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

It is well known that many drugs can induce tubulointerstitial nephropathy (DTIN) in the kidney. There are two kinds of onset mechanisms such as dose-dependent and allergic nephropathy. Risk factors inducing DTIN are known as aging, dehydration, preexisting renal damage, hypertension and serum electrolyte abnormalities. Treatment of DTIN is firstly to cease suggestive drugs of inducing nephropathy and then followed by diuresis, correcting serum electrolyte levels and sometimes hemodialysis or hemoadsorption to reduce the suggested drug levels in the circulation. In allergic nephropathy, high-dose glucocorticoid therapy is available for improving renal function rapidly. The prevention of DTIN is to know the patients background and monitor serum drug levels.
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PMID:[Clinical aspects of drug-induced tubulo-interstitial nephropathy]. 756 48

Neurons in the rostral hypothalamic areas were examined with physiologically hypertonic (+30 mOsm/kg, by NaCl or mannitol) and hypotonic (-30 mOsm/kg) artificial cerebrospinal fluids (ACSFs) applied by pressure through a multibarrel micropipette in urethane-anesthetized rats. Of 304 neurons tested, 39 were excited by the hypertonic ACSFs and/or inhibited by the hypotonic ACSF, and 35 were inhibited by the hypertonic ACSFs and/or excited by the hypotonic ACSF. The former cells were designated hypertonic-sensitive and the latter hypotonic-sensitive. Both types of osmosensitive neurons were diffusely scattered in the examined areas, but neurons in the lateral preoptic area and the bed nucleus of the stria terminalis responded more frequently (30-40%) to the osmotic stimuli. Osmosensitive and insensitive neurons were recorded during activation of the baro- and volume receptors of the cardiovascular system. Of seven neurons that were excited during temporal hypotension induced by intravenous administration of nitroprusside, five were hypertonic-sensitive and two were osmotically insensitive. Hypertonic-sensitive neurons may be activated during dehydration, which increases the osmotic pressure and decreases the volume of body fluids. Of six neurons that were excited during temporal hypertension induced by intravenous administration of phenylephrine, four were hypotonic-sensitive and two were osmotically insensitive. Hypotonic-sensitive neurons may be activated during rehydration or overhydration. Osmosensitive neurons probably integrate cardiovascular and osmotic information that is important for the central regulation of body fluids.
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PMID:Osmosensitive hypothalamic neurons and their responses to cardiovascular receptor activation. 771 97

Anaesthetists will encounter increasing numbers of patients who are receiving long-term treatment with ACE inhibitors for hypertension, congestive heart failure and prophylactically following myocardial infarction. Our understanding of the physiology and pharmacology of the renin-angiotensin system has dramatically increased in the last decade, and has led to the discovery of endogenous renin-angiotensin systems which may be physiologically more important than the better understood circulating system. There are several reports of adverse interactions between anaesthesia and ACE inhibitors, manifested as hypotension and bradycardia, which may be delayed until the postoperative period. The mechanism behind them is not understood and, as yet, no published studies have attempted to address this issue. It is possible, however, that dehydration associated with the pre-operative fast may play an important role. ACE inhibitors may, in the future, prove to be useful in the subspecialties of cardiac and vascular anaesthesia, where they might be used in an attempt to preserve cardiac function following periods of ischaemia and cardiopulmonary bypass, and to avoid renal damage following aortic cross-clamping. Meanwhile, it would seem prudent to exercise caution when anaesthetising patients taking ACE inhibitors and to be fully prepared to treat the hypotension and bradycardia which may occur.
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PMID:The renin-angiotensin system and angiotensin converting enzyme (ACE) inhibitors. 804 31

Resuscitation of the brain after a period of global ischemia is limited by two classes of post-ischemic pathologies: hemodynamic disturbances which prevent the adequate re-oxygenation of the ischemic brain, and metabolic disturbances which may lead to delayed neuronal death in so-called selectively vulnerable brain regions. The hemodynamic disturbances can be classified into the no-reflow phenomenon and the post-ischemic hypoperfusion syndrome. The no-reflow phenomenon results from a combination of increased blood viscosity and perivascular edema; the severity increases with the duration of ischemia, and the treatment is by combining arterial hypertension with dehydration and anticoagulation. The post-ischemic hypoperfusion syndrome is independent of the duration of ischemia, it develops after a delay and is due to an impairment of the metabolic/hemodynamic coupling mechanisms; there is no specific treatment at the present. The most important metabolic disturbance leading to delayed neuronal death is prolonged inhibition of protein synthesis. The injury is manifested already after 5 min ischemia but it progresses little if ischemia is prolonged to 1 h. Inhibition occurs at the translation level due to selective inhibition of polypeptide chain initiation. After brief periods of ischemia, the disturbance can be reversed by various anesthetics and hypothermia but there is no treatment if ischemia is prolonged. Exitotoxity, free radical-mediated reactions, disturbances of polyamine metabolism, acidosis and selective disturbances of gene expression may also be involved but are probably of lesser importance.
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PMID:Ischemia-mediated neuronal injury. 813 1

Female hormones are linked to migraine. Women who have had menstrual migraine and migraine onset at menarche tend to experience no migraine during pregnancy. Not all migraines improve during pregnancy, however. Some women experience migraine for the first time during pregnancy. Migraine developing during pregnancy may indicate an underlying structural or functional disorder, e.g., cerebral aneurysms. Headaches caused by cerebral arteriovenous malformations often present as migraine with aura. Cerebral venous thrombosis (common during pregnancy and the puerperium) may manifest with migraine-like visual disturbance and headache. Idiopathic intracranial hypertension or intracranial hypertension secondary to cerebral venous thrombosis or coincidental brain mass can manifest as a continuous and increasing headache. Physicians need to intensively evaluate such cases to achieve an accurate diagnosis. Spinal procedures linked to delivery can cause a low pressure headache. Oral contraceptive use is linked to migraine. Decreasing estrogen levels appear to precipitate migraine. Estradiol and progesterone therapy for menstrual migraine maintains high estrogen levels during the menstrual epoch, which generally prevents migraine. High but stable estrogen levels prevent migraine. Thus, migraines who do not suffer from migraine during pregnancy benefit from high estrogen levels. Pregnant women with migraine should not take drugs unless the frequency and severity of migraine is life threatening to the mother or fetus. Acetaminophen can be used to relieve pain. Meperidine suppositories can relieve severe pain. Pregnant women should not use aspirin, nonsteroidal anti-inflammatory drugs, or vasoconstrictors. Fluid replacement and acceptable antiemetic drugs can treat dehydration and vomiting. Behavioral modification, identification, and elimination of foods that trigger attacks, magnesium supplementation, and low doses of propranolol 3-4 times/day in severe cases may prevent migraine in pregnant women.
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PMID:Migraine and pregnancy. 829 77

The medical records of 90 patients with a clinical diagnosis of retinal vein occlusion (RVO) who were seen at two referral hospitals in Saudi Arabia were reviewed. Sixty-eight (75.6%) were men. Central RVO was present in 50 patients (55.6%); branch RVO, in 35 patients (38.9%); and hemiretinal occlusion, in five patients (5.6%). Arterial hypertension was present in 43 patients (47.8%); diabetes mellitus, in 28 patients (31%); and preexisting glaucoma, in 26 patients (28.9%). The date of onset of RVO was available in 61 patients. Eighteen attacks (29.5%) had occurred during the month of Ramadan. The Student's t test of paired samples indicated that the incidence of RVO during the month of Ramadan was significantly higher than that of the other months of the Gregorian year. These findings suggest that dehydration may play a role in the pathogenesis of RVO.
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PMID:Retinal vein occlusion in Saudi Arabia: possible role of dehydration. 830 94

Administration of hypertonic solutions is the method of choice for acute treatment of intracranial hypertension. Recording of the intracranial pressure during treatment facilitates adjustment of the dosis to the actual ICP-response, avoiding thereby administration of an excessive osmotic load as a basis to prolong therapeutical efficacy. The mechanisms underlying reduction of the intracranial pressure by hypertonic solutions are still controversially discussed. Dehydration of normal probably also of edematous brain parenchyma and constriction of cerebral resistance vessels as an autoregulatory response causing reduction of the intracranial blood volume are the most likely options. Administration of hypertonic/hyperoncotic solutions has regained attention on account of its unmatched therapeutical efficacy to reestablish normal conditions in severe hemorrhagic shock. Administration of, e.g. 7.2% NaCl/10% Dextran 60 in an amount equivalent of only 10% of the shed blood volume is immediately normalizing cardiac output and improving the microcirculation in peripheral organs. These therapeutical properties are relevant in head injury, since inflicted patients quite often are suffering from peripheral trauma and consequently from hemorrhagic shock. No evidence has been obtained in a variety of experimental studies that hypertonic/hyperoncotic solutions have adverse effects on the brain in the presence of a cerebral lesion. To the contrary, the fluid mixture has been found to lower the increased intracranial pressure. Administration of hypertonic/hyperoncotic solutions appears therefore appropriate in acute cerebral insults from head injury and impending circulatory failure from shock in order to inhibit development of secondary brain damage.
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PMID:[Hypertonic solutions in treatment of intracranial pressure]. 832 35

Mannitol is an osmotic diuretic used in acute oliguric renal failure, acute cerebral edema, and acute glaucoma. It is metabolically inert and is excreted through the kidneys. So once renal function is impaired, mannitol accumulates and the movement of water into the intravascular space with resultant cellular dehydration. Two patients suffered reversible acute oliguric renal failure following mannitol infusion given as treatment for intracranial hypertension. Both patients experienced nausea and vomiting and became increasingly lethargic with edema of general body. Congestive heart failure occurred. Laboratory data showed severe dilutional hyponatremia with hyperosmolality. We successfully treated them with extracorporeal ultrafiltration method (ECUM) and hemodialysis (HD). Some discussions were presented about acute renal failure following mannitol infusion.
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PMID:[Acute renal failure following mannitol infusion]. 837 73

Angio-oedema is a recognised complication of angiotensin converting enzyme (ACE) inhibitor therapy, occurring in 0.1% to 0.5% of patients taking captopril, enalapril, or lisinopril. This is the first report of severe angio-oedema complicating therapy with quinapril, a new, long-acting drug. CASE REPORT. A 74-year-old female had been taking quinapril (10 mg/day) and diuretics (fixed combination of triamterene and hydrochlorothiazide) for arterial hypertension for 18 months without any complication. After a fracture of the ankle, the patient received spinal anaesthesia uneventfully for an osteosynthesis. Ten days postoperatively, she noted swelling of the lips and the left half of the tongue. Following intravenous injection of antihistamines and prednisolone, these symptoms regressed. However, a relapse occurred on the 16th postoperative day with rapidly increasing oedema of the lips, face, ventral collar area, and entire tongue. Despite high-dose steroids, dyspnoea developed within 2 h. Direct laryngoscopy was impossible, and a flexible bronchoscope was used for nasotracheal intubation. At this point, the diagnosis of ACE inhibitor-induced angio-oedema was made and quinapril was withdrawn. The patient recovered, tracheal extubation was performed after 48 h, and the later course was uneventful. DISCUSSION. This is the second report of angio-oedema as a postoperative complication in a patient on long-term and previously unremarkable ACE inhibitor therapy. The first reported case occurred immediately after oral intubation and was perhaps precipitated by mechanical irritation. In this case, it is likely that postoperative deterioration of renal function due to dehydration and diuretic therapy was the precipitant, as has been reported in patients on lisinopril without surgery. Despite a significant increase in angio-oedema associated with the use of long-acting ACE-inhibitors, there appears to be a lack of familiarity among anaesthesiologist and other emergency physicians concerning this adverse effect. Withdrawal of the drug is the only effective treatment. High-dose steroids may be helpful, but if there is beginning dyspnoea or stridor, early endoscopically controlled intubation or emergency tracheostomy is essential to avoid hypoxaemia and death, as has occurred in the past.
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PMID:[Life-threatening postoperative angioedema following treatment with an angiotensin converting enzyme inhibitor]. 906 60

A 67-year-old male was admitted to our hospital because of watery diarrhea and pre-shock status at 10:30 am on March 20, 1995. He had travelled to Bali Island in Indonesia from March 13 to March 18, 1995. On admission, his systolic blood pressure was 60 mmHg and body temperature was 35.2 degrees C. His skin was very dry. Laboratory tests showed that s-Cr was 6.3 mg/dl and CPK was 5620 IU/l. A massive fluid transfusion was given immediately and then his blood pressure rose to 158/92 about two hours after admission. However, he developed a high grade fever and systemic cyanosis in the evening of the first hospital day and died at 0:20 am on March 21st. Salmonella Weltevreden was detected in the fecal and blood cultures obtained on admission. We considered that his acute renal failure was attributable to rhabdomyolysis due to dehydration and that the cause of death was probably septic shock. The patient had a previous history of cholecystectomy ten years ago and also suffered from hypertension, but his general condition was not so bad before this episode. Therefore, we were surprised that his illness became so severe. This case emphasizes that Salmonella enteritis may occasionally be a serious and lethal disease.
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PMID:[A fatal case of acute enteritis caused by Salmonella Weltevreden after travel to Indonesia]. 862 67


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