pituitrin and Bacterial-Infections

Pneumonia is one of the most serious infections in the neonate and is responsible for a large percentage of neonatal mortality. Pneumonia in a premature or term infant who is debilitated by an underlying problem such as hyaline membrane disease carries an extremely high morbidity and mortality. Since most of the bacterial pneumonias are treatable, early recognition and diagnosis and vigorous treatment are essential. X-ray findings, though helpful, serve only as a guideline. Prognosis is adversely affected if pneumonia results in generalized sepsis, leading to meningitis, disseminated intravascular coagulation, and osteomyelitis. Prompt antibiotic treatment should be begun before the etiologic agent or drug susceptibility is known.

Topics: Acute Disease; Ampicillin; Bacterial Infections; Gentamicins; Humans; Infant, Newborn; Infant, Newborn, Diseases; Kanamycin; Penicillins; Pneumonia; Pneumonia, Aspiration; Pneumonia, Viral; Syphilis, Congenital; Tuberculosis, Pulmonary; Vasopressins

Clinical and experimental studies with LPS injection have shown an increase in vasopressin (AVP) secretion in the early phase of severe sepsis, which is subsequently reduced despite persistent hypotension. The aim of this study was to evaluate the role of inducible nitric oxide synthase (iNOS)-derived NO in hypothalamic activation and in AVP release during severe sepsis induced by cecal ligation and puncture (CLP). Male Wistar rats received i.p. injections of aminoguanidine, an iNOS inhibitor, or saline 30 min before CLP or sham surgeries (controls). CLP led to increased plasma nitrate levels, protein leakage and hypotension and caused mortality of 80% by 24 h. Expression of c-fos in paraventricular (PVN), supraoptic (SON) and organum vasculosum of lamina terminalis (OVLT) nuclei, as well as plasma AVP concentration were increased at 6 h but reduced to basal levels 24 h after CLP. Aminoguanidine pre-treatment prevented the increase in plasma nitrate levels and hypotension in the first 6 h. It also reduced AVP secretion and hypothalamic c-fos expression. After 24 h, the pre-treatment reduced plasma nitrate levels, protein leakage and caused a partial recovery of c-fos expression in SON and OVLT but did not affect AVP release. Furthermore, mortality was reduced to 43%. We conclude that during the early phase of severe sepsis hypotension caused by the iNOS-derived NO is partially responsible for the hypothalamic activation and AVP release. In the late phase, however, the iNOS-derived NO prevents brain activation blunting AVP secretion contributing to hypotension, irreversible shock and animal death.

Topics: Animals; Bacterial Infections; Blood Pressure; Drinking; Enzyme Inhibitors; Gene Expression Regulation; Guanidines; Hypothalamus; Immunohistochemistry; Male; Nitric Oxide; Nitric Oxide Synthase Type II; Osmolar Concentration; Proto-Oncogene Proteins c-fos; Radioimmunoassay; Rats; Rats, Wistar; Sepsis; Time Factors; Vasopressins

Intra-abdominal sepsis was induced in rats by implanting into their abdominal cavities fecal-agar pellets impregnated with Escherichia coli and Bacteroides fragilis. Sham-operated rats received sterile pellets. A group of sterile- and septic-implanted rats was treated intraperitoneally with diltiazem (1.2 mg/kg) 8 h after implantations. Septic- and sterile-implanted rat hepatocytes were loaded with 1) the fluorescent dye indo-1 to quantify hepatocyte basal and vasopressin (100 nM)-elevated cytosolic Ca2+ concentration and 2) 45Ca to quantify Ca2+ flux and cellular content of exchangeable Ca2+. Lipid peroxidation was determined by measuring conjugated dienes (CD) and thiobarbiturate-reactive substances (TBA-RS) in liver homogenates. In septic-implanted rats, the basal cytosolic [Ca2+], cellular exchangeable Ca2+, Ca2+ flux, CD, and TBA-RS were significantly higher than in sterile-implanted rats. Although vasopressin caused a significant elevation in cytosolic [Ca2+] in septic rat hepatocytes, the magnitude of this elevation was significantly smaller than that found in the sterile group. Diltiazem treatment of septic rats significantly decreased basal cytosolic [Ca2+], cellular exchangeable Ca2+ content, Ca2+ flux, CD, and TBA-RS. Also, vasopressin-induced increase in hepatocyte cytosolic [Ca2+] in diltiazem-treated septic rats was significantly greater than that observed in untreated septic rats. Both Ca2+ and membrane lipid alterations were attenuated with diltiazem treatment of septic rats. These results suggest that prevention or attenuation of Ca2+ channel-mediated Ca2+ influx restores both Ca2+ homeostasis and membrane lipid alteration.

Topics: Abdomen; Animals; Bacterial Infections; Calcium; Diltiazem; Liver; Male; Rats; Rats, Sprague-Dawley; Reference Values; Thiobarbiturates; Vasopressins

We measured urine vasopressin (VP) once daily on days 1 through 3 in 18 patients hospitalized with meningitis. Urine VP values were 215 +/- 100, 116 +/- 44, and 69 +/- 23 pg/mL on days 1 through 3, respectively, for children with bacterial meningitis and 34 +/- 14, 20 +/- 4, and 15 +/- 4 pg/mL for those with aseptic meningitis. Urinary VP levels of infants with bacterial meningitis were significantly greater than those of healthy ambulatory subjects (n = 18) on all three study days; VP values of infants with bacterial meningitis were also greater than those of infants with aseptic meningitis on study days 2 and 3. The VP levels for the subjects with aseptic meningitis were significantly greater than those of the controls on day 1 only. None of the infants exhibited the clinical syndrome of inappropriate antidiuretic hormone secretion.

Topics: Bacterial Infections; Humans; Inappropriate ADH Syndrome; Infant; Meningitis; Meningitis, Aseptic; Osmolar Concentration; Risk Factors; Sodium; Time Factors; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone has been associated with many pulmonary diseases, including tuberculosis and bacterial and viral pneumonia: however, it has not been reported with anaerobic infections or empyema in the absence of pneumonia. We report a patient with empyema due to Bacteroides melaninogenicus, Bacteroides oralis, and Peptostreptococcus who developed the syndrome. Eight hours before the start of therapy, his serum sodium concentration was 127 mEq per liter; serum osmolality, 255 mOsm per kg; urine osmolality, 522 mOsm per kg; urinary sodium concentration, 39 mEq per liter. The creatinine clearance and the adrenocorticotropic hormone stimulation test were normal, and there was no evidence of dehydration. No other causes of the syndrome of inappropriate secretion of antidiuretic hormone were apparent. With drainage and antimicrobial drug therapy, the empyema cleared, and the syndrome resolved in 8 days. The patient has been well, without evidence of inappropriate secretion of antidiuretic hormone, for 9 months. Anaerobic infections and/or empyema without pneumonia can be associated with the syndrome of inappropriate secretion of antidiuretic hormone.

Topics: Adult; Anaerobiosis; Bacterial Infections; Bacteroides Infections; Empyema; Humans; Hyponatremia; Male; Osmolar Concentration; Peptostreptococcus; Prevotella melaninogenica; Syndrome; Vasopressins

Two patients developed spontaneous bacterial peritonitis after infusions of vasopressin into the superior mesenteric or gastroduodenal arteries for upper gastrointestinal hemorrhage. The peritonitis in these patients differed from the typical picture in which a single aerobic organism is responsible, by the presence of multiple organisms, some of which were anaerobic. These findings suggest that the arterial vasoconstriction decreased the integrity of the intestinal mucosal barrier and permitted the transmural migration of enteric organisms from the lumen of the bowel into the ascites-filled peritoneal cavity.

Topics: Anaerobiosis; Arteries; Ascitic Fluid; Bacterial Infections; Duodenum; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Intestines; Male; Mesenteric Arteries; Middle Aged; Peritonitis; Stomach; Stomach Ulcer; Vasopressins