Positive end-expiratory pressure and the damaged right ventricle. An experimental open versus closed chest study

Hemodynamic changes after isolated impairment of right ventricular function (produced by increasing afterload by temporary banding of the pulmonary artery) were studied in 22 ventilated pigs during increased levels of positive end-expiratory pressure (4, 8, 12, and 16 cm H2O). In the open chest group, application of positive end-expiratory pressure produced only a slight decrease of cardiac index. After right ventricular damage a decrease of cardiac index of more than 25% occurred only when higher levels of positive end-expiratory pressure were applied. In contrast to the open chest group, the closed chest group showed more distinct cardiovascular responses after positive end-expiratory pressure. In the damaged right ventricle with a positive end-expiratory pressure of 16 cm H2O, right ventricular end-diastolic pressure increased more than 100%. With positive end-expiratory pressure, cardiac index decreased 34% before and 47% after right ventricular damage. We conclude that positive end-expiratory pressure induces a more pronounced decrease in cardiac index if right ventricular function is impaired. During open chest conditions with lower levels of positive end-expiratory pressure, these changes are only small, however, and probably irrelevant. During closed chest conditions, the hemodynamic changes are much more pronounced. High right ventricular end-diastolic pressures resulting from impaired right ventricular contractility as well as from high levels of positive end-expiratory pressure may have an impact on biventricular function and right ventricular coronary driving pressure.     

Functional parameters before and after parathyroidectomy: a prospective, randomized long-term trial on different rat strains.

For clinical controls before and after parathyroidectomy and for evaluation of the function of transplants of parathyroid tissue, it is necessary to establish standard values of relevant laboratory parameters for donor and recipient animals as well as for different types of nutrition. Since no such data are yet available, it was the purpose to define such standards. In a prospective randomized trial on 400 rats of the Dark Agouti (DA) and Lewis strain, different functional laboratory parameters such as total calcium, intact parathyroid hormone, phosphate, 1.25-dihydroxyvitamin D, and alkaline phosphatase were measured under a standard and low calcium diet over a period of 40 weeks. Two hundred of these animals underwent a parathyroidectomy four weeks after the beginning of the study and specimens were evaluated histologically. For all eight different study groups normal values could be defined within tight limits for parameters which describe the function of the parathyroid gland or elements of calcium metabolism under different conditions. The optimal conditions for a transplantation model of parathyroid glands were established. Lewis-rats were identified as the ideal donor and DA rats as the better recipient animals. These data can serve as reference values for future studies on transplantation of the parathyroid without immunosuppression.     

Ontogeny of peroxidase activity in epithelium and eosinophils of the mouse uterus.

Outbred CD-1 mice treated for 1 or 4 days with 1 mg/kg of diethylstilbestrol (DES) at various ages after birth were examined for histochemical localization of peroxidase in the uterine epithelium. Peroxidase activity in uterine extracts was also measured by a radiometric assay and the conversion of [3H]DES to [3H]Z,Z-diensestrol (Z,Z-DIES). While no peroxidase activity was detected by a histochemical method in uterine epithelium from untreated 5-day old mice, the enzyme was apparent in mice treated for 4 days with DES; uterine eosinophils were absent at this age. By day 9, DES-induced staining for peroxidase in uterine epithelial cells and the number of uterine eosinophils had increased significantly. In addition, at this age, the biochemical assays for uterine peroxidase were sensitive enough to show that DES is converted to Z,Z-DIES and that [3H]estradiol gives rise to 3H2O and water-soluble radioactive metabolites. The peroxidase response to DES, determined by both histochemical and biochemical methods, increased with the age of the immature mice. These data indicate that the neonatal uterus, although deficient in eosinophils, demonstrates a peroxidase response to estrogen and that this response is localized primarily in the luminal epithelium. The role of this DES-induced peroxidase activity in converting DES to activated metabolites that may cause cell damage is discussed.     

Intraabdominal pressures during natural activities in patients treated with continuous ambulatory peritoneal dialysis

Intraabdominal pressures were measured during natural activities in 6 men, age 24-62 years, treated with continuous ambulatory peritoneal dialysis. The pressures were measured with a pressure transducer secured at the level of the umbilicus in the supine, sitting, and upright positions with 0-3 liters intraperitoneal fluid during talking, coughing, straining, changing position, walking, jogging, exercycling, jumping and weight lifting. Coughing and straining generated the highest intraabdominal pressures in every position. The pressures with weight lifting were proportional to the magnitude of the weight lifted up to 50 lbs, but were lower than those during coughing and straining. The pressures were generally higher with greater intraabdominal fluid volumes, especially with jumping and coughing. Exercycling was associated with lower intraabdominal pressure than was jogging, and the pressures were only minimally influenced by intraperitoneal fluid volumes. The results of this study can be used as a guide in establishing preventive measures in patients with intraperitoneal fluid to decrease complication rates related to raised intraabdominal pressures such as dialysate leaks, hernias and hemorrhoids.     

Rewarming from experimental hypothermia: comparison of heated aerosol inhalation, peritoneal lavage, and pleural lavage

This study compares the thermal transfer and rewarming characteristics of heated aerosol inhalation (HAI) alone and combined with peritoneal lavage (PEL) or pleural lavage (PLL). Closed-system PEL and PLL are equally efficient at rewarming hypothermic dogs and do so at a rate approximating 6 degrees C/h/m2. Cardiovascular responses to PEL and PLL were similar. Serum electrolytes, protein, Hct, and arterial blood gases were comparable and little changed when compared in prehypothermia and postrewarming periods. HAI alone provides little heat for rewarming; more heat is realized from endogenous metabolism. Nevertheless, HAI's ease of use and possible selective cardiac rewarming characteristics argue for its inclusion with other methods of active rewarming. The use of PEL or PLL is governed by clinical circumstances.     

Nucleation of calcium phosphate by surface-bound extracellular matrix

The native extracellular matrix (ECM) laid down on silicon and titanium surfaces by osteoblast-like SAOS-2 cells was exposed by selective removal of cells. This type of material surface ECM-Si, ECM-Ti was shown to promote the nucleation of calcium phosphate from a simulated body fluid (SBF). Microscopic and spectroscopic results revealed the effect was associated with a collagen fiber-free extracellular matrix.     

Kinetics of peptide uptake and tissue distribution following a single intranasal dose of peptide

Stimulation with the combination of PDB plus ionomycin induced LFA-l/ICAM-1-dependent homotypic adhesion of tonsil B cells. Adhesion of tonsil B cells in our system induced tyrosine phosphorylation of Pyk-2. Disruption of homotypic adhesion and concomitant inhibition of induction of protein tyrosine phosphorylation was achieved by physical separation of the cells and by treatment with methyl-2,5-dihydroxycinnamate (MDHC), an inhibitor of protein tyrosine phosphorylation. These results suggest that protein tyrosine phosphorylation that is associated with homotypic adhesion is mediated by LFA-l/ICAM-1 interactions.