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Biomedical subjects

N Voelkel

Publications and source records attributed to N Voelkel.

15 recordsLinked to original sources
PubMed2000

Plasma vascular endothelial growth factor in acute mountain sickness.

STUDY OBJECTIVES: To investigate the hypothesis that an increase in circulating vascular endothelial growth factor (VEGF) occurs in mountaineers at high altitude, particularly in association with acute mountain sickness (AMS) and/or low hemoglobin oxygen saturation. DESIGN: : Collection of medical histories, AMS scores, plasma samples, and arterial oxygen saturation (SaO(2)) measurements from mountaineers at 1,500 feet (sea level) and at 14,200 feet. SETTING: Mount McKinley ("Denali"), AK. PARTICIPANTS: Sixty-six mountaineers. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Plasma VEGF at 14,200 feet was not increased in any group. In fact, plasma VEGF was significantly lower in subjects who did not develop AMS (53 +/- 7.9 pg/mL; mean +/- SEM; n = 47) compared to control subjects at sea level (98.4 +/- 14.3 pg/mL; n = 7; p = 0.005). Plasma VEGF at 14, 200 feet for subjects with AMS (62 +/- 12 pg/mL; n = 15) did not differ significantly from subjects at 14,200 feet without AMS, or from control subjects at sea level. Of a small number of subjects with paired specimens at sea level and at base camp (n = 5), subjects who exhibited a decrease in plasma VEGF at 14,200 feet were those who did not develop AMS. Neither SaO(2), prior AMS, AMS symptom scores, or acetazolamide use were correlated with plasma VEGF. CONCLUSIONS: Subjects at high altitude who do not develop AMS have lower plasma VEGF levels compared to control subjects at sea level. Plasma VEGF at high altitude is not elevated in association with AMS or hypoxia. Sustained plasma VEGF at altitude may reflect a phenotype more susceptible to AMS.

Adult↗
PubMed1997

Editorial

Explore the source record for details and available documents.

Journal Article↗
PubMed1993

Microvascular hemodynamics in the sickle red blood cell perfused isolated rat lung.

In this study the effects of alveolar hypoxia on pulmonary microvascular hemodynamics in sickle red blood cell (HbSS-RBC) perfused rat lungs were studied under conditions of high and low oxygen tensions and compared with lung perfused with rat (HbRat) and normal human (HbAA) RBC controls. Independent of the RBC suspension (hematocrit 5%) used, ventilation with the room air gas mixture did not result in any significant differences in the pulmonary arterial pressure (Ppa), capillary pressure (Ppc), total pulmonary vascular resistance (RT), or angiotensin II pressor response. Ventilation of HbSS-RBC perfused lungs with a hypoxic gas mixture significantly increased the Ppa, Ppc, and RT above that which was seen in HbRat and HbAA controls. The increase in RT occurred mainly in the pulmonary artery independent of RBC suspension. In addition, no significant accumulation of lung water occurred in HbSS-RBC perfused lungs compared with HbRat and HbAA controls, as indicated by the change in capillary filtration coefficient and wet-to-dry lung weight ratio. In conclusion, deoxygenation of the HbSS-RBC and hypoxic pulmonary vasoconstriction is additive in altering pulmonary microvascular hemodynamics.

Anemia, Sickle Cell↗
PubMed1990

Leukotriene E4 elimination and metabolism in normal human subjects.

Radiolabeled leukotriene (LT) E4 was infused into three healthy subjects in order to assess the production and elimination of sulfidopeptide leukotriene metabolites in urine. Three different radiolabeled tracers were employed, [14,15-3H]LTE4, [35S]LTE4, and [14C] LTE4 in five separate infusion studies. There was a rapid disappearance of radioactivity from the vascular compartment in an apparent two-phase process. The first elimination phase had an apparent half-life of approximately 7 min. Radioactivity quickly appeared in the urine with 10-16% eliminated during the first 2 h following intravenous infusion; 7%, 2-5 h; 4%, 5-8 h; 4%, 8-15 h; and 1.5%, 15-24 h from the [14C] LTE4 experiments. Unmetabolized LTE4 was the major radioactive component in the first urine collection, but at later times two more polar compounds predominated. After extensive purification by normal phase-solid phase extraction and reverse-phase high performance liquid chromatography, these compounds were characterized by UV spectroscopy, co-elution with synthetic standards, negative ion electron capture gas chromatography/mass spectrometry, and tandem mass spectrometry. The two major urinary metabolites were structurally determined to be 14-carboxy-hexanor-LTE3 and the conjugated tetraene, 16-carboxy-delta 13-tetranor-LTE4. Three other minor metabolites were detectable in the first urine collection only and were characterized by co-elution with synthetic standards as 16-carboxy-tetranor-LTE3, 18-carboxy-dinor-LTE4, and 20-carboxy-LTE4. omega-Oxidation and subsequent beta-oxidation from the methyl terminus appeared to be the major metabolic fate for sulfidopeptide leukotrienes in man. The accumulation of the 14-COOH-LTE3 and 16-COOH-delta 13-LTE4 may reflect a rate-limiting step in further oxidation of these compounds which places a conjugated triene or conjugated tetraene, respectively, two carbons removed from the CoA ester moiety. Also in the first urine collection there was another minor metabolite identified as N-acetyl-LTE4, however, no subsequent beta-oxidation of this metabolite was observed. The major metabolites of LTE4 might be useful in assessing in vivo production of sulfidopeptide leukotrienes in humans.

Adult↗
PubMed1988

Current approach to treatment of primary pulmonary hypertension.

Based upon our experience with a cohort of 46 patients referred to the UCHSC from April, 1980 to April, 1987 for evaluation and treatment of PPH, we currently assess acute pulmonary vasoreactivity as defined by the patient's response to intravenous PGI2 during the initial diagnostic catheterization. A 3 to 5 day trial of high dose oral diltiazem treatment (720 mg/day maximum) is given while monitoring the patient in the clinical research center to detect significant side effects including arrhythmias, orthostatic systemic hypotension, arterial desaturation, and worsened right ventricular dysfunction. We believe it is necessary to recatheterize each patient to establish the efficacy of calcium antagonist treatment prior to discharge. Those patients who are responsive to diltiazem are discharged and followed in our pulmonary hypertension clinic. Since an occasional patient will deteriorate after several weeks of therapy, repeat right heart catheterization after 8 weeks of treatment is used to determine which patients should be continued on diltiazem for chronic therapy. Approximately 30 percent of our patients with PPH have been improved on diltiazem treatment. Most patients who have a good response to treatment after eight weeks continue to benefit from long-term treatment. It appears that the response to an acute infusion of PGI2 is useful in safely identifying those PPH patients who are likely to benefit from vasodilator therapy. Debilitated patients who are unresponsive to PGI2 and vasodilator therapy are considered potential candidates for cardiopulmonary transplantation.

Administration, Oral↗
PubMed1984

Metabolism of leukotrienes B4 and C4 in the isolated perfused rat lung.

Isolated rat lungs perfused with physiological buffer containing leukotriene C4 were found to rapidly metabolize leukotriene C4 to leukotriene C4 sulfoxide, leukotriene D4, and leukotriene E4. Addition of leukotriene C4 to the recirculating perfusion buffer was observed to cause a persistent increase in the pulmonary arterial pressure. Leukotriene C4 instilled into the airway of the perfused lung was also rapidly metabolized to these same products with retention of the products within the lung. In contrast, leukotriene B4 injected into the perfusion fluid was recovered unchanged in the lung effluent. Leukotriene B4 instilled into the airway of the perfused lung was observed to rapidly traverse the alveolar membranes and was recovered intact in the lung effluent. No evidence for formation of the 20-hydroxy or the 20-carboxy metabolites of leukotriene B4 by the isolated perfused rat lung was observed.

Animals↗
PubMed1980

Moderation of hypoxic vasoconstriction by infused arachidonic acid: role of PGI2.

To determine the role of prostaglandins in modulating pulmonary circulatory responses, we examined the effect of the prostaglandin precursor, sodium arachidonate, on the pulmonary vascular resistance of mongrel dogs during alveolar hypoxia. When infused intravenously for 5 min during hypoxia, sodium arachidonate (1 mg/min) decreased pulmonary vascular resistance from 6.9 +/- 1.1 to 4.9 +/- 0.6 U (P less than 0.05). The vasodilation produced by sodium arachidonate was blocked by sodium meclofenamate, a cyclooxygenase inhibitor. By infusing radiolabeled sodium arachidonate and collecting aortic blood samples, we found from chromatographic and mass spectrometric analysis that a major prostaglandin produced was 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2. Infusion of PGI2, but not PGE2, during hypoxia decreased pulmonary vascular resistance. We concluded that the prostaglandin precursor, sodium arachidonate, is a vasodilator of the pulmonary vasculature that has been constricted by alveolar hypoxia, probably because PGI2 is formed from the arachidonate. The pulmonary circulation may be similar to the systemic circulation where vasoconstriction results in the generation of vasodilatory prostaglandins that attenuate the constrictor effect.

Animals↗
PubMed1976

[Bronchospasmolysis with Atroven (SCH 1.000) (author's transl)].

A study was performed to evaluate the influence of Atrovent (SCH 1.000) and Ephedrine on the bronchial resistance in patients with obstructive airway diseases. The inhalation of SCH 1.000 was followed by a significant decrease in resistance reaching a maximum of 49.1% and lasting for four hours post inhalation. Ephedrine tablets were comparatively less effective. The second part of our study concerns the cardiovascular reaction of patients with coronary artery diseases after inhalation of SCH 1.000. Side effects involving the cardiovascular system due to inhalation therapy with SCH 1.000 were not registered. Atrovent is recommended as an excellent bronchodilator drug especially in patients with underlying coronary artery disease or tachycardial arrhythmias.

Airway Resistance↗