Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

Two diving incidents were investigated in which 1) an experienced professional diver (A) lost consciousness during an air dive to 69 meters, and 2) an amateur sports diver (D) lost consciousness during a 40-meter air dive. In subsequent tests both divers' ventilatory responses to inspired carbon dioxide were found to be extremely low. Under simulated diving conditions, Divers A and D exhibited marked carbon dioxide retention during exercise at 30 meters (end-tidal PCO2 = 65 and 57 mmHg, respectively) and at 70 meters, Diver A stopped work in less than 3 min because of severe dizziness. Reduced sensitivity to carbon dioxide, perhaps caused by the interaction of hypercapnia and nitrogen narcosis, is thought to have been partly responsible for these incidents.
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PMID:Observations after loss of consciousness under water. 67 82

Five subjects were compressed to 1000 ft (31 ATA) for 2 h breathing 3.2 ATA nitrogen, 0.5 ATA oxygen, and the remainder helium. The compression took 33 min with a 10-s stage at 50 ft (2.5 ATA), 1 MIN AT 320 FT (10.7 ATA), and 2 min at 700 ft (22 ATA). Hypothetically, this 1:10 ratio for nitrogen-helium partial pressures should induce neither nitrogen narcosis nor the High Pressure Nervous Syndrome (HPNS). Tests, therefore, were made during the experiment of postural tremor, spontaneous electroencephalogram, psychomotor and intellectual activities, and subjective sensations. One diver worked underwater for 40 min on a simulated engineering assembly while breathing with a closed-circuit breathing apparatus and wearing a battery-heated suit in water at 56 degrees F. Decompression was in 4 d using 0.8 ATA oxygen and helium. The performance tests indicated no narcosis and little or no signs of HPNS. No tremor or EEG changes were seen. The "wet" diver reported sensations of mild euphoria but the other four reported no difficulties. No nausea or dizziness of HPNS was reported. It is concluded that use of a ratio of 1:10::N2:He is effective in the control of narcosis and HPNS during rapid compression to 1000 ft (31 ATA).
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PMID:Optimal use of nitrogen to suppress the high pressure nervous syndrome. 111 94

A total of 930 patients have been evaluated for safety in a programme of clinical trials for lisinopril-hydrochlorothiazide combination treatment. Combination therapy with these two agents is generally well tolerated. In clinical trials, adverse experiences in patients treated with a lisinopril-hydrochlorothiazide combination were dizziness (7.5%), headache (5.2%), cough (3.9%), fatigue (3.7%), orthostatic effects (3.2%), diarrhoea (2.5%), nausea (2.2%) and upper respiratory tract infection (2.2%). Withdrawals from treatment have been relatively infrequent comprising dizziness (0.8%), headache (0.3%), cough (0.6%), fatigue (0.4%), diarrhoea (0.2%), orthostatic effects and nausea (0.1% each). The most common laboratory adverse experiences in patients on therapy with the lisinopril-hydrochlorothiazide combination are: increases in serum glucose, triglycerides, uric acid, serum creatinine, blood urea nitrogen and blood urea; and decreases in serum potassium. However, in individual controlled studies, the addition of lisinopril to treatment with hydrochlorothiazide results in attenuation of some of the potentially adverse metabolic affects of the diuretic. Adverse experiences in the patients treated for periods of 50 weeks or more, the elderly and the renally impaired are similar to those seen in the total population. Overall the available data indicate that a fixed dose combination of lisinopril-hydrochlorothiazide is a well-tolerated therapeutic option in patients with mild-to-moderate hypertension.
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PMID:Review of international safety data for lisinopril-hydrochlorothiazide combination treatment. 166 80

Carvedilol, a novel beta-blocker with a vasodilating action, was given either alone (monotherapy) or with diuretics (combination therapy) to 42 patients with renal hypertension. The hypotensive effect, safety, and optimal dose were investigated. In all, 23 untreated patients (16 men and 7 women; average age, 56.4 +/- 2.5 years) made up the monotherapy group and 19 diuretic-treated patients (11 men and 8 women; average age, 56.4 +/- 2.5 years) comprised the combined therapy group. All subjects had an initial blood pressure (BP) of greater than 160/95 mmHg and were started on 5 mg/day oral carvedilol. The dose was gradually increased to a maximum of 20 mg/day, or until either the BP was reduced to less than 149/89 mmHg or the reduction in mean BP was greater than 13 mmHg compared with baseline levels. The total study period was 8 weeks. With monotherapy, the BP and heart rate decreased significantly from 167/102 to 150/94 mmHg and from 81 to 74 beats/min, respectively. With combined therapy, the BP and heart rate fell significantly from 176/103 to 142/85 mmHg and from 81 to 70 beats/min, respectively. Responders were defined as subjects with a BP of less than or equal to 149/89 mmHg or those showing a fall of greater than or equal to 13 mmHg in mean BP. Responders accounted for 52.2% of the monotherapy group and 73.6% of the combination therapy group. Orthostatic hypotension was not seen in either group. Serum creatinine and blood urea nitrogen (BUN) levels were not altered by administration of carvedilol. Dizziness was noted by 1 of the 23 subjects in the monotherapy group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy and safety of carvedilol in renal hypertension. A multicenter open trial. 197 8

This report reviews the tolerability profile of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, in the treatment of patients with congestive heart failure. Data have been collected from 546 patients treated with enalapril for up to 9 months in clinical trials other than the Cooperative North Scandinavian Enalapril Survival Study. Results in patients treated with enalapril (n = 193) or placebo (n = 195) in double-blind, controlled clinical trials show that the incidences of death, serious adverse experiences, and adverse experiences requiring discontinuation of double-blind therapy, as well as the overall incidence of such experiences, were similar in the 2 groups. However, certain adverse experiences that are related to the mechanism of action of ACE inhibitors were seen more often after enalapril than after placebo treatment. Dizziness and hypotension were the most frequent adverse experiences reported in patients with heart failure treated with enalapril. The most frequent laboratory adverse experiences were increases in blood urea nitrogen and serum creatinine levels. hyperkalemia was also seen in patients receiving enalapril. It is possible to identify patients at risk of these experiences before initiating treatment with enalapril and to take certain measures (such as withholding or reducing the dose of diuretic drugs and discontinuing potassium supplements or potassium-sparing diuretic drugs) to reduce the likelihood that hypotension, increases in blood urea nitrogen and serum creatinine levels, or hyperkalemia will occur. Angioedema, a recognized adverse effect of ACE inhibitors, was not seen in the clinical trials reviewed here. Cough , another recognized adverse effect of these agents, was seen infrequently and rarely resulted in the discontinuation of enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerability of enalapril in congestive heart failure. 253 64

Benzoate and phenylacetate improve prognosis in inherited urea cycle enzyme deficiencies by increasing waste nitrogen excretion as amino acid acylation products. We studied metabolic changes caused by these substances and their pharmacokinetics in a biochemically different urea cycle disorder, lysinuric protein intolerance (LPI), under strictly standardized induction of hyperammonemia. Five patients with LPI received an intravenous infusion of 6.6 mmol/kg L-alanine alone and separately with 2.0 mmol/kg of benzoate or phenylacetate in 90 min. Blood for ammonia, serum urea and creatinine, plasma benzoate, hippurate, phenylacetate, phenylacetylglutamine, and amino acids was obtained at 0, 120, 180, and 270 min. Urine was collected in four consecutive 6-h periods. Alanine caused hyperammonemia: maximum increase 107, 28-411 microM (geometric mean, 95% confidence interval); ammonia increments were nearly identical after alanine + benzoate (60, 17-213 microM) and alanine + phenylacetate (79, 13-467 microM) (NS). Mean plasma benzoate was 6.0 mM when extrapolated to the end of alanine + benzoate infusions; phenylacetate was 4.9 mM at the end of alanine + phenylacetate. Transient toxicity (dizziness, nausea, vomiting) occurred in four patients at the end of combined infusions, and we suggest upper therapeutic plasma concentrations of 4.5 mM for benzoate and 3.5 mM for phenylacetate. Benzoate and phenylacetate then decreased following first-order kinetics with t1/2S of 273 and 254 min, respectively. Maximal plasma hippurate (0.24, 0.14-0.40 mM) was lower than maximal phenylacetylglutamine (0.48, 0.22-1.06 mM, p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Waste nitrogen excretion via amino acid acylation: benzoate and phenylacetate in lysinuric protein intolerance. 309 49

In patients with portal hypertension and tense ascites, large-volume paracentesis improves patient comfort and may improve systemic hemodynamics. However, it has been avoided in nonedematous patients because of concern for complications, including intravascular volume depletion. In this study, 12 nonedematous patients with chronic liver disease, portal hypertension and tense ascites underwent 14 large-volume (5-liter) paracenteses for the relief of discomfort and/or respiratory distress. Plasma volume was measured directly by a dilution method with 125I-labeled human serum albumin prior to and at 24 or 48 hr after 13 of the paracenteses. All patients felt better postparacentesis. No dizziness, hypotension, tachycardia, encephalopathy or change in mean serum sodium, creatinine or blood urea nitrogen occurred. Two patients experienced a decrease in hematocrit, which was not explained by blood loss or increase in plasma volume. Mean plasma volume was 3,713 +/- 129 ml (55.1 +/- 1.5 ml per kg ideal body weight) preparacentesis and 3,684 +/- 136 ml postparacentesis, the difference being -0.78% (p = 0.48, NS). Our results suggest that 5-liter paracentesis in nonedematous patients with tense portal hypertension-related ascites improves patient comfort and is not associated with a decrease in measured plasma volume.
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PMID:Large-volume paracentesis in nonedematous patients with tense ascites: its effect on intravascular volume. 335

Ciprofloxacin is a new quinolone antimicrobial agent with activity against a broad spectrum of gram-negative and gram-positive organisms, including Pseudomonas aeruginosa and methicillin-resistant strains of staphylococci. The efficacy and safety results of 80 clinical studies of the oral form of ciprofloxacin are reported. Drug safety was assessed in 2236 courses in 2203 adult patients treated primarily in the United States. Data from 1676 courses were suitable for analysis of drug efficacy. The unit dose for most patients ranged from 250 mg to 750 mg (median, 500 mg), usually given every 12 hours. The duration of treatment ranged from 3 to 231 days (median, 10 days). Predominant among 1722 infections were those of the urinary tract (43%), skin structures (29%), and respiratory tract (19%); the remainder were bone and joint infections (5%), bacteremias (2%), and intra-abdominal (1%), gastrointestinal (1%), and pelvic infections (less than 1%). Signs and symptoms of infection resolved in 79% of all cases; a further 15% improved, and 5% failed to improve. Pathogens were eradicated in 89% of urinary tract infections and persisted in 5%; 80% of patients still had sterile urine at the 3-to 6-week follow-up. In 81% of nonurinary tract infections, pathogens were eradicated; they persisted in 11%, and superinfection occurred in less than 5%. After treatment, 89% of the 2253 causative organisms were eradicated and 2% were reduced to clinically insignificant counts; 8% persisted. Of 411 isolates of P. aeruginosa, 77% were eradicated, as were 97% of 421 Escherichia coli and 80% of 248 Staphylococcus aureus isolates. Also eradicated were 95% of 166 Klebsiella, 96% of 139 Proteus mirabilis, 100% of 20 other Proteus, 94% of 123 Enterobacter, 100% of 68 Haemophilus influenzae, 96% of 49 Citrobacter, 89% of 45 Serratia, 95% of 41 Streptococcus pneumoniae, 91% of 43 Salmonella, 100% of 38 Morganella morganii, and 100% of 35 Providencia isolates. Adverse reactions were judged probably or possibly drug-related in 14.8% of courses; drug treatment had to be stopped prematurely in 3.5%. The most frequent reactions were gastrointestinal complaints (chiefly nausea, diarrhea, and vomiting), metabolic disorders (elevated SGOT, SGPT, serum creatinine, or blood urea nitrogen), and nervous system effects (dizziness, light-headedness, restlessness, tremor, and headache). Crystalluria, judged to be related to ciprofloxacin, occurred in two patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A survey of clinical experience with ciprofloxacin, a new quinolone antimicrobial. 336 Sep 68

Bennett (1975) reported that signs and symptoms of the High Pressure Nervous Syndrome (HPNS) appeared including nausea, dizziness, tremors of the hands and arms, increased slow wave activity in electroencephalogram, especially in the theta band (4-7 Hz) with depression of alpha (8-13 Hz) and beta (20 Hz and higher) on compression with oxygen-helium to depths greater than 500 ft (16 ATA). Earlier studies have indicated that the HPNS may be controlled by use of an increased nitrogen partial pressure, slowing compression rate or excluding subject who has higher susceptibility to HPNS. For determining the effect of slowing compression rate, it was changed to new compression profile of linear compression to 31 ATA with intermediate stops in SEADRAGON-VI carried out at JAMSTEC in 1983. All divers to compressed to 31 ATA using the new rate complained few and slight signs and symptoms involved HPNS than ever experienced.
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PMID:[On the compression rate for inhibiting high pressure nervous syndrome under high pressure helium atmosphere]. 372


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