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

In 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. Groups were formed by randomization, such that the effects of prostaglandin E1 (0.1 microgram/kg/min) and MPS (30 mg/kg) could be analyzed separately and in combination. Eight animals treated with prostaglandin E1 were compared with eight animals not receiving prostaglandin E1. The same method was applied to the MPS group. E. coli infusion resulted in an abrupt increase in pulmonary arterial pressure while systemic blood pressure gradually fell. Cardiac output decreased. Gated blood pool studies showed an increase in right ventricular end-diastolic volume and a decrease in right ventricular ejection fraction. Consequently, right-to-left ventricular end-diastolic volume ratio increased. Pulmonary arterial pressure was lowered in the treatment groups compared to control group. During volume loading right ventricular ejection fraction improved in the prostaglandin E1 group but remained low in the MPS group. Compared to control group, cardiac output did not change and mean systemic arterial pressure significantly decreased in the prostaglandin E1 group. Treatment with prostaglandin E1, MPS, or both drugs and volume loading did not reveal any difference between the four groups with respect to cardiac output, right and left ventricular volumes, and left ventricular ejection fraction. The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.
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PMID:Effects of vasodilators prostaglandin E1 and methylprednisolone on pulmonary hypertension and right ventricular performance during volume loading in porcine septic shock: a combined invasive and radionuclide study. 329 78

Group B Streptococcus (GBS) sepsis in humans may cause the persistent pulmonary hypertension syndrome. Infusions of GBS in animals elevate pulmonary artery pressure (PAP) and resistance and are associated with elevated thromboxane levels. We investigated the hemodynamic effects of the specific thromboxane synthesis inhibitor, dazmegrel, in a piglet model of GBS-induced pulmonary hypertension. PAP rose from 22 +/- 6 to 42 +/- 11 (SD) mm Hg during infusion of heat-killed GBS; pulmonary vascular resistance increased from 1440 +/- 400 to 4000 +/- 1040 dyne X sec/cm5. No significant changes in cardiac output, mean arterial pressure, or left atrial pressure were noted. Treatment with 1 mg/kg of dazmegrel resulted in a rapid return of PAP and resistance to control values. No other hemodynamic effects of either bacteria or drug were observed despite continued infusion of GBS.
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PMID:Thromboxane synthesis inhibition reverses group B Streptococcus-induced pulmonary hypertension. 329 89

Results with mechanical circulatory assistance for the treatment of profound cardiopulmonary failure after conventional heart surgery have been encouraging. Its usefulness after heart transplantation is not known. Since August 1982, eight patients (of 59 transplant patients) have required support 0 to 48 hours (mean, 19.5 hours) after transplantation. The ages of the patients ranged from 7 days to 52 years (mean, 28.4 years). Underlying recipient heart disease was ischemic in three patients, congenital in two, cardiomyopathic in two, and rheumatic in one patient. Preoperative North American Transplant Coordinators Organization (NATCO) classification was status 9 in one patient (on extracorporeal membrane oxygenation [ECMO]), status 1 in five patients, and status 3 in two patients. Reasons for graft failure, although usually multifactorial, were primarily pulmonary hypertension with right ventricular failure in five patients and pneumonia, hyperacute rejection, and fat embolus in one patient each. In three patients, there was a mismatch in graft size (too small in two adults and too large in one neonate). Graft ischemic times ranged from 75 to 229 minutes (mean, 171 minutes). Two patients received mechanical support with an intra-aortic balloon (IAB), three with ECMO, and three with a right ventricular assist device (RVAD). One of the patients on ECMO and two of the patients with an RVAD also had IABs. Duration of support ranged from 4 hours to 8 days (mean, 3.2 days). Initial hemodynamic stability was achieved in all patients. Complications were common, including sepsis in seven patients and kidney failure in five patients. Only three patients were weaned. One patient with pulmonary hypertension, who was treated with ECMO, died 36 hours after being weaned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanical circulatory assistance after heart transplantation. 330 17

Pulmonary microvascular occlusive disease has been investigated using balloon occlusive pulmonary angiography in 31 patients with severe adult respiratory distress syndrome (ARDS) of different origins (14 patients with pneumonia, nine with multiple injury, eight with sepsis). Multiple pulmonary artery filling defects (PAFD) were detected in 13 (42%) patients, with a seven (78%) in nine incidence among those with posttraumatic ARDS. The presence of PAFD did not correlate with the severity of the respiratory failure, with the pulmonary hemodynamic alterations (pulmonary hypertension and increased vascular resistance), or with the final outcome (mortality rate was 54% among patients with PAFD and 61% among those with normal angiograms). These findings suggest that widespread pulmonary microthrombosis is a common event in patients with polytrauma and respiratory failure, with an important pathophysiologic role in the onset of posttraumatic ARDS.
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PMID:Pulmonary microthrombosis in severe adult respiratory distress syndrome. 334 22

In a patient who died of complications of severe pulmonary hypertension, right ventricular failure, and sepsis, antemortem two-dimensional (2-D) echocardiography and magnetic resonance imaging (MRI) studies demonstrated a right ventricular mass which at autopsy proved to be thrombus. The diagnostic features of this mass as imaged by these two methods are compared. This case was complicated in that the patient had a history of right atrial myxoma that had been successfully removed three years previously, and a history of several prior pulmonary emboli. Gated MRI depicted the size, shape, and surface characteristics of the mass more clearly than 2-D echocardiography because MRI provided better contrast and spatial resolution. Both techniques were useful in localizing the mass and showing if it was fixed or mobile. Depiction of tumor attachment was unclear with echocardiography but very clear with MRI. MRI also showed a left pulmonary artery thrombus that was not visualized by 2-D echocardiography. Both techniques provided chamber dimension measurements showing enlargement of the right atrium and ventricle. This case demonstrates that gated MRI provides high-quality images of cardiac anatomy and masses. Gated cardiac MRI should be considered at least complementary and potentially superior to two-dimensional echocardiography in the evaluation of intracardiac masses in certain patients.
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PMID:Comparison of gated cardiac magnetic resonance imaging and two-dimensional echocardiography for the evaluation of right ventricular thrombi: a case report with autopsy correlation. 339 69

Thromboxane A2 has been implicated as a mediator of cardiorespiratory dysfunction in sepsis. This study evaluated whether or not thromboxane A2 was necessary or sufficient for these adverse effects to occur during bacteremia. Fourteen adult swine under barbiturate anesthesia and breathing room air were monitored with arterial and pulmonary artery catheters. Animals were studied for 4 hours in three groups: group I, graded infusion of 10(9)/ml Aeromonas hydrophila; group II, Aeromonas hydrophila infusion plus SQ 29,548 (thromboxane A2 antagonist); and group III, U46619 (thromboxane A2 agonist) infusion in normal swine to pulmonary artery pressures observed in group I. Hemodynamic parameters, arterial and mixed venous blood gases, and plasma thromboxane B2 and prostaglandin 6-keto-F1 were measured. At sacrifice after 4 hours, wet-to-dry lung weights were calculated. Results indicated that thromboxane A2 was necessary and sufficient for the development of pulmonary hypertension and impaired alveolar-capillary oxygen diffusion in graded bacteremia. It was necessary but not sufficient for increased lung water to occur and sufficient but not necessary for decreased cardiac index and stroke volume index. Thromboxane A2 was neither sufficient nor necessary to the pathophysiology of systemic hypotension during graded bacteremia. Plasma prostaglandin 6-keto-F1 levels were increased in hypotensive animals with sepsis, suggesting its involvement in hypotension during sepsis.
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PMID:Thromboxane A2 mediates hemodynamic and respiratory dysfunction in graded bacteremia. 352 3

The effects of intravenous phenylephrine (PE) on aortic blood pressure (AOP), pulmonary artery pressure (PAP), and cardiac output (CO) were evaluated in piglets with normal PAP and piglets with sepsis-induced pulmonary hypertension. Anesthetized, ventilated piglets (1-4 weeks; n = 22) were divided into four groups - group 1 (n = 5) received group B beta streptococci (GBS) followed by PE (300 micrograms/kg); group 2 (n = 6) received GBS alone; group 3 (n = 6) received placebo infusion; group 4 (n = 5) received PE alone (300 micrograms/kg). Infusion of GBS in piglets (groups 1 and 2) elevated PAP by 149 and 176%, reduced CO by 34 and 28%, and did not affect AOP. Administration of PE (groups 1 and 4) raised AOP by 30 and 27% without significantly affecting PAP. However, CO fell after PE by 31 and 39%, respectively. If selective elevation of systemic blood pressure is to become an effective strategy for human newborns with right-to-left shunts caused by sepsis-induced pulmonary hypertension, agents other than PE, with less associated reduction of CO, need to be identified.
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PMID:Effects of phenylephrine on systemic and pulmonary artery pressure during sepsis-induced pulmonary hypertension in piglets. 353 Jun 73

Infusions of group B streptococci cause pulmonary hypertension in several neonatal animal models. A continuous infusion of prostaglandin D2 reduced the magnitude of this pulmonary hypertensive response; indomethacin completely blocked the response. Prostaglandin D2 or cyclooxygenase inhibitors may be important therapeutic agents for infants with group B streptococcal sepsis who manifest pulmonary hypertension.
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PMID:Influence of prostaglandin D2 on hemodynamic effects of group B streptococcus in neonatal lambs. 353 Jun 74

An evaluation was made of 106 surgical patients with Gram-negative septic shock, both for clinical criteria as well as the biochemical mediators endotoxin, prostaglandin F2 alpha, prostaglandin I2 (prostacyclin), and thromboxane. These data were correlated to various defined shock phases, functional data of vital organs, and clinical outcome. Patients underwent invasive organ function monitoring and the usual laboratory tests of intensive care. Prostaglandins and thromboxane were measured radioimmunologically, endotoxin by the limulus amebocyte lysate test. Endotoxin proved to be a more accurate predictor of severe sepsis than did positive blood cultures. Endotoxin as well as prostaglandins and thromboxane are predominantly released in early shock phases, appearing in plasma concentrations, which correlate with the severity of organ failure. Sepsis-induced respiratory failure coincides with a deterioration of pulmonary prostaglandin inactivation, which contributes to the release mechanism. High systemic prostacyclin activity benefits the patients' organ functions and clinical outcomes, while a predominance of thromboxane seems to effect the opposite. Transpulmonary-thromboxane gradients correlate significantly with pulmonary hypertension in the early phases of septic shock.
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PMID:The clinical significance of prostaglandins and thromboxane as mediators of septic shock. 355 Feb 66

Eleven of 30 patients with MCTD, followed for a mean of 10 years, developed immune complex nephropathy (five membranous, two mesangial, one mixed, and one sclerosing) with NS in nine of 11. Another patient had membranous nephropathy at autopsy. Patients with renal disease tended to have more systemic manifestations than those without. NS was at times of abrupt onset, recurrent, and/or persistent. Anti-RNP and serum complement were not helpful in predicting nephritis. Seventy-two percent of nephropathy and 62% of NS episodes resolved or improved after corticosteroid therapy. Five patients became hypertensive, two developed chronic renal failure and required chronic dialysis, and one needed acute dialysis twice. One patient progressed to focal proliferative crescentic nephritis with necrotizing arteritis. Three patients with nephropathy died, two of pulmonary hypertension with acute cor pulmonale and one of overwhelming sepsis. Nephropathy is relatively common in MCTD, is associated with substantial morbidity, and with the risk of hypertension and chronic renal failure.
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PMID:Renal involvement in mixed connective tissue disease: a longitudinal clinicopathologic study. 356 25


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