Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of an anaphylactoid shock in a patient treated with beta-adrenergic blocking agents during a long time prior to surgery constitutes a high risk because beta-receptors are refractory to adrenergic substances and compensatory mechanisms are obtunded. The shock is characterized by severe hypotension and bradycardia, both resistant to adrenaline. These signs were observed in a patient treated with metoprolol for hypertension several months prior to surgery. The intravenous injection of an iodine containing contrast medium during general anaesthesia was followed by a lethal anaphylactoid shock resistant to adrenaline, atropine and isoprenaline. The treatment of the shock needs, besides adrenaline, massive vascular filling, high doses of beta-agonists and glucagon.
 ...
PMID:[Fatal anaphylactic shock in a patient treated with beta-blockers]. 615 72

A 31 year-old inhabitant of French Guiana was prescribed mercuric iodide per os for two and a half months. Shortly before the end of the treatment he developed fasciculations in the trunk and particularly the lower limb muscles, distal painful paresthesias with vasomotor disorders, episodes of excessive perspiration and palmoplantar erythema, moderate fluctuating hypertension, progressive loss of weight and irritability with insomnia. Clinical and electrical signs of neuropathy were lacking. The clinical picture was that of Morvan's fibrillary chorea with acrodynia, the conditions of onset strongly suggesting a mercurial intoxication. Blood and particularly urine mercury levels were elevated. Administration of dimercaprol (BAL) considerably increased urinary excretion of mercury and there was progressive improvement and finally recovery after two months of BAL treatment. This case exemplifies the possible co-existence of fibrillary chorea and acrodynia. Whereas in many cases of fibrillary chorea a precise etiology cannot be determined, the affection can be induced by mercury as by gold administration. The fact that cases of fibrillary chorea due to mercury poisoning are rarely reported may be the result of individual patient hypersensitivity or particular metabolic absorption and excretion features of mercury. This case cannot be included within the continuous activity syndrome of muscle fibers described by Isaacs, since muscle contractures were absent and there was associated acrodynia. Moreover, there was no latent polyneuropathy, in spite of the intense fasciculations. It must be concluded, therefore, that in spite of its rarity fibrillary chorea should keep its semiologic autonomy.
 ...
PMID:[Morvan's fibrillary chorea and acrodynic syndrome following mercury treatment]. 652 13

Salt once was a scarce commodity and for some governments salt tax was an important income. The Na content of a diet without any processed foods or added salt would be approximately 400-500 mg. Food industry contributes substantial amounts of salt. A nutrition policy on Na should include regulation of the Na content in infant formulas and a decreased Na intake to reduce the risk of hypertension and possibly also gastric cancer. Iodized salt is an important source of iodine in many countries. Recommendations regarding Na intake have been given in some recommended dietary intakes and in several dietary guidelines. During the last years a few Western countries have published action programmes regarding Na and hypertension. Very few countries have standards regulating the salt content of certain products but in case any claims are made related to the Na content, this usually has to be declared. Special dietary foods with low Na content and salt substitutes are available in many countries. Standards for such products have been published by the FAO/WHO Codex Alimentarius Commission.
 ...
PMID:Sodium in nutrition policy. 653 38

A 48-year-old woman with a known history of hypothyroidism was admitted to the intensive care unit with a diagnosis of thyroid storm secondary to acute thyroid hormone poisoning and the possible hyperfunction of a singular thyroid nodule. Her clinical manifestations included pyrexia, tachycardia, tachypnea, hypertension, RUQ abdominal pain, psychotic behavior, and pharyngitis. She was successfully treated with sodium iodide, PTU, propranolol, antibiotics, and a hypothermia mattress, with her serum T4 level returning to normal range prior to discharge. The patient was discharged 9 days after admission in good medical health with no medication. This article clearly shows that the functions of the endocrine system remain a frontier in today's medicine. With research, perhaps one day we might fully understand the intricate pathophysiology that results in thyroid storm. The potential problem format has been utilized in the development of the nursing care plan to assist the nurse with identifying and defining her patient's problems, as well as directing her assessment and nursing intervention. As more is learned about thyroid storm, nurses should update their knowledge so that they will be prepared to care for the patient with these difficult nursing problems.
 ...
PMID:Thyroid storm--a nursing crisis. 655 51

Iodine-labeled ([125I]) rat urinary kallikrein and rat urinary TAME esterase A2 were used as probes to look for urinary and plasma proteins that bind to these enzymes. Such proteins are presumptive enzyme inhibitors. Complexes formed with labeled enzymes were identified by polyacrylamide gel electrophoresis followed by autoradiography. Urine from young (6 weeks old) Dahl salt-sensitive (S) rats showed no, or only traces, of protein binding to kallikrein. Concomitant with the slow development of hypertension and proteinuria in S rats fed normal rat chow, one of the six kallikrein-binding proteins demonstrable in plasma was readily found in S-rat urine. This kallikrein-binding protein was called "KBP-1." R rats showed either no or much less KBP-1 in the urine, compared to S rats up to 5 months of age. A partly purified preparation of KBP-1 was shown to inhibit the TAME esterase activity of rat urinary kallikrein in the radiometric TAME assay. Urine of proteinuric S rats also contained two TAME esterase-binding proteins, TEBP-1 and TEBP-2, detected with the [125I]-esterase A2 probe. As S rats aged from 3 to 8 months, free KBP-1 disappeared from the urine in spite of increased and marked proteinuria and the continued presence of KBP-1 in plasma. Concomitant with this age-related loss of urinary KBP-1 there was a marked shift in S urinary proteins binding to [125I]-esterase A2 from TEBP-1 to TEBP-2. It was speculated that KBP-1 and TEBP-1 were the same protein detectable with either labeled kallikrein or labeled esterase A2. The concomitant disappearance of free KBP-1 (TEBP-1) and the appearance of free TEBP-2 in the urine of old, hypertensive, proteinuric S rats suggests that: 1) most of the KBP-1 (TEBP-1) is bound to enzyme(s) in old rats; or 2) KBP-1 (TEBP-1) is largely converted to TEBP-2 in old rats; or 3) both are true and that binding of KBP-1 (TEBP-1) to enzymes is associated with the generation of TEBP-2.
Hypertension
PMID:Proteins binding to kallikrein and esterase A2 in the urine of salt-sensitive and salt-resistant rats. 675 95

Carcinoid tumors with hepatic involvement can produce intense flushing, tachycardia, hypotension or hypertension and diarrhoea. Patients with limited cardiac reserve may not tolerate these effects under anaesthesia. Valvular heart disease associated with carcinoid tumors has been reported, but there is no record in the literature of such an association with coronary artery disease. This report presents the anaesthetic management of a patient with coronary artery disease and carcinoid tumor undergoing myocardial revascularization. Emphasis is placed on the rational use of anaesthetic and adjunctive agents which will minimize the incidence of carcinoid symptons. The salient features of the management are prevention of release of vasoactive substances by the use of promethazine hydrochloride during operation, the avoidance of stropine, prophylactic administration of corticosteroids and smooth induction of anaesthesia by the use of diazepam and dimethyl-tubocurarine iodide (Metocurine).
 ...
PMID:Anaesthetic management of a patient with carcinoid tumor undergoing myocardial revascularization. 696 32

It has been shown that the blood-brain barrier (BBB) of chronically hypertensive adult spontaneously hypertensive rats (SHR) is less susceptible to disruption during acute superimposed hypertension than normotensive controls. The purpose of this study was to determine if the BBB of young SHR, not yet markedly hypertensive, was similarly protected during super-imposed acute hypertension. Spontaneously hypertensive rats (n = 22) and normotensive Wistar-Kyoto rats (WKY) (n = 23) 4-5 weeks of age were anesthetized with secobarbital sodium (50 mg/kg) intraperitoneally and acute hypertension was produced by an intravenous injection of norepinephrine (75 micrograms). Permeability of the BBB was studied with radioactive iodine serum albumin (RISA) injected intravenously. The ratio of brain-to-blood RISA X 100 was used as an index of permeability of the BBB expressed as % protein transfer. In WKY exposed to acute hypertension mean arterial pressure increased by 52 +/- 2 mmHg and in SHR the increase was 49 +/- 3 mmHg. The protein transfer of the cerebral hemispheres was 1.17 +/- 0.30% in WKY and 0.90 +/- 0.20% in SHR (P less than 0.40). These data indicate that BBB protein transfer during acute superimposed hypertension does not differ between young SHR and WKY. Thus, the reduced susceptibility to BBB disruption in chronically hypertensive adult SHR is not present in young SHR, making them as susceptible as WKY to cerebral complications related to protein transfer during acute hypertension.
 ...
PMID:The blood-brain barrier in young spontaneously hypertensive rats. 711 67

In patients with arterial hypertension as most frequent disturbance of the electrolyte balance a hypopotassaemia is observed. Examinations of our working team on 517 patients with hypertension exhibited a prevalence of the hypopotassaemia of 3%, in which case in the greater part of these patients (1.6%) a decrease of the serum potassium levels induced by diuretics was present. In the other patients in 1.2% of the cases a secondary and only in 0.2% of the patients a primary aldosteronism was diagnosed as underlying cause. The leading clinical symptom of the primary aldosteronism is a hypopotassaemic hypertension. The diagnosis of the disease is ascertained by the proof of a pathologically increased plasma aldosterone concentration and of a decreased and non-measurable renin activity, respectively. Since these peripheral hormone values do not allow a differential diagnosis between an adenoma producing aldosterone and an idiopathic hyperplasis of the adrenal cortex, further investigations for the differentiation of these two main forms of the primary aldosteronism must be performed. These investigations are: Phlebography of the suprarenal bodies, determination of the aldosterone concentration in the blood of the adrenal veins and iodine-131-cholesterol scintigraphy. Patients with an adenoma producing aldosterone are unilaterally adrenalectomized, while an operative intervention has no essential influence of the behaviour of the blood pressure in cases with idiopathic hyperplasia of the adrenal cortex. Therefore, these cases must be treated antihypertensively. A pseudo-primary aldosteronism, also shows a hypopotassaemic hypertension as leading symptom. In contrast to the genuine primary aldosteronism this disease, differs by the proof of low plasma aldosterone levels. A pseudo-primary aldosteronism is caused by the exogenic supply of mineralocorticoid-effective substances. A hypopotassaemia in patients with Cushing's syndrome should, above all when it is very expressed, attract the suspicion to a cortisol-producing carcinoma of the adrenal cortex. The hypopotassaemia in these patients is caused by additional abnormally high tumour production of mineralocorticoid-effective steroids.
 ...
PMID:[Electrolyte balance in arterial hypertension (continuation)]. 721 Jul 51

Physostigmine (P) was used as a model in anesthetized rats for the development of hypertension by a central cholinergic mechanism. P (25-100 micrograms/kg i.v.) produced a dose-related increase in mean arterial pressure which was inhibited 30 to 90% by preinjection of clonidine (100 micrograms/kg i.v.). This dose of clonidine was without effect on the pressor response to ganglionic stimulation produced by 1,1-dimethyl-4-phenylpipera-zinium iodine. To examine further the central inhibitory effect of clonidine on the pressor response to P, regional brain acetylcholine turnover rate was measured in control and clonidine-pretreated rats. Clonidine significantly reduced turnover in hypothalamus (69%), pons-medulla (43%) and midbrain (39%) but not in striatum or hippocampus. These observations are consistent with an inhibitory effect of clonidine on central cholinergic neurons involved in cardiovascular regulation.
 ...
PMID:Mechanism of the antihypertensive action of clonidine on the pressor response to physostigmine. 735 26

Hypertension may be induced by pharmacologic activation of central cholinergic receptors either indirectly, through the injection i.v. of physostigmine, or directly, through the injection of i.v. of arecholine in anesthetized rats. Activation of peripheral preganglionic cholinergic receptors with dimethylphenylpiperazinium iodide (DMPP) also produced a hypertensive response. Pretreatment with various doses of clonidine caused inhibition of the pressor response to central cholinergic stimulation but was without effect on the response to ganglionic cholinergic stimulation.
 ...
PMID:Influence of clonidine on experimental hypertension induced by cholinergic stimulation. 741 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>