Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of central nervous system (CNS) complications was studied retrospectively in 150 patients with bacteremia caused by Staphylococcus aureus, Streptococcus pneumoniae, beta-hemolytic streptococci or Escherichia coli. The incidence and clinical manifestations of different CNS complications were noted during 1 month after the bacteremia. Special attention was paid to vascular complications (infarction or hemorrhage), infections (meningitis or brain abscess) and mental changes when they were the only signs of CNS origin (lowered level of consciousness, confusion or delirium). The risk of cerebral infarction was elevated in the patients with bacteremia during the first month after the positive blood culture as compared with the overall risk of stroke in the general population. 10/150 patients (7%) developed cerebral infarction during that month. Two of these cases were associated with bacterial meningitis and 1 with endocarditis. Mental changes as a main symptom of CNS origin occurred in 27% of patients with bacteremia. Increasing patient age predisposed to this complication. Mental changes were not associated with any bacterial species studied. Altogether 40% of the patients developed CNS complications, which were a significant risk factor for death during the first month after the bacteremia.
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PMID:Central nervous system complications in patients with bacteremia. 266 96

Twenty-six episodes of Pseudomonas aeruginosa bacteremia treated with intravenous ceftazidime, 4-6 g/day were evaluated. Treatment was begun within the first 24 hours after the isolation of the microorganism and was maintained for 10-12 days. In two patients with neutropenia amikacin was added during the initial 48-72 hours until the susceptibility to ceftazidime was known. All isolates were sensitive to ceftazidime. The most common underlying diseases were neoplasia (12), diabetes with stroke (4), neurosurgical and vascular procedures (4), rheumatoid arthritis (2), burns (2), cor pulmonale (1), and hypertension (1). The origins of bacteremia were urinary (12), pulmonary (9), and unknown (5). The infection was hospital-acquired in 77% and community-acquired in 23%. A critical clinical status and the presence of complications were significantly (p less than 0.01) associated with an increased mortality rate. Clinical outcome was good in 18/26 (70%), with a 30% mortality rate. The microbiological evolution showed 14 eradications, 6 persistences, 3 relapses and 3 colonizations. Resistance did not develop during therapy. Ceftazidime may be a good alternative therapy for these severe infections, although wider comparative studies are required for a better evaluation.
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PMID:[Evaluation of ceftazidime monotherapy in Pseudomonas aeruginosa bacteremias. Prospective study]. 268 60

In both neutropenic and normal dogs a significant and sustained fall in mean arterial pressure (MAP) occurred within 2 h (P less than .01) of the onset of E. coli bacteremia. The MAP remained depressed (P less than .001) in the neutropenic dogs while it increased to normal by 4 h in the control dogs. The fall in MAP was primarily related to a fall in total peripheral resistance (TPR). Although myocardial performance curves declined in both groups over the 4-h period, cardiac index (CI) and left ventricular stroke work index (LVSWI) were not significantly different from baseline in either group; nor was LV filling as assessed by the pulmonary artery wedge pressure (PAWP). No significant differences between groups were demonstrated between the mean pulmonary vascular resistance (PVR), dead space, shunt, or oncotic pressure for either group. A significant (P less than .01) percent reduction of arterial PO2 (PaO2) occurred in the neutropenic dogs. The pH of both groups fell during the course of the experiment and was significantly lower (P less than .02) in the neutropenic dogs at the termination of the study. A similar percent fall in platelet count, factor VIII, and fibrinogen levels was observed in both groups. Circulating endotoxin levels were paradoxically higher in normal animals and did not correlate with any hemodynamic alteration in either group--except that the earlier, higher endotoxin levels in the normal animals were associated with a more rapid decline in myocardial performance. However, the vasodilation of the neutropenic group was clearly related to the higher level of E. coli circulating since the concentration of E. coli in both groups at 4 h was significantly inversely correlated with the MAP (P less than .001).
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PMID:Effects of granulocytopenia on the hemodynamic responses of dogs during E. coli bacteremia. 330 Oct 52

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

We have modified our previously described experimental model of neonatal sepsis using group B beta hemolytic streptococci (GBS) in piglets and report here early and late hemodynamic responses to GBS infusion in the systemic, pulmonary, and mesenteric circulations. Piglets were anesthetized, intubated, and ventilated. Aortic blood pressure (AOP), pulmonary artery pressure (PAP), central venous pressure (CVP), left atrial pressure (LAP), cardiac index (CI), mesenteric blood flow index (MBFI), and heart rate (HR) were measured directly. Systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), mesenteric vascular resistance index (MVRI), and stroke volume index (SVI) were calculated. Sepsis was induced by continuous IV infusion of live GBS beginning at 0.5 X 10(7) organisms/kg/min. LAP was held constant throughout the sepsis protocol. PAP and PVRI were the most sensitive hemodynamic indices of early GBS sepsis, rising to greater than two times baseline levels within 11 min of the onset of bacteremia (approximately 1.0 X 10(8) cumulative organisms/kg). In contrast, AOP was unaffected during the first 83 min of GBS sepsis (approximately 25 X 10(8) organisms/kg) but fell from 84 to 47 mmHg in the final 31 min of the experiment. Both CI and MBFI fell monotonically as a function of cumulative GBS dose, reaching 72% and 64% of baseline at 55 min (approximately 12.5 X 10(8) organisms/kg) and 40% and 34% of baseline by 3 hr of sepsis (approximately 125 X 10(8) organisms/kg), respectively. At every GBS dose, the fall in CI was entirely accounted for by a reduction in SVI. SVRI, MVRI, and PVRI were elevated at all times during GBS sepsis. Despite a 34% reduction in systemic oxygen delivery during the first 83 min of GBS infusion (approximately 25 X 10(8) organisms/kg), arterial pH and base excess did not change significantly. Thereafter, pH fell monotonically reflecting the progressive development of metabolic acidosis.
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PMID:Early and late hemodynamic consequences of group B beta streptococcal sepsis in piglets: effects on systemic, pulmonary, and mesenteric circulations. 352 68

A synthesis of the postulated sequence of events for development of the inappropriate response of the myocardium to a demand for increased cardiac index is schematically represented in Fig. 10. In sepsis, bacteremia and/or the release of endotoxin activate the macrophages which release a spectrum of mediators. Some of these mediators (and possibly also endotoxin itself) have a negative influence on myocardial contractile function either directly and/or through altering cellular calcium flux. This results in impaired myocardial function manifested initially by decreased stroke volume. Subsequently, stroke volume will be either partially or completely restored to normal through the action of circulating catecholamines, the concentration of which is markedly elevated due to the presence of endotoxin and/or macrophage-produced mediators. Endotoxin and/or these mediators also act on the SA node increasing its sensitivity to beta-adrenergic stimulation. This will result in elevated heart rates. The latter, combined with the restored stroke volume, will yield an increased cardiac index which is the hallmark of the hyperdynamic phase of sepsis. In the cecal ligation and puncture model of sepsis, where cardiac index is maintained at the original level, the partially restored stroke volume and the elevated heart rate will combine to maintain cardiac index. Although this mechanism of increasing cardiac index through tachycardia is not energy efficient, the myocardium is able to cope with these changes and also to maintain its high energy phosphate concentrations, since the utilization of the three major myocardial substrates (fatty acids, lactate and glucose) is not affected by sepsis. Although this putative sequence of events is consistent with the observed experimental findings, further work is needed to substantiate its applicability to the etiology of myocardial dysfunction in man during sepsis.
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PMID:Myocardial dysfunction in sepsis. 361 52

A canine sepsis model that simulates the human cardiovascular response to septic shock was produced in 10 conscious unsedated dogs by implanting an Escherichia coli-infected clot into the peritoneum, resulting in bacteremia. By employing serial, simultaneous measurements of radionuclide scan-determined left ventricular (LV) ejection fraction (EF) and thermodilution cardiac index (CI), the end-diastolic volume index (EDVI) was calculated (EDVI = stroke volume index divided by EF). By using three different methods of quantifying serial ventricular performance (EF, shifts in the Starling ventricular function curve using EDVI vs. stroke work index, and the ventricular function curve response to volume infusion), this study provides evidence (P less than 0.01) that septic shock produces a profound, but reversible, decrease in systolic ventricular performance. This decreased performance was not seen in controls and was associated with ventricular dilatation (P less than 0.01); the latter response was dependent on an adequate volume infusion. Further studies of EDVI and pulmonary capillary wedge pressure during diastole revealed a significant, though reversible, shift (P less than 0.001) in the diastolic volume/pressure (or compliance) relationship during septic shock.
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PMID:Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock. 372 79

We studied the effects of systemic sepsis on peripheral microcirculatory fluid exchange by examining changes in flow (Qlymph) and lymph-to-plasma [L/P] total protein and albumin ratios from lymph draining, the efferent duct of a prefemoral lymph node in sheep, before and during surgically-induced peritonitis. After baseline study, peritonitis was produced by cecal ligation, perforation, and devascularization. By 24 hours blood cultures revealed a polymicrobial bacteremia. The hemodynamic response to the septic insult during the 72-hour study period was characterized by an increase in heart rate and an initial fall in stroke volume index; yet, the mean blood pressure remained unchanged from baseline levels throughout the study protocol. The intrapulmonary shunt fraction increased (p less than 0.05) by 48 hours, as did both the Qlymph (2.6 +/- 1.9 ml/hr to 6.8 +/- 4.6 ml/hr; p less than 0.05) and the calculated lymph albumin clearance (1.6 +/- 1.2 ml/hr to 3.1 +/- 1.7 ml/hr; p less than 0.05). Although the calculated serum to interstitial colloid osmotic pressure gradient fell (F = 4.37; p less than 0.04), both the [L/P] total protein and albumin ratios were unchanged from baseline throughout 72 hours of study. Further, [L/P] total protein ratios were unrelated to Qlymph (r = -0.20); as Qlymph (experimental/baseline) increased with sepsis, [L/P] total protein ratio (experimental/baseline) did not fall (r = +0.62). We therefore conclude that systemic sepsis, as represented by this model of bacterial peritonitis, results in increased peripheral microcirculatory fluid flux that is primarily a consequence of an increase in permeability of the peripheral microvascular exchanging membrane.
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PMID:Peripheral lymph flow in sheep with bacterial peritonitis: evidence for increased peripheral microvascular permeability accompanying systemic sepsis. 389 Feb 43

This study investigates the interaction of thromboxane, prostacyclin, and the hemodynamic dysfunction of graded bacteremia. Arterial, venous, and pulmonary artery catheters were inserted into eight adult female pigs under barbiturate anesthesia. After a 60-min control period Aeromonas hydrophila (1.0 X 10(9)/ml) was infused intravenously at 0.2 ml/kg/hr, increasing gradually to 4.0 ml/kg/hr at 4 hr. Hemodynamic measurements, blood gases, and radioimmunoassay of thromboxane B2 (TxB) and prostaglandin 6-keto-F1 (PGI) were performed during the control period, at 10, 20, 30, 45, 60, 75, and 90 min of bacteremia and at 30-min intervals thereafter. During the bacterial infusion, cardiac index (CI), mean arterial pressure (MAP), paO2, pvO2, stroke volume (SV), and left ventricular stroke work (LVSW) decreased significantly, and pulmonary vascular resistance (PVR), pulmonary artery pressure (PAP), and intrapulmonary shunt (Qs/Qt) increased significantly. TxB was significantly increased at 30 min and remained elevated thereafter. PGI did not rise above control levels until after 240 min of bacterial infusion. TxB cross-correlated most frequently with CI, PVR, SV, paO2, and Qs/Qt, changes in TxB preceding the other variables by 0-60 min. PGI cross-correlated significantly with MAP, LVSW, CI, paO2, and Qs/Qt, changes in PGI preceding MAP, LVSW, and CI by 0-60 min, but following paO2 and Qs/Qt by 30-60 min. TxB is increased early in graded bacteremia and appears related to cardiorespiratory dysfunction. PGI increases late in graded bacteremia, following the onset of respiratory failure, and may mediate the arterial hypotension of septic shock.
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PMID:Thromboxane, prostacyclin, and the hemodynamic effects of graded bacteremic shock. 391 37

Hemodynamic and respiratory effects of a continuous 5-h intravenous infusion of live Escherichia coli were studied in rats. Control animals were infused with saline. Rats infused with 1.8 +/- 0.4 X 10(10) bacteria/h did not survive a 5-h infusion. These animals developed early hypotension and reduced cardiac output (CO) measured by thermal dilution technique. Rats infused with 8.0 +/- 0.4 X 10(9) bacteria/h survived a 5-h infusion with hypotension and reduced CO occurring later in the course of bacteremia. Heart rate was markedly elevated in both septic groups. Arterial blood gas measurements revealed that partial pressure of O2 was not affected by bacteremia, but partial pressure of CO2 was significantly decreased. Arterial pH remained within the normal range indicating respiratory compensation of a metabolic acidosis. Since hypotension and reduced CO were accompanied by a fall in right atrial pressure (RAP) during bacteremia, a third septic group was studied to evaluate cardiac performance during volume loading. After 3-5 h of bacteremia, a 40% reduction in CO was associated with a significant drop in arterial pressure and RAP. Despite volume loading, ventricular stroke work and arterial pressure were significantly reduced compared with control animals. The results indicate that severe gram-negative bacteremia produces myocardial depression in the rat. This model can be useful for further studies of cardiac dysfunction during sepsis.
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PMID:Cardiopulmonary response of the rat to gram-negative bacteremia. 636 87


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