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Biomedical subjects

J J Lunn

Publications and source records attributed to J J Lunn.

11 recordsLinked to original sources
PubMed1998

Early extubation after abdominal aortic reconstruction.

OBJECTIVE: To assess the safety of early (<2 hrs) extubation after elective infrarenal aortic surgical procedures. DESIGN: A retrospective chart review of 192 consecutive elective infrarenal aortic surgical procedures from January 1990 to March 1994 at Mayo Clinic Scottsdale was undertaken. MEASUREMENTS AND MAIN RESULTS: Combined general and epidural anesthesia was used extensively (187 patients; 97.4%). Early extubation was accomplished in 166 (86.5%) patients. Time to extubation was dependent on clinical factors and not by protocol. All early extubations occurred in the operating room or recovery room with a median time from skin closure of 12 minutes. Ten patients were extubated from 2 to 12 hours after the procedure, 14 patients more than 12 hours after the procedure, and 2 patients were not extubated and subsequently expired. Of the 166 patients extubated within 2 hours, 8 (4.8%) required reintubation. Factors found univariantly to be significantly associated with failure of early extubation include obesity, abnormal chest x-ray postoperatively, prior myocardial infarction, and prior coronary revascularization (p < 0.05). CONCLUSION: Early extubation (<2 hrs) after elective infrarenal aortic procedures may be performed safely and should be undertaken unless clinical features suggest failure of extubation.

Aged↗
PubMed1994

Comparing drugs for short-term sedation.

Selected benzodiazepines and a phenol derivative are reviewed in relation to their appropriateness as short-term sedatives in settings such as noninvasive and invasive medical procedures. Terminating sedation with flumazenil is also a focus of interest.

Anesthesia↗
PubMed1993

Postpneumonectomy pulmonary edema. A retrospective analysis of associated variables.

STUDY OBJECTIVE: Evaluate the correlation between intravenous fluid administration and postpneumonectomy pulmonary edema. DESIGN: Retrospective chart review. SETTING: Large multispecialty group practice hospital. PATIENTS: Adults who had a pneumonectomy performed between 1977 and 1988. MEASUREMENTS AND RESULTS: Patients were identified who had postpneumonectomy pulmonary edema (PPE). Fluid administration and fluid balance information was found in records and compared with age- and sex-matched control patients who did not develop PPE. The side of pneumonectomy was noted for patients in each group. Autopsy findings were recorded for patients who died. Twenty-one patients met PPE criteria. No significant difference was found between groups for fluid administration or fluid balance. Patients who had right pneumonectomy had a significantly higher incidence of PPE. Patients with PPE had a 100 percent mortality rate and histologic evidence of the adult respiratory distress syndrome (ARDS) at autopsy. CONCLUSIONS: PPE is caused by noncardiogenic pulmonary edema rather than excess intravenous fluid administration. There is a greater incidence of the syndrome with right pneumonectomy for unknown reasons. The mortality rate is high despite interventions for ARDS.

Aged↗
PubMed1990

Halothane decreases the release of neuropeptide Y and 3,4-dihydroxyphenylglycol from superfused segments of dog pulmonary artery.

Neuropeptide Y (NPY), norepinephrine (NE), and 3,4-dihydroxyphenylglycol (DOPEG), the metabolite of NE that arises intraneuronally, were measured in superfusates before, during, and after nerve stimulation and in extracts of dog pulmonary artery after superfusion and electrical stimulation (ES) at 12, 6, and 1 Hz. NE and DOPEG were quantified by high-pressure liquid chromatography with electrochemical detection; peptides were quantified by radioimmunoassay. The rate of overflow of NPY, NE, and DOPEG into superfusate was measured over time. The overflow of DOPEG into superfusate during basal conditions was 3.0 times that of NE. Efflux of DOPEG and NPY increased during ES; peak effluxes were not reached, however, until after cessation of stimulation. NE efflux peaked during ES. Effluxes of NE, NPY, and DOPEG were frequency-dependent at 12 and 6 Hz; at 1 Hz efflux of only NE was greater than basal. Halothane decreased significantly the rates of NPY and DOPEG efflux during and after 12 Hz ES; DOPEG efflux evoked by 6 Hz stimulation was also decreased by halothane. The percentage of the total tissue content of NPY that overflowed was decreased by halothane. Halothane did not affect the molar ratios of NE:DOPEG or NE:NPY during basal conditions or ES. These studies provide evidence that halothane slows efflux of NPY that is released along with NE from dog pulmonary artery during high frequencies of stimulation. Halothane also reduces the metabolism of NE to DOPEG.

Animals↗
PubMed1990

Endotoxin does not directly alter norepinephrine release or vasoactivity in dog pulmonary artery and portal vein.

The direct effect of Escherichia coli endotoxin on the release of norepinephrine (NE) and the contractile response consequent to the release of NE were studied in isolated, superfused segments of dog pulmonary artery and portal vein during resting conditions and during electrical stimulation (ES). High-pressure liquid chromatography with electrochemical detection was used to quantify the endogenous NE released and that remaining in the tissue after stimulation. Endotoxin (1 micrograms/ml and 10 micrograms/ml in superfusate) had no effect on the release of NE from either pulmonary artery or portal vein. Endotoxin also had no effect on vasoactivity in response to ES. Thus, in isolated pulmonary artery and portal vein, endotoxin, in the doses employed, does not directly affect release of NE from adrenergic nerve endings, nor does it affect the sequence of events that starts with transmitter-receptor interaction and ends with contraction of smooth muscle cells.

Adrenergic Fibers↗
PubMed1984

Halothane-induced changes in the release and disposition of norepinephrine at adrenergic nerve endings in dog saphenous vein.

The effect of halothane on the release and metabolism of norepinephrine during resting conditions and in response to electrical stimulation at 2 Hz was studied in isolated superfused segments od dog saphenous vein. Liquid chromatography with electrochemical detection was used to measure endogenous norepinephrine overflowing in response to electrical stimulation and the content of norepinephrine remaining in the tissue after stimulation. In other preparations, norepinephrine stores were labeled with [3H]norepinephrine, and measurements were made of [3H]norepinephrine and its metabolites (separated by column chromatography) in superfusates. Radiolabeled metabolites of norepinephrine produced intraneuronally (3,4-dihydroxyphenylglycol) and extraneuronally (O-methylated) were quantitated by liquid scintillation spectrometry. Electrically stimulated release and overflow of endogenous norepinephrine was decreased 11.9% at 0.75% halothane, 17.7% at 1.5% and 19.2% at 2.5% halothane. At each halothane concentration studied, the per cent of tissue NE content released in response to electrical stimulation was less. Halothane decreased the fraction of radioactivity lost during basal conditions and during stimulation. Less oxidative deamination of norepinephrine occurred in the presence of halothane.

Animals↗