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D J Krellenstein

Publications and source records attributed to D J Krellenstein.

7 recordsLinked to original sources
PubMed1992

Pleural effusion in non-Hodgkin's lymphoma.

Intrathoracic non-Hodgkin's lymphoma (NHL) usually presents with roentgenographic evidence of mediastinal lymph node enlargement, pulmonary masses, pleural effusion, and a clinical picture of a systemic disease with lymphadenopathy. The presentation of NHL with pleural effusion as the major roentgenographic abnormality and no clinical peripheral lymphadenopathy or organomegaly is unusual. During a seven-year period, we encountered 19 patients with NHL in whom pleural effusion was the major roentgenographic and clinical finding. Pleural fluid cytologic results were diagnostic in only two patients. Closed pleural biopsy was positive in three. Eight of 11 patients had diagnostic immunophenotypic lymphocyte cell marker studies. Seven of nine patients had diagnostic thoracoscopy and one thoracotomy. The CT scan identified biopsy sites when pleural fluid and tissue studies were nondiagnostic. Lymphomatous tissue was obtained from the pleura in 17 of the 19 patients supporting the contention that pleural effusion in patients with NHL is usually due to pleural lymphoma rather than obstruction to mediastinal lymphatics.

Adult↗
PubMed1978

Factors affecting overdrive suppression of idioventricular pacemakers and associated potassium shifts.

A characterization of the factors controlling overdrive suppression of idioventricular pacemakers was investigated in canine hearts with complete atrioventricular block perfused in vitro. The following results were obtained: 1) overdrive suppression increases as a function of driving rate in a sigmoidal fashion; 2) overdrive suppression is maximal after 3 min; 3) the pause is a function of spontaneous rate prior to overdrive; 4) overdrive causes an initial net K loss; 5) overdrive is followed by a transient net K grain; 6) increasing [K]o does not affect K loss; 7) net K loss with drive is less in pre-driven hearts; 8) net K uptake after overdrive is little affected by ventricular activity; 9) acetylcholine does not alter ventricular K balance; and 10) paired stimulation increases overdrive suppression and K loss whether or not each stimulus is followed by a contraction. The following conclusions are drawn. The factors controlling overdrive suppression include the spontaneous rate prior to drive, the rate, duration and pattern of drive, an increase in [K]o during the drive and a decrease in [K]o after drive, but not on acetylcholine-mediated inhibition.

Acetylcholine↗
PubMed1977

Extracorporeal membrane oxygenation for massive pulmonary thromboembolism.

This study was undertaken to determine whether extracorporeal membrane oxygenation (ECMO) could modify the effects of massive lethal thromboembolism and prevent death. Twenty anesthetized dogs were prepared for venoarterial perfusion with a demand pump and membrane lung and were perfused slowly for 1 1/2 hours to lessen homologous blood shock; 1 ml per kilogram of 24-hour-old tantalum-impregnated thrombus was injected intravenously. The dogs had profound systemic hypotension with an elevated mean pulmonary artery pressure (62.9 +/-4.5 mm Hg) immediately after embolization. Control animals generally died within 15 minutes. Four of the 10 ECMO-supported animals lived for six days, at which time they were restudied and killed. Not only can ECMO maintain an animal that would otherwise die quickly of massive pulmonary thromboembolism, but such support, even though temporary, can greatly improve the chances of survival.

Animals↗
PubMedDate not supplied

Norepinephrine, potassium and overdrive suppression.

The influence of norepinephrine on ventricular overdrive suppression and attendant potassium shifts has been studied in isolated perfused canine hearts with complete atrioventricular block. It was found that: 1) there is a potassium loss during the drive and a potassium uptake after the drive); 2) reducing the driving rate from 240 to 120/min decreases potassium loss; 3) norepinephrine increases potassium uptake and spontaneously beating ventricles and during the recovery from 120/min drive; 4) norepinephrine enhances K loss during and after a 240/min drive; 5) norepinephrine shortens the overdrive pause under all the conditions tested; 6) in ventricles driven at a constant rate, norepinephrine causes a small loss of ptoassium; 7) reserpinized hearts show a small potassium loss during drive and a larger potassium uptake after drive; yet, the suppression is longer; 8) norepinephrine increases K loss with drive and decreases overdrive suppression in reserpinized hearts; 9) norepinephrine enhances the increase in oxygen consumption caused by overdrive; and 10) norepinephrine antagonizes the depressant effect of high [K]0 on automaticity. It is concluded that norepinephrine shortens the pause independently of potassium levels and antagonizes the inhibittory influence of high K. The effect or norepinephrine on K movements depends on the ventricular rate and such rate-dependence is related to oxygen availability with respect to the increased metabolic demand.

Animals↗