Adrenal epinephrine increases alveolar liquid clearance in a canine model of neurogenic pulmonary edema.
Adrenal Glands/*metabolism; Adrenalectomy; Adrenergic beta-Agonists/blood/*pharmacology/therapeutic use; Adrenergic beta-Antagonists/therapeutic use; Amiloride/therapeutic use; Animal; Animals; Blood; Blood Pressure; Brain Diseases/chemically induced/*complications; Central Nervous System Agents/adverse effects; Cisterna Magna; Disease Models; Diuretics/therapeutic use; Dogs; Epinephrine/blood/*physiology/therapeutic use; Extravascular Lung Water/chemistry/*metabolism; Female; Hypertension; Injections; Male; Propanolamines/therapeutic use; Proteins/analysis; Pulmonary Alveoli/*metabolism; Pulmonary Artery; Pulmonary Edema/etiology/*metabolism/prevention & control; Pulmonary/prevention & control; Sodium Channel Blockers; Veratrine/adverse effects
Case reports of neurogenic pulmonary edema (NPE) often indicate that the edema resolves quickly. Because plasma epinephrine concentration may be elevated in NPE, and epinephrine has been shown to increase the rate of alveolar liquid clearance (ALC), we determined if ALC was increased in a canine model of NPE produced by the intracisternal administration of veratrine. ALC was determined by instilling autologous plasma into a lower lung lobe and using the increase in instillate protein concentration after 4 h to calculate the volume of fluid cleared from the airspaces by mass balance. To prevent pulmonary hypertension and edema, which would confound the mass balance analysis, carotid arterial blood was allowed to drain into a reservoir as pulmonary arterial pressure started to rise after veratrine administration. ALC in animals administered veratrine (n = 6) was 30.4 +/- 1.6 (SE)% of the instilled volume compared with 14.1 +/- 2.1% observed in control animals. The increase in ALC could be inhibited by adrenalectomy, beta2-adrenergic blockade using ICI 118,551, or sodium channel blockade using amiloride and could be duplicated by infusing epinephrine to increase plasma epinephrine concentration to levels observed in NPE. These data indicate that the increased ALC was mediated by adrenal epinephrine and suggest that edema resolution in patients with NPE might be accelerated by endogenous epinephrine.
Lane S M; Maender K C; Awender N E; Maron M B
American journal of respiratory and critical care medicine
1998
1998-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1164/ajrccm.158.3.9802031" target="_blank" rel="noreferrer noopener">10.1164/ajrccm.158.3.9802031</a>
Humoral hypercalcemia of malignancy in squamous cell carcinoma of the skin: parathyroid hormone–related protein as a cause.
Aged; Carcinoma; Fatal Outcome; Humans; Hypercalcemia/blood/*etiology; Male; Paraneoplastic Syndromes/blood/etiology/therapy; Parathyroid Hormone-Related Protein; Parathyroid Hormone/blood; Prognosis; Proteins/analysis; Skin Neoplasms/*complications; Squamous Cell/*complications; Treatment Refusal
The second most common cause of hypercalcemia is humoral hypercalcemia of malignancy (HHM), a condition associated with increased mortality. Although hypercalcemia is usually seen in squamous cell cancers, only 13 cases have been described in association with squamous cell skin cancer, and only 5 of these had characteristics of HHM. We report a case of hypercalcemia due to squamous cell skin cancer confined to the chest wall in a 67-year-old semi-comatose patient. Aggressive treatment with intravenous fluid hydration, furosemide, and etidronate corrected the hypercalcemia. A thorough workup ruled out bone metastasis and confirmed increased parathyroid-related protein, the hallmark of HHM. After regaining consciousness, the patient refused further therapy and subsequently died.
Cisneros G; Lara L F; Crock R; Whittier F C
Southern medical journal
2001
2001-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1097/00007611-200194030-00010" target="_blank" rel="noreferrer noopener">10.1097/00007611-200194030-00010</a>