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

No therapeutic agent consistently decreases pulmonary arterial pressure (PAP) more than aortic pressure in neonates with persistent pulmonary hypertension of the newborn. We have investigated whether nitroglycerin (NG) or nitroprusside (NP) selectively decreases PAP in an animal model of sepsis-induced pulmonary hypertension. Piglets were anesthetized, intubated, and ventilated. Pulmonary hypertension was induced by an iv infusion of group B Streptococci. Piglets were then divided into three groups with group B Streptococci infusion ongoing. Neither PAP nor the pulmonary vascular resistance index was decreased significantly by either NP or NG. NP decreased significantly both mean aortic pressure and the systemic vascular resistance index. Cardiac index decreased significantly during both NG and placebo infusion. These data suggest that neither NP nor NG is likely to be beneficial in sepsis-induced pulmonary hypertension in newborns.
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PMID:Neither nitroglycerin nor nitroprusside selectively reduces sepsis-induced pulmonary hypertension in piglets. 311 93

We studied the effects of prostaglandin D2 (PGD2) in six newborn infants, 1 to 2 days of age, who had persistent pulmonary hypertension syndrome and a PaO2 less than 75 torr during mechanical hyperventilation with an inspired oxygen concentration of 100%. Tolazoline and dopamine were used to treat some of the patients. No patients had congenital heart disease or sepsis. Catheters were placed to measure pulmonary and systemic arterial blood pressures. PGD2 was infused intravenously at doses of 1 to 25 micrograms/kg/min. Pulmonary and systemic arterial blood pressures, heart rate, and descending aortic blood gas values were measured before each dose change. Only two of six patients had a transient increase in PaO2. All had an increase in heart rate. Two of six patients had an increase in pulmonary arterial blood pressure. No deleterious effects occurred during the infusion. Four of six patients subsequently died. Although PGD2 is a specific pulmonary vasodilator in fetal and newborn animals, it did not lower pulmonary arterial blood pressure nor improve oxygenation in newborn infants with persistent pulmonary hypertension syndrome.
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PMID:Effects of prostaglandin D2 on pulmonary arterial pressure and oxygenation in newborn infants with persistent pulmonary hypertension. 316 78

Live Pseudomonas aeruginosa (2.5.10(9).kg-1.h-1) were administered to awake (Group A, n = 10) and anesthetized piglets, which were given intravenous ketamine (Group K, 10 mg.kg-1.h-1, n = 8) or pentobarbital (Group P, 15 mg.kg-1.h-1, n = 8). The anesthetized animals were mechanically ventilated. In addition, a pentobarbital group (Group CP, n = 6) and a ketamine control group (Group CK, n = 6) were studied. The mean survival time was 10.5 +/- 3.0 h in Group A, 10.6 +/- 2.8 h in Group K, and 1.8 +/- 1.3 h in Group P. In Group P the arterial pressure, the cardiac output and the systemic vascular resistance declined soon after start of the bacterial infusion, whereas the pulmonary artery pressure increased. The animals died of irreversible circulatory failure. In Group K pronounced pulmonary hypertension and lethal pulmonary edema developed. There was no circulatory failure in Group A, but the animals also died of marked pulmonary edema. Groups CP and CK exhibited stable hemodynamics for a period of 8 h. The results of this study suggest a deleterious effect of pentobarbital on hemodynamics and survival time, and a minor suppressive action of ketamine on the circulation in septicemia. Therefore, data obtained from septic shock studies applying pentobarbital have to be evaluated carefully. Investigation of the effects of gram-negative bacteria or endotoxin should be performed in unanesthetized or, if anesthesia is necessary, in ketamine-anesthetized animals.
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PMID:Comparison of ketamine and pentobarbital anesthesia with the conscious state in a porcine model of Pseudomonas aeruginosa septicemia. 318 20

Inhalation injury increases the likelihood of sepsis. We tested the hypothesis that preexisting inhalation injury would diminish bacterial clearance across the pulmonary vasculature and induce greater hemodynamic response. Live Pseudomonas aeruginosa were infused centrally for one hour in three groups of awake sheep. Inh + Ps (n = 10), with a seven to 10-day-old inhalation injury; Ps-LOW (n = 8) both received 10(7) Ps/min; and Ps-HI (n = 9) received 5 x 10(7) Ps/min. for one hour. Pulmonary hypertension was more severe in Ps-HI and Inh + Ps. A hyperdynamic response with high cardiac index and low mean arterial pressure developed in Inh + Ps and Ps-HI from six to 18 hr, while Ps-LOW, only the cardiac index was elevated at six to eight hr. The Inh + Ps and Ps-LOW groups had equivalent pulmonary artery and aortic bacterial levels, while Ps-HI had levels approximately five times higher. All groups removed bacteria efficiently in the lungs. However, preexistent inhalation injury exaggerated the pulmonary and systemic hemodynamic response.
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PMID:Effect of preexisting inhalation injury on response to bacteremia in sheep. 319 2

There were 37 maternal deaths among the 109,221 livebirths registered during the period 1977-86 in Bahrain, Arabian Gulf. The maternal mortality rate was 33.9/100,000 for the 10-year study period; however, disaggregation reveals a decline in this rate from 42.3/100,000 in 1977-81 to 26.9/100,000 in 1982-86. This decline presumably reflects streamlining of the Ministry of Health's maternity services, including a central maternity hospital with all modern facilities that serves as a referral center for all of Bahrain, 2 peripheral hospitals with provision for blood transfusion and surgical deliveries, and 3 maternity units managed by fully qualified midwives. About 80% of deliveries are covered by these maternity services; only 2.5% of deliveries occur in the home. Despite this highly developed maternity care system, 18 of the maternal deaths were due to direct obstetric cause: hemorrhage, 7; pre-eclampsia and eclampsia, 5; abortion septicemia, 2; bowel perforation during cesarean section, 1; thromboembolism, 2; and amniotic fluid embolism, 1. The causes of the 19 indirect maternal deaths were: pulmonary embolism, 5; infection, 7; cardiac failure, 2; cerebrovascular accident, 2; pulmonary hypertension, 1; and uncertain, 2. Of interest is the finding that sickle cell disease was the underlying cause of maternal death in 12 of the 37 deaths in this series. Sickle cell disease was implicated in 3 of the deaths from hemorrhage, all 5 deaths from pulmonary embolism, 2 deaths from septicemia, and the 2 cases of cardiac failure. In this series, 50% of the patients with sickle cell disease had thromboembolic crises following treatment of anemia with packed cell transfusion. Blood transfusion, especially of packed cells, should be given with caution to these patients since it may precipitate vaso-occlusive crisis by increasing blood viscosity. Since sickle cell disease represents a high risk during pregnancy in this Arab population, such patients should have frequent prenatal check-ups and deliver in a well-equipped hospital.
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PMID:Maternal mortality in Bahrain with special reference to sickle cell disease. 321 81

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

Lipid X (2,3-diacylglucosamine-1-phosphate) is a novel monosaccharide precursor of lipid A that has some of the physiologic activities of endotoxin but little toxicity. To determine whether lipid X would interfere with the toxic effects of endotoxin, we pretreated sheep with either 100 or 200 micrograms of lipid X per kg of body weight and then challenged them with a potentially fatal dose of Escherichia coli endotoxin (20 micrograms/kg). Twenty-one sheep underwent pulmonary artery catheterization and were monitored for changes in pulmonary artery pressure, temperature, pH, partial O2 pressure, partial CO2 pressure, blood pressure, and cell counts over 7 h. Overall mortality for control animals was 37% versus 5.3% for pretreated animals. None of the 13 animals pretreated with 100 micrograms of lipid X per kg died. These differences in survival were significant (P less than 0.05). Animals pretreated with 100 micrograms of lipid X per kg had significantly lower pulmonary artery pressure during both phases 1 and 2 of endotoxin-induced pulmonary artery hypertension. A higher dose of lipid X, 200 micrograms/kg, produced pulmonary hypertension. Perhaps because lipid X is a subunit of lipid A, lipid X shows a partial pyrogenic effect while also decreasing the pyrogenic activity of complete lipopolysaccharide (LPS). Lipid X did not prevent endotoxin-induced neutropenia or moderate hypotension in response to LPS. Lipid X is a potential prototype compound for a new type of chemotherapy directed at blocking the harmful effects of LPS during bacterial septicemia.
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PMID:Lipid X ameliorates pulmonary hypertension and protects sheep from death due to endotoxin. 330 7

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


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