Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 19 patients (aged 17-66 years) with priapism received primarily conservative treatment in the form of aspiration of blood from the cavernous bodies and subsequent intracavernous (i.c.) administration of the alpha-adrenergic drug metaraminol. In 15 patients the priapism was due to i.c. injection of vasoactive agents; 1 patient each it had developed after hemodialysis, during oral prazosin medication, and in conjunction with Fabry's disease; and in 1 patient the etiopathogenesis was unknown. Treatment of priapism with metaraminol was successful in the first 15 patients and in 2 patients with priapism due to hemodialysis and oral prazosin medication. Therapy failed in long-lasting priapism associated with Fabry's disease and in priapism of unknown etiopathogenesis. Penile detumescence took place in the first 15 patients 3 min to 2.5 h after the injection of 2-4 mg metaraminol. Hemodialysis- and prazosin-linked priapism was treated with 5 and 2 mg metaraminol, respectively; in these patients erection subsided within 15 and 4 min after onset of therapy. In a further 2 patients in whom therapy had failed Al-Ghorab shunts were constructed, with the subsequent postoperative complication of erectile impotence. Injection of metaraminol must be carried out under strict supervision of the patient's circulatory system: doses of 4 mg metaraminol or more led to an increase in blood pressure and heart rate. In 15 patients with priapism induced by i.c. application of vasoactive agents, the analysis of blood gas parameters demonstrated a severe hypercapnia (70.3 +/- 10.0 mm Hg) and acidosis (pH 7.08 +/- 0.08) 5-10 h after the onset of erection, but severe hypoxia (37.0 +/- 16.6 mm Hg) was not found until erection had lasted for more than 10 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metaraminol in therapy of various forms of priapism]. 314 Apr 63

Priapism is a persistent erection which fails to subside after climax and is accompanied by penile pain and tenderness. The most common form of priapism to confront contemporary urologists is persistence of erection following pharmacologic stimulation. We reviewed our experience over 18 months with initial diagnostic intracavernous challenges of prostaglandin E1. Three-hundred and sixty-six new impotence patients presented to our center and underwent PGE1/color duplex Doppler assessment; 14 patients developed persistent rigidity of two or more hours accompanied by penile discomfort. Each of these patients was successfully managed with penile aspiration and direct corporal instillation of the alpha-adrenergic agonist phenylephrine. The mean PGE1 dosage injected was 6 micrograms and mean duration of erection preceding aspiration 180 minutes. Penile blood gases were obtained from the initial aspirate in all cases. The duration of pharmacologic erections were correlated with the partial pressures of oxygen, carbon dioxide, bicarbonate and the pH using linear regression analysis. There was a clear trend towards deoxygenation, acidosis, and hypercarbia with prolonged erection (105-342 minutes). The relationship between duration of pharmacologic erection and acidosis/hypercarbia was highly significant.
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PMID:Pharmacologic erection: time-dependent changes in the corporal environment. 801 18

A wide range of clinical consequences may be associated with obstructive sleep apnea (OSA) including systemic hypertension, cardiovascular disease, pulmonary hypertension, congestive heart failure, cerebrovascular disease, glucose intolerance, impotence, gastroesophageal reflux, and obesity, to name a few. Despite this, 82 % of men and 93 % of women with OSA remain undiagnosed. OSA affects many body systems, and induces major alterations in metabolic, autonomic, and cerebral functions. Typically, OSA is characterized by recurrent chronic intermittent hypoxia (CIH), hypercapnia, hypoventilation, sleep fragmentation, peripheral and central inflammation, cerebral hypoperfusion, and cerebral glucose hypometabolism. Upregulation of oxidative stress in OSA plays an important pathogenic role in the milieu of hypoxia-induced cerebral and cardiovascular dysfunctions. Strong evidence underscores that cerebral amyloidogenesis and tau phosphorylation--two cardinal features of Alzheimer's disease (AD), are triggered by hypoxia. Mice subjected to hypoxic conditions unambiguously demonstrated upregulation in cerebral amyloid plaque formation and tau phosphorylation, as well as memory deficit. Hypoxia triggers neuronal degeneration and axonal dysfunction in both cortex and brainstem. Consequently, neurocognitive impairment in apneic/hypoxic patients is attributable to a complex interplay between CIH and stimulation of several pathological trajectories. The framework presented here helps delineate the emergence and progression of cognitive decline, and may yield insight into AD neuropathogenesis. The global impact of CIH should provide a strong rationale for treating OSA and snoring clinically, in order to ameliorate neurocognitive impairment in aged/AD patients.
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PMID:Death by a thousand cuts in Alzheimer's disease: hypoxia--the prodrome. 2340 Jun 34