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Biomedical subjects

B B Silver

Publications and source records attributed to B B Silver.

5 recordsLinked to original sources
PubMed1980

Intestinal distribution of Trichinella spiralis in rats.

Intestinal distribution of Trichinella spiralis was studied in mature and suckling Sprague-Dawley rats. Position of Trichinella along the small intestine was defined by a median value for the population. A range, 90% of total population, gave a relatively precise determination of microhabitat width. The normal position of Trichinella following an oral infection is in the duodenum, but position of Trichinella in mature rats is more anterior than position of Trichinella in suckling rats. Intestinal inoculation of Trichinella larvae into the jejunum and ileum revealed that worms remained at the site of inoculation and did not migrate to the duodenum. Trichinella is able to utilize the entire small intestine but its normal position is the duodenum. The position of Trichinella in the anterior region of the small intestine probably is related to physiological factors of the intestine and thereby host dominated.

Aging↗
PubMed1980

Concurrent infections of Hymenolepis diminuta and Trichinella spiralis in the rat intestine.

The intestinal distribution of Trichinella spiralis and Hymenolepis diminuta in rats was studied in single and concurrent infections. Results showed that the location of T. spiralis was not significantly changed in concurrent infections, but higher populations of T. spiralis in single and concurrent infections resulted in a posterior shift in position. Trichinella spiralis affected H. diminuta distribution significantly by causing a posterior shift in the position of scoleces and biomass and a loss of circadian rhythm. Infection with 4,000 T. spiralis larvae resulted in decreased tapeworm weight and fecundity, and destrobilation of H. diminuta from day 8 to 18 of the T. spiralis intestinal stage. Hymenolepis diminuta moved anteriorly to its preferred microhabitat as the T. spiralis intestinal stage decreased.

Animals↗
PubMed1979

Hepatic cellular hypoxia in murine peritonitis.

Reduced oxygen consumption and lactic acidosis were observed frequently in patients with peritonitis. This study was designed to evaluate whether reduced oxygen consumption is secondary to deficient oxygen delivery or is a function of primary injury to mitochondria. Peritonitis was produced in rats by cecal ligation and perforation. Animals were killed at 2, 4, and 6 hours and agonally. Oxygen utilization was studied polarographically in isolated hepatic mitochondria with glutamate, pyruvate, and succinate substrates. State 3, state 4, respiratory control index (RCI), and ADP:O ratios were determined. Whole tissue and isolated mitochondrial ultrastructure were examined by electron microscopy. Systemic blood pressure and oxygenation were monitored. Hepatic tissue oxygenation was examined using a surface oxygen electrode. Peritonitis resulted in acceleration of state 3 respiratory rates and increased respiratory control indices at all time intervals. Maximal respiratory control was observed at 4 hours with all substrates. Whole tissue mitochondria demonstrated mild swelling and thinning of membranes and matrix. Experimental and control isolates showed similar orthodox-to-condensed conformational changes. Hepatic tissue oxygenation declined to less than 10% of control by 6 hours, while arterial Po2 was unchanged. The conclusions of this study are that lethal peritonitis results in (1) no primary injury to the hepatic mitochondria, (2) increased efficiency of hepatic mitochondrial oxygen utilization, and (3) reduced hepatic tissue oxygenation. The exact mechanisms of defective oxygen delivery require further study.

Animals↗
PubMed1975

Pathological accumulation of calcium by mitochondria: modulation by magnesium.

Magnesium causes a marked decrease in the initial rates of respiration-supported calcium uptake by isolated heart mitochondria. Differential responses of mitochondrial respiration and cytochrome b redox states in the presence and absence of magnesium indicate that with magnesium present, heart mitochondria retain the ability to phosphorylate ADP after calcium uptake. Electron microscopy of the isolated mitochondria after calcium accumulation revealed markedly different crystal structures within the matrix space depending on the presence or absence of magnesium. The results suggest a "protective" effect of magnesium on the phosphorylating mechanism of mitochondria during active calcium uptake. Further, magnesium appears to determine the type of crystal structure formation within the intramitochondrial compartment.

Animals↗