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Biomedical subjects

E Haas

Publications and source records attributed to E Haas.

At least 109 records · Page 6Linked to original sources
PubMed1975

Effects of renal failure and dialysis on cefazolin pharmacokinetics.

Serum and urinary levels of cefazolin were determined after a 500-mg parenteral dose in eight azotemic volunteers. The mean peak serum concentration was 1.5 to 5 times the levels obtained in nonazotemic patients. The serum half-life of cefazolin was increased significantly. In patients on dialysis, the mean serum half-life of cefazolin was 4.05 h during (or after) hemodialysis, and 32.1 h during (or after) peritoneal dialysis. There was a significant decrease in cefazolin removal when dialysate flow or membrane surface area of the dialyzer were decreased. It was also shown that one circuit through the dialysis unit caused measurable decrease in cefazolin concentration. These data and previously published reports suggest: (i) the maintenance dose of cefazolin can be decreased in azotemic patients; (ii) patients on hemodialysis will require an additional half dose after dialysis because of efficient removal during hemodialysis; and (iii) patients on peritoneal dialysis do not require an extra dose.

Cefazolin↗
PubMed1975

Kinetics of renin-antirenin reaction: micromethods for the assay of renin and antirenin.

Indirect micromethods were designed for the assay of human renin (lower limit 0.25 times 10-4 U and of antirenin to human renin (lower limit 3 times 10-4 U), with the rat used for the bioassay of the angiotensin produced by the action of renin on renin substrate. This made possible the assay of unusually small amounts (0.01 mu1) of serum for antirenin. The Michaelis-Menten concept of a dissociating complex can be applied to the antireninrenin reaction: the rate constants for the formation and for the breakdown of the complex were k1 equal to 1.65 (ml/U antirenin per min) and k3 equal to 1.97 times 10-3 (U inactivated renin/U antirenin per min), respectively; the apparent Michaelis constant was 12 times 10-4 (U renin/ml). A second method of analysis was also applied by assuming the formation of a rather tight complex, with antirenin functioning as an irreversible inactivator of renin. Both methods of analysis yielded practically the same rate constant (k1 equal to 1.65 and k1 equal to 1.71), but the treatment according to the Michaelis-Menten equation affords a slightly better fit of the experimental data (accuracy equal to plus or minus 15.5 percent) than the second method of calculation (accuracy equal to plus or minus 21.6 percent).

Angiotensin II↗
PubMed1975

Release of antirenin to human renin by anaphylactic shock or by antihypertensive agents.

In dogs that have had repeated intravascular injections of small doses of human renin, even for long periods, the development of antirenin to human renin in the blood has not been previously noted, and their pressor response (30 mmHg) to 1 U of human renin has remained unchanged for years. In such dogs, however, a profound, abrupt fall of the systemic blood pressure, due to an anaphylactic reaction to human renin, or to the infusion of depressor agents, such as Arfonad, histamine, or diazoxide, resulted in the appearance in the blood of an inhibitor specific for human renin. This inhibitor was suddenly released into the blood-stream from the tissues in which it presumably had been stored, and it persisted, in a relatively high concentration, in some animals for months. It did not occur in dogs that had not previously received many injections of human renin. This study has shown that the inhibitor has all of the properties of antirenin to human renin. It abolished the pressor response to hog, dog, and rat renin or to angiotensin and norepinephrine. It inactivated human renin, but not dog renin, duringits incubation with renin substrate to form angiotensin.

Anaphylaxis↗
PubMed1975

[Report of a cased of carcinoma of the hypopharynx successfully treated by immediate pharyngogastrostomy (author's transl)].

The treatment of carcinoma of the lower part of the pharynx and upper oesophagus presents many difficulties. One of the outstanding problems being that of repair of the defect after excision of the pharyngo-oesophageal portion of the alimentary tract. This paper describes an operation in which the mobilized stomach is transposed after blunt dissection of the oesophagus via a posterior mediastinal tunnel without thoracotomy to a position high in the neck, with anastomosis of the fundus to the pharynx at the level of vallecula. This type of oesophagectomy was first tried bei Turner 1936 for carcinoma of the thoracic oesophagus. The main advantage of this form of repair is that it can restore normal swallowing within a few days in this difficult clinical situation.

Adult↗