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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 15 year old girl presented with excessive thirst and hypertension (170/110 mm Hg). Biochemical investigations revealed serum sodium 118 meq/liter, serum osmolality 238 mosmol/liter, urine sodium 90 meq/liter, urine osmolality 700 mosmol/liter, persistenly elevated serum antidiuretic hormone (ADH) levels (5.8 to 11.9 pg/ml) and no obvious cause for the hypertension. The hypertension is, at least in part, volume-related, diminishing with fluid restriction. Features of gross water intoxication (e.g., confusion, coma) have not occurred. The etiology of the inappropriate secretion of ADH is not obvious but is not thought to be due to "resetting of osmoreceptors" as evidenced by failure to maximally dilute urine following a water load test and persistently elevated serum ADH levels. A similar patient described by Epstein and associates in 1962 is presently well with persistent features of inappropriate secretion of ADH.
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PMID:Idiopathic, sustained, inappropriate secretion of ADH with associated hypertension and thirst. 47 98

Autonomic failure in patients with the Shy-Drager syndrome may produce cardiovascular instability during anaesthesia and surgery. The syndrome is reviewed and the anaesthetic management of a case is described. The choice between general and regional anaesthesia seems to be less important than adequate cardiovascular monitoring and the maintenance of blood pressure with intravenous fluids. Sympathomimetic drugs, if used at all, should be administered in very dilute solutions to avoid hypertension from denervation hypersensitivity. In the postoperative period, symptoms from orthostatic hypotension may be severe and their control requires prolonged postural training, by elevation of the head of the bed, and therapy with 9-alpha-fludrocortisone.
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PMID:Shy-Drager syndrome. A review and a description of the anaesthetic management. 53 23

A 41-year-old man, complaining of leg cramps, was found to have persistent hyperkalemia. Except for mild hypertension, his physical examination and laboratory values to exclude connective tissue diseases and diabetes mellitus were normal. Renal function testing revealed a normal glomerular filtration rate and tubular capacity to acidify and dilute, as well as near-normal ability to concentrate his urine. Hormonal evaluation revealed a normal cortisol, as well as normal resting and stimulated renin and aldosterone levels. A selective defect in tubular potassium secretion was demonstrated. In the absence of aldosterone deficiency or renal dysfunction, it was assumed that the patient had primary renal resistance to aldosterone, known as pseudohypoaldosteronism. Treatment with hydrochlorothiazide controlled his hyperkalemia and hypertension. His case emphasizes the diagnostic and therapeutic factors that should be considered in evaluating and treating a non-hospitalized patient with sustained hyperkalemia.
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PMID:Pseudohypoaldosteronism: case report and discussion of the syndrome. 178 91

During an 18-month period 33 patients in whom there were contraindications to the use of iodinated contrast arteriography underwent 40 carbon dioxide/digital subtraction arteriograms for lower extremity ischemia (19), severe hypertension and renal insufficiency (12), or arterial aneurysm (2). Contraindications to iodinated contrast agents included renal insufficiency, congestive heart failure, and contrast hypersensitivity. Sixteen aortic, 15 iliac-femoral-popliteal-tibial, five aorta-iliac-femoral and four aorta-iliac-femoral-popliteal-tibial carbon dioxide/digital subtraction arteriography studies were performed. In 11 studies, imaging of selected arterial segments required the addition of 10 to 60 ml of dilute nonionic contrast. Guided by carbon dioxide/digital subtraction arteriography studies four femoral-tibial bypasses, three aneurysmorrhaphies, two aortorenal bypasses, one aortofemoral bypass and one femoral-femoral bypass were successfully performed in 11 patients. In addition, carbon dioxide/digital subtraction arteriography directed angioplasties of the common iliac (4), superficial femoral (6), popliteal (3), or tibioperoneal trunk (1) were performed in 10 patients. Complications of carbon dioxide/digital subtraction arteriography included transient deterioration in renal function in three patients in whom 20 ml of nonionic contrast was used, a nonfatal myocardial infarction after a popliteal percutaneous transluminal angioplasty in one patient, and transient tachypnea and tachycardia during a carbon dioxide/digital subtraction arteriography study in one patient. Diagnostic arteriograms are obtainable using carbon dioxide as the contrast agent. Carbon dioxide/digital subtraction arteriography permits patients with symptomatic arterial disease at high risk for contrast related complications to safely undergo arteriography and subsequent arterial reconstruction or endovascular intervention.
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PMID:Clinical applications of carbon dioxide/digital subtraction arteriography. 189 74

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. In response to acute environmental stress (air jet), the borderline hypertensive rat exhibits a diuretic response, whereas the parental strains exhibit an antidiuretic response (spontaneously hypertensive rat) or no change in urine flow rate (Wistar-Kyoto rat). This study sought to investigate the role of the periventricular tissue surrounding the anteroventral third ventricle and vasopressin release in the diuretic response of the borderline hypertensive rat to acute environmental stress. Sixteen-week-old borderline hypertensive rats who had consumed a 1% NaCl diet for 10-12 weeks were given either electrolytic lesions of the anteroventral portion of the third ventricle or sham lesions. When exposed to acute environmental stress 4 weeks later, the increase in volume of dilute urine seen in the sham-lesion rats was not observed in the lesion rats. Plasma vasopressin concentration was decreased by acute environmental stress in the sham-lesion rats (15.2 +/- 4.0 to 10.9 +/- 1.7 pg/ml, p less than 0.05) but was unchanged in the lesion rats (12.3 +/- 2.0 to 13.4 +/- 4.0 pg/ml). In a separate group of intact borderline hypertensive rats, a constant intravenous infusion of vasopressin prevented the diuretic response to acute environmental stress. The results suggest that acute environmental stress produces a diuresis in the borderline hypertensive rats via a decrease in plasma vasopressin concentration that is dependent on the integrity of the periventricular tissue of the anteroventral portion of the third ventricle.
Hypertension 1991 Jun
PMID:Role of anteroventral third ventricle and vasopressin in renal response to stress in borderline hypertensive rats. 204 36

To investigate the diagnostic value of carbon dioxide arteriograms in patients with peripheral vascular disease, ten patients in whom standard contrast arteriography was contraindicated underwent carbon dioxide digital subtraction arteriography. Lower extremity ischemia or severe hypertension with renal insufficiency were the indications for arteriography. Standard contrast arteriography was precluded by chronic nondialysis-dependent renal insufficiency, severe congestive heart failure or contrast hypersensitivity. All critical arterial segments were well visualized with the exception of the infrapopliteal arterial tree in three patients. Adequate imaging of this segment required the addition of 20 cc of dilute nonionic contrast. Guided by carbon dioxide digital subtraction arteriography, four percutaneous transluminal angioplasties and three reconstructive procedures were successfully performed. One patient did not have surgically reconstructible disease and two had renal arteries without critical stenoses. Renal function transiently deteriorated in one patient who received 20 cc of nonionic contrast. No adverse events occurred due to carbon dioxide. Clinically useful diagnostic arteriograms are possible using carbon dioxide as the contrast agent.
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PMID:Carbon dioxide digital subtraction arteriography: a pilot study. 212 Dec 15

The tumescent technique for local anesthesia permits regional local anesthesia of the skin and subcutaneous tissues by direct infiltration. The tumescent technique uses large volumes of a dilute anesthetic solution to produce swelling and firmness of targeted areas. This investigation examines the absorption pharmacokinetics of dilute solutions of lidocaine (0.1% or 0.05%) and epinephrine (1:1,000,000) in physiologic saline following infiltration into subcutaneous fat of liposuction surgery patients. Plasma lidocaine concentrations were measured repeatedly over more than 24 hours following the infiltration. Peak plasma lidocaine levels occurred 12-14 hours after beginning the infiltration. Clinical local anesthesia is apparent for up to 18 hours, obviating the need for postoperative analgesia. Dilution of lidocaine diminishes and delays the peak plasma lidocaine concentrations, thereby reducing potential toxicity. Liposuction reduces the total amount of lidocaine absorbed systemically, but does not dramatically reduce peak plasma lidocaine levels. A safe upper limit for lidocaine dosage using the tumescent technique is estimated to be 35 mg/kg. Infiltrating a large volume of dilute epinephrine assures diffusion throughout the entire targeted area while avoiding tachycardia and hypertension. The associated vasoconstriction is so complete that there is virtually no blood loss with liposuction. The tumescent technique can be used with general anesthesia or IV sedation. However, with appropriate instrumentation and surgical method, the tumescent technique permits liposuction of large volumes of fat totally by local anesthesia, without IV sedation or narcotic analgesia.
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PMID:Tumescent technique for regional anesthesia permits lidocaine doses of 35 mg/kg for liposuction. 217 48

A case of inadvertent intravascular injection of PGF2alpha during induction of labor by intraamniotic injection for fetal demise, involving alternating extreme hypotension and hypertension, is described. The woman was a 29-year old in late 2nd trimester with oligohydramnios, but no other related history. She was given epidural anesthesia, 7.5 mg midazolam and 5 mg morphine S04 for anxiety. Because of oligohydramnios, 300 ml Ringers lactate was instilled to dilute the PG. A test dose of 1 mg PGF2alpha was tolerated well. 80 g urea and 20 mg PGF2alpha were injected over 10 minutes. A few minutes later contractions began, followed by complaints of burning on face and chest and dyspnea. Oxygen was given by mask. Systolic pressure fell to 70 mm by cuff; peripheral pulses could not be palpated, but the patient remained alert and oriented. She was given 35 mg ephedrine and increased iv fluids. She remained dyspneic, her extremities became mottled, and she complained of chest pressure, severe headache and severe breast tenderness. Blood pressure rose to 220/135 mm Hg; pulse to 95, and respiratory rate to 44. Pulse oximetry, detectable at the earlobe only, was 94% saturation. After 50 mg labetalol, blood pressure fell to 134/77, but symptoms remained. For 2 hours blood pressure swung between 76/50 and 225/125, until delivery of the fetus. An arterial line could not be started because of extreme vasoconstriction. Central venous pressure was 13 cm H20. After artificial rupture of the membranes and removal of remaining PG, blood pressure stabilized. Delivery was accomplished without incident. The symptoms and labile blood pressure were considered to be due to intravascular injection of PGF2alpha, caused by repeated bolus injection at each uterine contraction. In case of PG induction for fetal demise, it is recommended that anesthesiologists be prepared to treat intravascular collapse, hypertension and bronchoconstriction.
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PMID:Life-threatening effects of intravascular absorption of PGF2 alpha during therapeutic termination of pregnancy. 318 4

The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

DMSO is a clear odorless liquid, inexpensively produced as a by-product of the paper industry. It is widely available in the USA as a solvent but its medical use is currently restricted by the FDA to the palliative treatment of interstitial cystitis and to certain experimental applications. Cutaneous manifestations of scleroderma appear to resolve (albeit equivocally) following topical applications of high concentrations of DMSO. A limited number of small clinical trials indicate that intravenous DMSO may be of benefit in the treatment of amyloidosis, possibly by mobilizing amyloid deposits out of tissues into urine. Dermal application of DMSO seems to provide rapid, temporary, relief of pain in patients with arthritis and connective tissue injuries. However, claims for antiinflammatory effects or acceleration of healing are currently unwarranted. There is no evidence that DMSO can alter progression of degenerative joint disease, and, for this reason, DMSO may be considered for palliative treatment only and not to the exclusion of standard antiinflammatory agents. The safety of DMSO in combination with other drugs has not been established; neurotoxic interactions with sulindac have been reported. In experimental animals, intravenous DMSO is as effective as mannitol and dexamethasone in reversing cerebral edema and intracranial hypertension. An initial clinical trial in 11 patients tends to support this latter application. DMSO enhances diffusion of other chemicals through the skin, and, for this reason, mixtures of idoxuridine and DMSO are used for topical treatment of herpes zoster in the UK. Adverse reactions to DMSO are common, but are usually minor and related to the concentration of DMSO in the medication solution. Consequently, the most frequent side effects, such as skin rash and pruritus after dermal application, intravascular hemolysis after intravenous infusion and gastrointestinal discomfort after oral administration, can be avoided in large part by employing more dilute solutions. Most clinical trials of DMSO have not incorporated the components of experimental design necessary for objective, statistical evaluation of efficacy. Randomized comparisons between DMSO, placebo and known active treatments were rarely completed. Final approval of topical DMSO for treatment of rheumatic diseases in particular will require a multi-center, randomized comparison between high and low concentrations of DMSO and an orally-active, nonsteroidal antiinflammatory agent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Medical use of dimethyl sulfoxide (DMSO). 391 2


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