Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old female with a 30-year history of untreated essential hypertension was noted to have a blood pressure of 290/175 mmHg during evaluation for elective gynecological surgery. At the time of hospitalization she complained chiefly of chronic frontal headaches. Physical examination revealed grade two hypertensive retinopathy, and laboratory studies showed left ventricular hypertrophy. Over the next 12 days the patient's blood pressure was successfully lowered to 178/106 mmHg. During revision of her therapy her mean blood pressure rose to 244/144 mm Hg (88% of the admission level) over 36 hours and she developed hypertensive encephalopathy with papilledema, headaches and projectile vomiting. Concomitant resolution of neurological symptoms and control of blood pressure occurred over the next nine days. The course of this patient suggests that autoregulation of cerebral blood flow may be acutely reversed and that the occurrence of hypertensive encephalopathy depends not only on the magnitude and duration of the blood pressure elevation but, more important, on the rate at which that blood pressure is attained.
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PMID:Iatrogenically induced hypertensive encephalopathy. 45 3

The efficacy of fixed dose PGE2 (prostaglandin E2) in inducing labor was studied in 40 multiparous patients. Low amniotomy was performed, and 1 tablet of 6.5 mg PGE2 was given orally in the absence of uterine activity after 30 minutes, and hourly thereafter until the patient delivered. Successful induction was defined as the establishment of effective uterine contractions and cervical dilatation within 12 hours of amniotomy. Indications for induction are postmaturity (n=15); pre-eclampsia (n=10); essential hypertension (n=6); weight loss (n=4); bad obstetric history (n=2); and others (n=3). 38 patients (95 percent) had successful labor induction, with 37 delivering vaginally within 18 hours of amniotomy and 1 delivering by Cesarian section because of fetal distress. In the remaining 2 patients, labor did not commence within 12 hours and consequently necessitated intravenous oxytocin. Mean amniotomy-delivery interval was 7.53 hours. Maternal side effects included vomiting (12.5%); diarrhea (5%); pyrexia (15%); ketonuria (22.5%); and postpartum hemorrhage (12.5%). There were no apparent fetal side effects. Advantages of oral PGE2 for labor induction include: 1) ease of administration; 2) increased patient acceptability; 3) greater convenience for medical and nursing staff; 4) absence of complications associated with intravenous infusion such as sudden changes in infusion rate, air emboli or occasional pyrogen reactions. Advantages of using a low fixed dose are: 1) excessive administration and subsequent uterine hypertonus are less likely to occur; 2) low incidence of vomiting/diarrhea; and 3) absence of uterine hypertonus and apparent fetal side effects.
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PMID:Fixed dose prostaglandin E2 tablets in the induction of labour in multipara. 108 93

A multicenter open trial involving 50 hypertension patients enabled evaluation of the efficacy and tolerability of Isoptine L.P. (sustained release verapamil) in mild to moderate essential hypertension. Following a 2-week placebo run-in period, patients were given Isoptine L.P. (240 mg/24 h) as a morning dose for 3 months, with a possible dose increase (360 mg/24 h) in case of diastolic blood pressure of 95 mmHg or more at the 30-day evaluation. Blood pressure was measured by mercury sphygmomanometer and, in 20 patients, by a Dinamap type Automatic device. After 3 months of treatment, blood pressure levels in supine and standing position, measured manually and automatically, showed a highly significant decrease, with a mean fall of 18.4 mmHg for systolic (13.7 percent) and 13.2 mmHg diastolic (-14.6 percent). 67 percent of patients were responders after 1 month of treatment and 79 percent at 3 months, including one-fifth at the dose of 360 mg/24 h. Seventeen patients, i.e. 34 percent, reported one or more adverse reactions. Among these, four patients had to stop treatment, twice because of headache and twice for constipation. Adverse events seen most frequently were constipation, headache, tiredness and vomiting. No cardiac adverse events were reported with the exception of one case of atrial premature contractions. The electrocardiogram revealed significant slowing of heart rate, as well as slight prolongation of PR and QT intervals and slight widening of the QRS complex. Tolerability on the basis of laboratory parameters was good.
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PMID:[Efficacy and tolerability of isoptine LP in mild to moderate hypertension. A multicenter study with 50 patients]. 130 Sep 22

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c) AMP is known to act as a second messenger for inhibition of platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side-effects, primarily, nausea, emesis, flushing, diaphoresis, and restlessness. In hypertensive patients blood-pressure responses are complex and are influenced to some extent by renin secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and it also has an indirect effect by activating the sympathetic nervous system. Thus, it is useless as an antihypertensive agent even apart from its debilitating side-effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize large amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be greatly reduced. Some drugs (thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to reduce their antihypertensive effects. The effects of low- and high-dose aspirin on prostacyclin and thromboxane synthesis are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostacyclin in hypertension]. 149 51

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

The efficacy of bromocriptine in the treatment of hypertension was assessed in a double-blind placebo controlled cross-over study preceded by a dose titration phase. A diuretic and/or a beta-blocker were administered concomitantly in constant dosage to 11 of the 20 patients who received bromocriptine. A wide range of doses of bromocriptine was tolerated. Side-effects of vomiting and postural hypertension did not occur, possibly due to the gradual increase in the administered doses. Plasma prolactin was not raised in this population of hypertensives. In the dose titration phase (n = 20), a small fall in diastolic but not in systolic blood pressure occurred with bromocriptine, but only with the patient standing and after exercise. In the double-blind phase (n = 9), there was no significant difference in blood pressure between the bromocriptine and placebo treatments. It is concluded that bromocriptine was not effective in lowering blood pressure in the present patients with essential hypertension.
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PMID:Bromocriptine in the treatment of hypertension. 351 42

One thousand four hundred and two patients with essential hypertension were treated by their general practitioners for 3 months with one tablet daily consisting of 200 mg acebutolol plus 12.5 mg hydrochlorothiazide: 813 were newly diagnosed and 589 were known hypertensives already on treatment. There was no 'wash-out' period before the latter changed to the study treatment. Newly diagnosed hypertensives had an average initial mean arterial pressure (MAP) of 129.9 mm Hg which fell on average by 18.2% during the study: 79% of patients had good results with final MAP levels less than 113 mm Hg (equivalent to e.g., 160/90 mm Hg), and a further 7% also had good results in that MAP fell more than 15%, another 12.5% had moderate results (falls of 5% to 15%): and only 1.5% had poor results (fell less than 5%). Known hypertensives had an average MAP of 127 mm Hg on previous treatment, which fell on average by 15.4% during this study: 70% of patients had good results with final MAP levels less than 113 mm Hg and a further 7% also had good results in that MAP fell more than 15%: 18% had moderate results and 3% poor results. Pulse rate fell by 12.5% in newly diagnosed and 10% in known treated hypertensives. If allowance is made for withdrawals due to side-effects and to the need for more than one tablet of Secadrex daily, then over all 75.7% had a good blood pressure response to study medication, 13.7% a moderate response and 10.7% a poor response. Adverse effects caused the withdrawal of 4% of newly diagnosed and 5% of treated hypertensives, predominantly nausea/vomiting, lassitude/fatigue and malaise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of essential hypertension with beta-blocker plus diuretic: a study of 1402 patients treated by general practitioners with acebutolol 200 mg combined with hydrochlorothiazide 12.5 mg ('Secadrex') once daily for 3 months. 637 43

Essential hypertension is a heterogenous disease made up of several still unspecified subgroups. According to the dual theory of hypertension, acquired and genetic factors can lead to vascular muscle defects and increased sympathetic drive, which, either both or each alone, can lead to an increased vascular resistance. Acquired factors can either help a predisposition to become a manifest disease, act by itself to cause a disease or prevent a genetic trait from becoming manifest. Among the acquired factors, we differentiate those lying inside the personality, which means they are early acquired in life and those lying outside of the individual such as job-stress, noise exposure etc. How the external stressors are perceived depends upon the personality make up and the social support system. Within the presented model the Greek word 'crisis' plays an important role, since it characterizes a state in which a decision has to be made. In a situation in which a decision cannot be made in reality or tried out in fantasy life, the organism will activate the autonomic nervous system in a planless fashion, alternating very rapidly between its two branches, with concomitant symptoms of trembling, piloerection, salivation, vomiting, urination, defecation etc. In case this persists for a longer period of time the reciprocity between the two systems may break down, the organism seems to be psychologically immobilized. In the beginning of stress exposure, increased sympathetic nervous system activity is seen as an adaptive response, thereby enabling the individual to cope, but if the attempts to cope meet with constant failure, the stress becomes unbearable. The attitude of giving up which then develops is accompanied by a low level functioning of the sympathetic nervous system. This goes along with an adaptation for the baroreceptor depressor mechanism. As a consequence, any kind of additional stress would not lead to a relieving counterregulation. This might be a small stone within the mosaic of essential hypertension.
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PMID:[Essential hypertension: psychosomatic aspects]. 794 88

The use of diuretics leads to a negative sodium and fluid balance without primary effects on serum sodium concentration. This parameter is regulated by the activity of the antidiuretic hormone (ADH) system. Secondary changes in other electrolyte systems and in acid base homeostasis also are induced by diuretic therapy. Especially diuretic induced hypokalemia is important as it is responsible for the excess mortality observed in patients with diuretic treated essential hypertension and cardiac abnormalities. All adverse metabolic effects of diuretic therapy are, in contrast to the antihypertensive action, dose dependent. Changes in fluid and electrolyte metabolism induced by diuretics occur within the first 2 or 3 weeks after initiation of medication. Counterregulatory mechanisms are activated and a new steady state is established. Serial laboratory determinations after this period are not necessary as long as this steady state is not affected by additional events (like a change in therapy or diet as well as the occurrence of vomiting or diarrhea).
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PMID:[Effects of diuretic therapy on electrolyte and acid-base homeostasis]. 903 78

We designed a study to determine the efficacy and safety of amlodipine given once daily in the pediatric population. Twenty-one patients (mean age 13.1 years) with either essential (n=160) or renal (n=5) hypertension, and newly diagnosed (n=15) or poorly controlled or intolerant on existing antihypertensive therapy (n=6), were included. Patients received amlodipine once daily at a starting mean dose of 0.07+/-0.04 mg/kg per day. The total daily dose of amlodipine was increased 25%-50% every 5-7 days if the mean home blood pressure measurements (HBPM) were above the 95th percentile for age and gender. A baseline followed by a repeat 24-h ambulatory blood pressure monitor study (ABPM) was performed in 20 patients when the mean HBPM was below the 95th percentile goal. The mean titrated dose required to control BP was 0.29+/-0.11 mg/kg per day for those < 13 years, 0.16+/-0.11 mg/kg per day for those > or = 13 years, 0.23+/-0.14 mg/kg per day for essential, hypertension and 0.24+/-0.13 mg/kg per day for renal hypertension. The ABPM demonstrated that amlodipine provided effective BP control as primary therapy in 14 essential patients. Adverse effects included fatigue (n=6), headache (n=5), facial flushing (n=4), dizziness (n=3), edema (n=3), abdominal pain (n=3), chest pain (n=2), nausea (n=1), and vomiting (n=1). Quality of life appeared to improve during therapy. Amlodipine was an effective once daily antihypertensive agent with an acceptable safety profile. Higher doses of amlodipine were required for younger patients, and monotherapy was effective in patients with essential hypertension.
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PMID:Efficacy of amlodipine in pediatric patients with hypertension. 1045 79


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