Biomedical subjects
D L Fritz
Publications and source records attributed to D L Fritz.
Different high-frequency ventilator strategies: effect on the propagation of tracheobronchial histopathologic changes.
To assess the role of high-frequency ventilator strategy in the propagation of airway injury, we compared the tracheobronchial histologic alterations in 20 newborn piglets ventilated for 8 hours with high-frequency flow interruption (HFFI). Ten animals were assigned to HFFI with a strategy of continuous pulsations at a frequency of 10 Hz and a mean airway pressure of 16 cm H2O. Ten piglets were treated at identical settings except for 10 one-second baseline pauses per minute to a positive end-expiratory pressure of 5 cm H2O. A semiquantitative scoring system was used to grade light microscopic tissue alterations in the trachea, carina, and mainstem bronchi. Ultrastructural changes were evaluated with scanning electron microscopy. The HFFI-continuous-treated piglets had significantly more damage in all areas than the HFFI-baseline pause group (P less than .001). The upper tracheas of animals in both groups were altered to a greater extent than the lower tracheas (P less than .007). In addition, numerous "skip" areas of injury were noted throughout the tracheas. High-frequency ventilator strategy is a determinant of the severity of airway histologic changes. Factors that adversely affect tissue oxygenation or cause direct mechanical trauma may also influence the degree of injury. Optimal operating characteristics and limitations of different high-frequency devices must be assessed before their use in human neonates.
Determinants of tracheobronchial histologic alterations during conventional mechanical ventilation.
It was hypothesized that diverse mechanisms may influence upper airway injury during mechanical ventilation. To assess the roles of several factors in the propagation of such injury, the tracheobronchial histologic changes in 53 newborn piglets were compared following conventional positive pressure ventilation. Eight animals were assigned to each of four positive pressure ventilation groups at "low" settings (an FiO2 of 0.25, a frequency of 10 breaths per minute, a peak inspiratory pressure of 20 cm H2O, a positive end-expiratory pressure of 4 cm H2O, a flow rate of 10 L/min, and an inspiratory time to expiratory time ratio of 1:2): (1) positive pressure ventilation with no hypotension or hypoxemia; (2) positive pressure ventilation with hypotension; (3) positive pressure ventilation with hypoxemia; and (4) positive pressure ventilation with both hypotension and hypoxemia. In addition, eight piglets were assigned to each of two positive pressure ventilation groups at "high" settings (greater frequency [40 breaths per minute], higher peak inspiratory pressure [40 cm H2O], and greater flow rate [17 L/min]): (1) positive pressure ventilation with no hypotension or hypoxemia; and (2) positive pressure ventilation with both hypotension and hypoxemia. The changes were mild and similar among the first three positive pressure groups at low settings. However, the injury scores of the combined hypotension and hypoxemia group (group 4) were greater than those of the former three positive pressure ventilation groups (P less than .004). The piglets receiving positive pressure ventilation at high settings with no hypotension or hypoxemia (group 5) had no more injury than those in the first three groups receiving positive pressure ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
Characterization of the plasmid from Escherichia coli RDEC-1 that mediates expression of adhesin AF/R1 and evidence that AF/R1 pili promote but are not essential for enteropathogenic disease.
RDEC-1, an Escherichia coli strain that adheres to rabbit mucosa and causes an attaching, effacing lesion, expresses the pilus adhesin AF/R1 which determines in vitro attachment to rabbit intestinal brush borders. In order to determine the role of AF/R1 pili in the pathogenesis of enteropathogenic diarrhea in rabbits, we localized the genes for AF/R1 expression, constructed an AF/R1- strain, and compared the virulence of the AF/R1+ and AF/R1- strains with particular attention to the development of attaching, effacing lesions. We introduced Tn5 into the 86-megadalton (MDa) conjugative plasmid known to mediate expression of AF/R1 pili and transferred the derivative plasmids into laboratory strain HB101. Transconjugant M5 was found to contain the 86-MDa plasmid from RDEC-1 and to express AF/R1 pili. Pilus expression on M5 was confirmed by reaction with antiserum raised against purified AF/R1 pili and allowed the bacteria to adhere to the rabbit ileum in an in vitro assay. Three Tn5 insertions in the 86-MDa plasmid were obtained which resulted in loss of AF/R1 expression. Part of the plasmid was mapped, including a region necessary for AF/R1 pilus expression. AF/R1- mutant strain M34 was constructed, and its pathogenesis was investigated. M34 produced disease in rabbits but was less virulent than the parent. The characteristic effacing lesions of RDEC-1 and enteropathogenic E. coli developed in the intestine of rabbits infected with either M34 or RDEC-1, although with M34 they were much less frequent and did not involve the small bowel. We conclude that AF/R1 pilus expression is not essential for the attaching, effacing lesion but serves as an accessory virulence factor which promotes an initial interaction of RDEC-1 with normal epithelial cells.