Gene/Protein Disease Symptom Drug Enzyme Compound
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The efficacy of a recently marketed posttesticular male oral contraceptive, Contrasperm, was assessed in a clinical trial involving 32 Malaysian volunteers ages 21-39 years. Contrasperm is claimed to be a pure botanical extract free of toxic chemicals, steroids, and hormones. The drug is believed to cause cells surrounding the sperm in the seminiferous tubules to secrete carbon dioxide, producing a weakly acidic environment that greatly increases the sperms' metabolism and reduces the pH of semen from its normal level of 7.5 to 1.5. The manufacturer claims that this drop in pH decreases motility from 95% to 0%. Semen samples were collected by masturbation from subjects to provide baseline data. 3 days after the initial sperm analysis, subjects were given 1 capsule of Contrasperm containing 10 mcg of the active ingredient. Additional semen analyses were conducted 30 minutes, 6 hours, and 24 hours after ingestion. Sperm count and sperm motility were greatly reduced in most subjects 30 minutes after ingestion. However, 6 subjects had increased sperm counts and 4 subjects demonstrated increased sperm motility, indicating an enhancing effect. At 6 hours after ingestion, 20 subjects had lowered sperm motility and 12 subjects showed normal sperm motility, contradicting the manufacturer's claim that motility is reduced to 0%. Although Contrasperm is claimed to be effective for 6-8 hours after ingestion, its effect wore off in less than 6 hours in 37% of subjects. Both sperm count and sperm motility returned to normal levels 24 hours after ingestion, confirming the reversibility of this drug. Most subjects reported mild side effects such as muscle weakness, blurred vision, dizziness, perspiration, urgency, abnormal muscle tension, and dry throat which persisted longer than 24 hours. Further studies, with proper controls, are needed to assess the reliability and toxicity of this preparation.
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PMID:Efficacy of Contrasperm as a male contraceptive: clinical trials in Malaysian men. 1227 93

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

The 'Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - International Consensus on Science' recommend an artificial ventilation volume of 10 ml/kg bodyweight (equivalent to a tidal volume of 700-1000 ml) without the use of supplemental oxygen in adults with respiratory arrest. For first aid providers using the mouth-to-mouth or mouth-to-nose-ventilation technique, respectively, a ventilation volume of approximately 9.6 l/min results. Additionally, a deep breath is recommended before each ventilation to increase the end-expiratory oxygen concentration of the air exhaled by the first aid provider. To investigate the effects of these recommendations in healthy volunteers, test persons were asked to ventilate an artificial lung model for a period of up to 10 min. The tidal volume was set at 800 ml at a breathing rate of 12/min. End-tidal carbon dioxide, oxygen saturation (measured by pulse oximetry), and heart rate were measured continuously. Capillary blood gas samples were collected and non-invasive blood pressure readings were recorded prior to the start of ventilation and immediately after the end of the measuring period. The data reveal a statistically significant and clinically relevant decrease in end-tidal carbon dioxide pressure (P<0.001, median decrease 14 mmHg), and the occurrence of hyperventilation-associated symptoms such as paraesthesia, dizziness, and carpopedal spasms in more than 75% of the participants. Clinically and statistically significant hyperventilation results in first aid providers performing artificial ventilation according to the guidelines. This artificial ventilation is associated with a significant decrease in capillary and end-tidal carbon dioxide pressure as well as with multiple symptoms of an acute hyperventilation syndrome. Ventilation performed according to these guidelines may cause injury to the health of the first aid provider. Rescuers ventilating the victim should be replaced at regular intervals and the recommendation to take a deep breath before each ventilation should not be upheld in order to minimise the risk of hyperventilation.
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PMID:Artificial ventilation for basic life support leads to hyperventilation in first aid providers. 1280 4

Clinical reports on unintentional mass exposure to extreme concentrations of carbon dioxide are rare. We describe an industrial incident caused by a container of liquid carbon dioxide that was unintentionally opened in an enclosed working environment. Twenty-five casualties reached our emergency department. Symptoms included dyspnea, cough, dizziness, chest pain, and headache. ECGs (n=15) revealed ST-segment changes in 2 (13.3%) patients, atrial fibrillation in 2 patients, and non-Q wave myocardial infarction in 1 patient. Chest radiographs (n=22) revealed diffuse or patchy alveolar patterns, consistent with pneumonitis, in 6 (27%) patients and pulmonary edema in 2 (9%) patients. Eleven (44%) patients were admitted to the hospital: 8 were discharged 24 hours later and the others within 8 days. No patient died. Exposure to high concentrations of carbon dioxide resulted in significant but transient cardiopulmonary morbidity with no mortality when victims were promptly evacuated and given supportive therapy. Cardiac complications were frequently observed and should be actively sought.
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PMID:Exposure to extremely high concentrations of carbon dioxide: a clinical description of a mass casualty incident. 1474 8

This stratified cross-sectional epidemiological study included 1053 school children aged 13-17 years. All pupils filled in a questionnaire on building-related symptoms and other relevant health aspects. The following exposure measurements were carried out: room temperature, CO2 level, and relative humidity; building characteristics including mold infestation were assessed, and dust was collected from floors, air, and ventilation ducts during a working day. Dust was examined for endotoxin level, and cultivated for viable molds. We did not find a positive association between building-related symptoms and extent of moisture and mold growth in the school buildings. Five of eight building-related symptoms were significantly and positively associated with the concentration of colony forming units of molds in floor dust: eye irritation, throat irritation, headache, concentration problems, and dizziness. After adjusting for different potentially confounding factors in separate analyses of each symptom, the above-mentioned associations between molds in dust and symptoms were still present, except for concentration problems. However, in none of the analyses was mold exposure the strongest covariate, being secondary to either asthma, hay fever, recent airway infection, or psychosocial factors.
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PMID:Molds in floor dust and building-related symptoms in adolescent school children. 1475 47

Based on prior studies, the hypothesis that hyperventilation (HV) may have a pressor effect and play a causal role in hypertension has been suggested. The objective of this study was to correlate HV with blood pressure (BP)-change during a postural challenge. Consecutive subjects referred for evaluation of syncope, dizziness, chronic fatigue syndrome (CFS), fibromyalgia, or non-CFS fatigue were assessed with a 10-min supine 30-min head-up tilt test combined with capnography. We selected for analysis the records of patients aged 17-70 years, not taking vasoactive medications, having sitting systolic BP (SBP) < 140 mmHg, sitting diastolic BP (DBP) < 90 mmHg, and who completed 30 min of tilt. HV was diagnosed when end-tidal pressure of CO2 < 30 mmHg was recorded consecutively for > or = 10 min. Postural hypertension (PHT) was diagnosed when DBP on tilt > or = 90 mmHg was recorded consecutively for > or = 10 min. DBP-change was computed as (median DBP on tilt) -(median DBP supine). PHT and DBP-change were correlated with HV. A total of 320 patient charts were reviewed. PHT was present in 30 cases. The mean DBP-change in patients with PHT was +9.9 mmHg (s.d. 5.8), with three patients manifesting HV. Of the remaining 290 patients, 56 had HV, their mean DBP-change was -0.3 mmHg (s.d. 7.2). The other 234 patients without HV had a mean DBP-change +0.95 mmHg (s.d. 5.7), comparable to the DBP-change in patients with HV. In, conclusion, posturally induced HV was not associated with an increase in BP, nor was PHT associated with HV, except in a small minority of cases.
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PMID:Hyperventilation and amplified blood pressure response: is there a link? 1583 38

Carbon monoxide, a byproduct of incomplete hydrocarbon combustion, has been responsible for many accidental poisonings worldwide. The signs and symptoms of poisoning are diverse, ranging from headache, dizziness, and confusion to cardiac and neurological disturbances. Oxygen is the cornerstone of treatment, because it accelerates the dissociation of carbon monoxide from heme proteins. The role of hyperbaric oxygen in the treatment of CO poisoning is still questionable. Only a few randomized, controlled studies have been conducted, and their results are inconsistent. In the present review, we discuss the conclusions of four randomized controlled studies and propose a hyperbaric oxygen treatment protocol based on these conclusions.
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PMID:Hyperbaric oxygen in the treatment of carbon monoxide poisoning. 1590 92

Carbon monoxide is an insidious poison that accounts for thousands of deaths each year in North America. Clinical effects maybe diverse and include headache, dizziness, nausea, vomiting,syn-cope, seizures, coma, dysrhythmias, and cardiac ischemia. Children, pregnant women, and patients who have underlying cardiovascular disease are particularly at risk for adverse out-comes. Treatment consists of oxygen therapy, supportive care, and, in selected cases, hyperbaric oxygen therapy.
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PMID:Toxicity associated with carbon monoxide. 1656 27

This study investigated whether sick building syndrome (SBS) complaints and indoor air pollution for office workers are associated with oxidative stress indicated by urinary 8-hydroxydeoxyguanosine (8-OHdG). With informed consent, 389 employees in 87 government offices of 8 high-rise buildings in Taipei city completed self-reported questionnaires on SBS complaints at work in the past month. Urinary 8-OHdG was determined for each study participant and on-site air pollutants were measured for each office in both indoor and outdoor air. The results showed that urinary 8-OHdG had significant associations with volatile organic compounds and carbon dioxide levels in offices, and with urinary cotinine levels. The mean urinary 8-OHdG level was also significantly higher in participants with SBS symptoms than in those without such complaints (6.16 vs. 5.45 mug/g creatinine, p = .047). The mean 8-OHdG increased as the number of SBS symptoms increased. The multivariate logistic regression analyses showed that the adjusted odds ratios (OR) in relation to micrograms per gram creatinine increase in 8-OHdG were statistically significant for eye dryness (1.12), upper respiratory syndrome (1.17) with particularly nose itching (1.25), sneezing (1.51), dry throat (1.21), skin dryness (1.31), and dizziness (1.19). This study indicates that the 8-OHdG level was significantly associated with SBS complaints after controlling for air pollution and smoking. Whether the 8-OHdG can be used as an effective predictor for SBS symptoms deserves further study.
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PMID:Oxidative stress associated with indoor air pollution and sick building syndrome-related symptoms among office workers in Taiwan. 1712 43

Carbon monoxide (CO) is a colorless, odorless, tasteless toxic gas produced by incomplete combustion in fuel-burning devices such as motor vehicles, gas-powered furnaces, and portable generators. Persons with CO poisoning often overlook the symptoms (e.g., headache, nausea, dizziness, or confusion), and undetected exposure can be fatal. Unintentional CO exposure accounts for an estimated 15,000 emergency department visits and 500 unintentional deaths in the United States each year. The most recent state-level estimates of CO-related deaths were described in 1991 for the years 1979-1988. Using the most recent mortality data available, this report updates national and state-specific unintentional, non-fire-related CO mortality rates and describes the demographic, seasonal, and geographic patterns for 1999-2004. During this period, an average of 439 persons died annually from unintentional, non-fire-related CO poisoning, and the national average annual death rate was 1.5 per million persons. However, rates varied by demographic subgroup, month of the year, and state. Rates were highest among adults aged > or =65 years, men, non-Hispanic whites, and non-Hispanic blacks. The average number of deaths was highest during January. Among the states, Nebraska had the highest reliable CO mortality rate. These findings indicate that improved population-based prevention measures, including educating the public about the dangers of CO exposure, are needed at the state and national levels.
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PMID:Carbon monoxide--related deaths--United States, 1999-2004. 1809 42


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