The cell wall structure of Selenomonas ruminantium

The cell wall structure of Selenomonas ruminantium subsp. lactilytica Str GA192 and subsp. ruminantium Str PC18 was examined. Whole cell walls of strain GA192 contained: - 11% total carbohydrate; 1% phosphorus; rhamnose; fucose; mannose; glucose; galactose; glucosamine; galactosamine; muramic acid; and two unidentified amino sugars; while Str PC18 walls contained 10% total carbohydrate; 0.9% phosphorus; mannose; glucose; galactose; glucosamine; galactosamine; muramic acid and two unidentified amino sugars. The peptidoglycan layer of Str GA192 was purified by extraction with sodium dodecyl sulphate and phenol. It contained: muramic acid; glucosamine; alanine; glutamic acid and diaminopimelic acid; indicating that the peptidoglycan structure is similar to that of other gram negative bacteria. Lipoprotein does not appear to be a major component of this peptidoglycan. Two lipopolysaccharides (LPS) were extracted from PC18 cell walls with phenol/water. One lipopolysaccharide appeared in the aqueous phase (PC18Aq) and one in the phenol phase (PC18Phe). One phenol phase lipopolysaccharide (GA192Phe) and one aqueous phase polysaccharide (GA192Aq) were extracted from str GA192 walls. All three lipopolysaccharides contained mannose, glucose, heptose, 3-deoxy-octulosonic acid, glucosamine and galactosamine in common. The main fatty acids were C₁₁:₀' C₁₃:₀ and 30H C₁₃:₀ . Both PC18 lipopolysaccharides contained a second heptose which was not present in GA192Phe . Sugars unique to each lipopolysaccharide were; PC18Aq, two unidentified amino sugars; GA192Phe, fucose. Each of the phenol soluble lipopolysaccharides could be further separated into chloroform/methanol soluble and insoluble fractions. GA192Aq contained rhamnose, glucose and two unidentified amino sugars. A glycogen/amylopectin type polysaccharide (presumably the main storage polysaccharide) was isolated from the cytoplasmic fraction of each strain. The results are discussed in terms of known LPS structure and data previously published for S. ruminantium

Antecedent hypertension and heart failure after myocardial infarction

AbstractObjectivesWe sought to assess the relationship of antecedent hypertension to neurohormones, ventricular remodeling and clinical heart failure (HF) after myocardial infarction (MI).BackgroundHeart failure is a probable contributor to the increased mortality observed after MI in those with antecedent hypertension. Hence, neurohormonal activation, adverse ventricular remodeling and a higher incidence of clinical HF may be expected in this group. However, no previous report has documented serial postinfarction neurohumoral status, serial left ventricular imaging and clinical outcomes over prolonged follow-up in a broad spectrum of patients with and without antecedent hypertension.MethodsInpatient events were documented in 1,093 consecutive patients (436 hypertensive and 657 normotensive) with acute MI. In 68% (282 hypertensive, 465 normotensive) serial neurohormonal sampling and radionuclide ventriculography were performed one to four days and three to five months after infarction. Clinical outcomes were recorded over a mean follow-up of two years.ResultsPlasma neurohormones were significantly higher in hypertensives than in normotensives one to four days and three to five months after infarction. From similar initial values, left ventricular volumes increased significantly in hypertensives, compared with normotensives. Left ventricular ejection fraction rose significantly in normotensive but not hypertensive patients. Together with higher inpatient (8.1% vs. 4.4%, p < 0.002) and post-discharge mortality (9.5% vs. 5.5%, p = 0.043), hypertensive patients incurred more inpatient HF (33% vs. 24%, p < 0.001) and more late HF requiring readmission to hospital (12.4% vs. 5.5%, p < 0.001). Antecedent hypertension predicted late HF in patients >64 years of age with neurohormonal activation and early left ventricular dilation.ConclusionsAntecedent hypertension interacts with age, neurohumoral activation and early ventricular remodeling to confer greater risk of HF after MI

Urocortin 2 Infusion in Healthy Humans Hemodynamic, Neurohormonal, and Renal Responses

ObjectivesWe sought to examine the effects of urocortin (UCN) 2 infusion on hemodynamic status, cardiovascular hormones, and renal function in healthy humans.BackgroundUrocortin 2 is a vasoactive and cardioprotective peptide belonging to the corticotrophin-releasing factor peptide family. Recent reports indicate the urocortins exert important effects beyond the hypothalamo-pituitary-adrenal axis upon cardiovascular and vasohumoral function in health and cardiac disease.MethodsWe studied 8 healthy unmedicated men on 3 separate occasions 2 to 5 weeks apart. Subjects received placebo, 25-μg low-dose (LD), and 100-μg high-dose (HD) of UCN 2 intravenously over the course of 1 h in a single-blind, placebo-controlled, dose-escalation design. Noninvasive hemodynamic indexes, neurohormones, and renal function were measured.ResultsThe administration of UCN 2 dose-dependently increased cardiac output (mean peak increments ± SEM) (placebo 0.5 ± 0.2 l/min; LD 2.1 ± 0.6 l/min; HD 5.0 ± 0.8 l/min; p < 0.001), heart rate (placebo 3.3 ± 1.0 beats/min; LD 8.8 ± 1.8 beats/min; HD 17.8 ± 2.1 beats/min; p < 0.001), and left ventricular ejection fraction (placebo 0.6 ± 1.4%; LD 6.6 ± 1.5%; HD 14.1 ± 0.8%; p < 0.001) while decreasing systemic vascular resistance (placebo −128 ± 50 dynes·s/cm5; LD −407 ± 49 dynes·s/cm5; HD −774 ± 133 dynes·s/cm5; p < 0.001). Activation of plasma renin activity (p = 0.002), angiotensin II (p = 0.001), and norepinephrine (p < 0.001) occurred only with the higher 100-μg dose. Subtle decreases in urine volume (p = 0.012) and natriuresis (p = 0.001) were observed.ConclusionsBrief intravenous infusions of UCN 2 in healthy humans induced pronounced dose-related increases in cardiac output, heart rate, and left ventricular ejection fraction while decreasing systemic vascular resistance. Subtle renal effects and activation of plasma renin, angiotensin II, and norepinephrine (at high-dose only) were observed. These findings warrant further investigation of the role of UCN 2 in circulatory regulation and its potential therapeutic application in heart disease