PubMed HealthSearch

Biomedical subjects

P J Boor

Publications and source records attributed to P J Boor.

13 recordsLinked to original sources

Juxtaposition of the atrial appendages.

Juxtaposition of the atrial appendages is a rare congenital cardiac anomaly almost universally associated with severe conotruncal abnormalities, especially transposition of the aorta. This presentation describes a case of right sided juxtaposition of the atrial appendages without concomitant conotruncal malformations. This finding contradicts previous hypotheses concerning the genesis of juxtaposition.

Ductus Arteriosus, Patent

Papillary-cystic neoplasm of the pancreas.

A case of an unusual pancreatic tumor with a characteristic papillary-cystic microscopic morphology is presented. Review of four previously reported similar cases suggests a distinct clinical picture of a large abdominal mass occurring in a young person which apparently, after resection, does not rapidly recur. The histopathology of this tumor consists of papillary and cystic patterns, regular homogeneous cells with a few mitoses, glassy eosinophilic cytoplasm, and mucin and PAS positivity. Ultrastructural detail, including eccentric nucleoli, numerous mitochondria, sparse endoplasmic reticulum, and little evidence of secretory activity, suggests a duct cell origin for this rare tumor.

Adolescent

Myocardial infarct size: clinicopathologic agreement and discordance.

An accurate postmortem method of planimetrically estimating the extent of myocardial infarction was employed in 16 cases. Delineation of necrotic myocardium was enhanced by a macroscopic staining technique, which utilizes a tetrazolium dye. Comparison of infarct size with peak serum creatine phosphokinase levels showed a general correlation between the two that was not statistically significant. Two markedly disparate cases serve to emphasize the need for clinical awareness of the temporal relationship between myocardial infarction and creatinine phosphokinase analysis as well as the possibility of other anatomic sources of elevation of serum enzyme levels. Comparison of infarct sizes in cardiogenic shock and nonshock patients confirms the existence of a significant relationship between a larger myocardial infarct and shock. However, the data from several patients in the group again emphasize the possibility of maintaining a reasonable blood pressure in the face of a massive myocardial infarction or, more importantly, of manifesting "cardiogenic" shock when only a small amount of left ventricular damage has been sustained. The latter possibility may be related to other anatomic events, e.g., bowel infarction, hemorrhage, or possibly right ventricular ischemia, infarction, or dysfunction.

Creatine Kinase

Trichloroethylene-induced deactivation of cytochrome P-450 and loss of liver glutathione in vivo.

Liver microsomal enzyme activities and glutathione (GSH) contents of fasted male rats pretreated with phenobarbital (PBT) or vehicle controls were measured during and after exposure to trichloroethylene (TRI) (1% x 2 hr). TRI caused morphologic liver injury only in the pbt animals. Cytochrome P-450 and b5 contents were diminished by the end of the first hr of TRI exposure and NADH-cytochrome c reduction increased three-fold by eight hr in the PBT animals. The only change in vehicle animals exposed to TRI was a decrease in NADPH-cytochrome c reductase activity by eight hr. Hepatic GSH contents of vehicle animals, constant during TRI exposure, rose with time. In contrast, in PBT animals, hepatic GSH contents decreased during TRI exposure and then rebounded. Decreases in GSH were most profound in the microsomal fraction. When fed animals with approximately two-fold higher hepatic GSH levels than fasted animals were exposed to TRI, they had shorter anesthesia recovery times and less liver injury, although excreting similar or slightly more trichlorinated metabolite into their urine in 24 hr than their fasted counterparts. We suggest that the hepatoxic effects of trichloroethylene are caused by inadequate detoxification of its reactive intermediates.

Alanine Transaminase

Neurotoxicity of digitoxin in adult and newborn rats: drug distribution.

Electrocardiographic monitoring of adult and 1 week old (newborn) rats during severe acute digitoxin toxicity demonstrated a lack of acrdiotoxicity despite marked neurotoxicity in both age groups. To examine the possibility that drug disposition is a factor in the unusual digitoxin sensitivity of newborn rats, 3H-digitoxin distribution in liver, heart, brain, kidney, adrenal, blood and fat was compared in 1 and 3 week old (weanling) rats at 2, 12 and 24 hr. H3-label was rapidly sequestered by the liver in weanlings but not in newborn rats. Newborns had significantly higher concentrations of 3H-substance in all other organs, particularly in brain (greater than 25% of the administered dose at 24 hr), indicating a cerebrotoxic basis for the newborn's sensitivity to digitoxin. Only trace amounts of 3H-substance were recovered from adult rat brain during severe neurotoxicity (72 hr) suggesting that digitoxin metabolites may be potent cerebrotoxins. Extremely high adrenal concentrations were noted in all animals.

Aging

Host response to implanted dacron grafts. A comparison between mesh and velour.

Segments of open Dacron mesh grafts were subcutaneously implanted in rats and harvested for a period of up to 12 weeks after operation at serial intervals. The gross and histologic events of the host response to the external surface were compared to that of segments of low-porosity Dacron velour implanted in a similar fashion. Mature collagen, generously vascularized with new capillaries, was noted throughout the mesh within three to four weeks, while a tightly bonded inner fibrous layer had formed from the surrounding tissues. Major segments of velour floated in amorphous caseous material for up to five weeks. These pools of debris with their concomitant inflammatory response slowly resolved during a ten-week period. This prolonged healing may contribute to eventual graft closure by progressive fibrosis and extrinsic contracture.

Animals