenous leukotriene D4. For comparison, several lambs received bolus injections of live GBS, either alone or after pretreatment with LY171883. The hemodynamic response to live GBS and attenuation of that response by LY171883 were similar to those caused by similar doses of heat-killed GBS. Thus, bolus injections of heat-killed GBS provide a reproducible model of pulmonary hypertension in conscious newborn lambs. In addition, the sulfidopeptide leukotrienes appear to be important mediators of GBS-induced pulmonary hypertension in newborn lambs.
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PMID:Hemodynamic effects of heat-killed group B beta-hemolytic streptococcus in newborn lambs: role of leukotriene D4. 131 29

The type-specific polysaccharide capsule of group B streptococcus (GBS) is thought to be an important factor in the pathogenesis of disease. We used an acutely instrumented piglet model to assess the hemodynamic effects of rapid infusions of two heat-killed GBS type Ib strains isolated from the spinal fluid of an infant with late-onset meningitis and from the vaginal culture of his mother. These strains expressed different amounts of capsule, as determined by buoyant density centrifugation and electron micrographs, and they produced different hemodynamic effects in the piglets. The mother's strain, which had a smaller capsule, caused significantly higher increases in pulmonary artery pressure and vascular resistance than did the infant's strain, which had a larger capsule. Transposon mutants were then made from the infant's isolate to further study the role of capsule in pulmonary hypertension. Two mutants lacking detectable capsular type-specific polysaccharide were compared with the original isolate and with an isogenic mutant containing transposons but having a large capsule. The nonencapsulated mutants caused significantly higher changes in pulmonary artery pressure and resistance than did the encapsulated strains. Pulmonary hypertension may play a role in the pathophysiology of GBS sepsis, but the presence of a large capsule may partially cloak the hemodynamically active component(s) of the bacteria. The lower initial host response to heavily encapsulated GBS may play a role in pathogenesis by helping the organisms avoid host defense mechanisms.
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PMID:Role of capsule in pulmonary hypertension induced by group B streptococcus. 131 21

We report our experience from May 1985 to January 1991 with surgical complications and procedures performed in neonates on extracorporeal membrane oxygenation (ECMO) (218 venoarterial and 7 venovenous bypass). Eleven children older than 1 month were excluded. Total complications were 96 in 67 patients and included: bleeding (37), problems with initial cannula placement (17), thrombus formation (15), hemothorax, pneumothorax, or effusions (11), mechanical problems (11), and miscellaneous (5). Forty-eight procedures were performed in 37 patients while on ECMO. These were recannulation or reposition of cannulas (14), tube thoracostomy (11), cardiac surgery (6), cardiac catheterization (4), repair of congenital diaphragmatic hernia (5), thoracotomy (4), and others. Twenty-eight complications occurred in 15 of the 27 patients who died. Mortality rate was 12% for the entire group. Primary causes of death were hypoplastic lung (11), cardiac (8), sepsis (4), intraventricular hemorrhage (2), and pulmonary hypertension (2). No deaths were due solely to complications except for the two patients with intraventricular hemorrhage. Mortality in neonates who had complications while on ECMO was significantly higher (P less than .005) than in patients without complications. Hemorrhagic and thoracic complications were associated with higher mortality (P less than .001). Mortality was not affected by mechanical problems, thrombus formation, or catheter-related problems. While on ECMO cardiac defects, diaphragmatic hernia, lobar emphysema, and other conditions can be safely corrected. The use of echocardiography to position the cannulas, better control of coagulation factors and improvement in equipment may ultimately decrease complications.
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PMID:Surgical complications and procedures in neonates on extracorporeal membrane oxygenation. 140 45

One hundred ten infants with congenital diaphragmatic hernia (CDH) developed life-threatening respiratory distress in the first 6 hours of life. Associated anomalies were present in 33%. Twenty-eight of 65 infants (43%) treated before 1987 (pre-extracorporeal membrane oxygenation [ECMO] era) survived after immediate CDH repair, and mechanical ventilation with or without pharmacologic support. Only two of 16 (12.5%) infants requiring a prosthetic diaphragmatic patch survived. Since 1987, 31 of 46 (67.4%) infants with birth weight, gestational age, and severity of illness similar to the pre-1987 group survived. All patients were immediately intubated and ventilated. Seven (four with lethal chromosomal anomalies) infants died before treatment, and 30 stabilized (partial pressure of carbon dioxide [PCO2] < 50; partial pressure of oxygen [PO2] > 100; pH > 7.3) and underwent delayed CDH repair at 5 to 72 hours. Fifteen did well on conventional support and survived. Fifteen infants deteriorated after operation: 11 were placed on ECMO with eight survivors, and four infants were not considered ECMO candidates. Nine babies failed to stabilize initially and were placed on ECMO before CDH repair (alveolar-arterial gradient > 600 and oxygenation index > 40), and seven survived. The overall survival rate was 80% at 3 months in this ECMO-treated group. Early mortality was due to inability to wean from ECMO (one), intracranial hemorrhage (one), liver injury (one), and pulmonary hypoplasia (one). Nine of 11 babies requiring a prosthetic patch in the post-1987 ECMO group survived (81.8%). There were three late post-ECMO deaths (3 to 18 months) of right heart failure (two) and sepsis (one). Symptomatic gastroesophageal reflux occurred in nine cases, six requiring a fundoplication in the bypass babies. Recurrent diaphragmatic hernia occurred in nine cases (five ECMO). The overall survival rate was significantly improved in the delayed repair/ECMO group (67% versus 43%; p < 0.05) and was most noticeable in infants requiring a prosthetic diaphragm (81.2% versus 12.5%; p < 0.005). These data indicate that early stabilization, delayed repair, and ECMO improve survival in high-risk CDH. Early deaths are related to pulmonary hypertension and can be reversed by ECMO.
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PMID:Delayed surgical repair and ECMO improves survival in congenital diaphragmatic hernia. 141 95

Significant progress has been made since the first successful human heart-lung transplantation (HLT) for pulmonary vascular disease performed in 1981. The refinement of surgical techniques, use of cyclosporin as the main immunosuppressant, technique of distant organ procurement to expand the donor organ pool, and improved diagnosis and management of pulmonary infection and rejection have all contributed to this accomplishment. This has inevitably coincided with the extension of this procedure to other groups of patients with end stage heart and lung disease. Initially, HLT was offered to patients with cardiac disease associated with pulmonary hypertension. Because of the success, consideration was given to transplantation for parenchymal pulmonary diseases, initially pulmonary fibrosis and emphysema, and then suppurative lung disease such as in cystic fibrosis (CF). However, the application of HLT to patients with CF lagged behind because of concern related to the risk of sepsis, the systemic nature of the disease, malnourishment, and fear of recurrence of the epithelial CF defect in the transplanted lungs.
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PMID:Lung transplantation for cystic fibrosis. 145 9

Increased resistance in the pulmonary vessels in children with ventriculo-atrial shunts is a rare and often unrecognized permanent complication. We report 2 children in whom this diagnosis was detected by two-dimensional echocardiography. The first patient received a ventriculo-atrial shunt at age 9 days for congenital internal hydrocephalus. At 17 months it had to be replaced because of infection of the efferent catheter limb. At 22 months at a routine follow-up the echocardiographic diagnosis of pulmonary hypertension was made. Invasive studies confirmed the presence of irreversible increased resistance in the pulmonary circulation. The second patient received a ventriculo-atrial shunt at age 13 months because of a cerebral cyst. After repeated catheter infections, at 28 months a ventriculo-peritoneal shunt was placed. At age 4 years the diagnosis of pulmonary hypertension was made by routine echocardiography. This finding was confirmed by invasive studies. The left pulmonary artery was completely occluded. Both patients had developed microemboli, caused or aggravated by catheter sepsis, in the second case probably through contiguous clot growth up to complete occlusion of the left pulmonary artery. Therapeutic measures seemed not to be indicated. Two-dimensional echocardiography proved to be a reliable method for diagnosing increased resistance and pulmonary hypertension. We recommend routine echocardiography for follow-up in all children with ventriculo-atrial shunts.
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PMID:Echocardiographic proof of pulmonary hypertension with irreversible increased resistance in the pulmonary circulation as a complication after placement of a ventriculo-atrial shunt for internal hydrocephalus. 147 66

Unilateral thalamic bleeding with associated intraventricular hemorrhage is reported in three full-term neonates. The first presented within 48 hours from birth with early onset streptococcal meningitis, persistent pulmonary hypertension, tonic seizures and a tense fontanelle. The second presented 6 days after birth with irritability, opisthotonus, a tense fontanelle and tonic seizures. The third was admitted three days after birth with seizures and a tense fontanelle. In the latter two infants NMR and CT imaging documented thrombosed superficial and deep cerebral veins. The etiopathogenesis of intracranial venous thrombosis in the neonate is diverse: asphyxia, dehydration, polycythemia, sepsis-meningitis and difficult delivery are the main causes. In one of our patients jugular vein compression by the collar of a negative-pressure ventilation chamber probably initiated the intracranial events. More than half of the survivors sustain severe neurological impairment.
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PMID:Deep cerebral venous thrombosis in thalamo-ventricular hemorrhage of the term newborn. 150 40

It has been suggested that the effects of high-dose corticosteroid therapy (HDC) in gram-positive (G+) and gram-negative (G-) septicemia differ. As few data are available on HDC in G+ septicemia, pulmonary and cardiovascular function was studied for 44 hr in five anesthetized pigs subjected to brief infusion of live Staphylococcus aureus (approximately 10(11) cfu) followed by intravenous methylprednisolone (MP, 30 mg/kg) administered as a bolus every 8 hr. Comparisons were made with six septic pigs given no MP but otherwise identically managed. Six control pigs received no bacteria or MP. Infusion of bacteria induced identical transient pulmonary hypertension in both septic groups (52 +/- 7 mm Hg, mean +/- SD), but MPAP remained significantly lower in the pigs with MP (18 +/- 1 mm Hg vs. 30 +/- 9 mm Hg at 8 hr, P less than 0.05). MAP was better maintained in the MP group (107 +/- 9 mm Hg vs. 80 +/- 16 mm Hg at 8 hr, P less than 0.05). Pulmonary function also was less affected in the MP group at 8 hr, with significantly better maintenance of arterial oxygenation (13.5 +/- 1.2 kPa vs. 9.4 +/- 2.2 kPa, P less than 0.05) less venous admixture (11 +/- 6% vs. 34 +/- 23%, P less than 0.05) and superior lung-thorax compliance (29 +/- 5 ml/cm H2O vs. 15 +/- 5 ml/cm H2O, P less than 0.05). Five of five with MP survived, whereas two of six without MP survived (P = 0.045). MP thus attenuated pulmonary and hemodynamic abnormalities induced by S. aureus septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methylprednisolone improves pulmonary function and hemodynamics in experimental gram-positive septicemia. 151 6


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