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

Taking into consideration the role of pancreatic enzymes in the etiology of cholecystitis and cholecystopancreatits, the authors examined amylase in 92 patients, bile lipase--in 39 patients during cholecystectomy and also amylase in the choledochus bile during external drainage of the duct in 15 patients in the early postoperative period. The investigations inducated different levels of pancreatic enzymes in bile. Their level is found to depend on the occurrence of hypertension in the bile tract both pre- and postoperatively.
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PMID:[Enzymatic cholecystitis and cholecystopancreatitis]. 85 25

The capacity of cultured renal medullary interstitial cells derived from Dahl salt-sensitive and salt-resistant rats to synthesize prostaglandin E2 (PGE2) was compared. Basal and arginine vasopressin (AVP)-induced PGE2 production by interstitial cells from salt-resistant rats was fourfold to fivefold higher than corresponding values of those from the salt-sensitive rats. Similarly, basal and AVP-responsive release of [3H]arachidonate were twofold higher by interstitial cells from salt-resistant compared with salt-sensitive rats. Differences in PGE2 production were abolished by the calcium inophore A23187 or the addition of exogenous arachidonate. The latter findings suggested a role for altered availability of endogenous arachidonate, possibly mediated by reduced calcium-responsive lipase activity. Basal and AVP-induced increases in cytosolic free calcium concentration, assessed by the aequorin method, were significantly lower in interstitial cells from salt-sensitive versus salt-resistant rats, further supporting a possible role for altered cellular calcium homeostasis. Studies of the potential contribution of various phospholipases and of triglyceride lipase to the release of arachidonate for PGE2 synthesis in interstitial cells implicated phospholipase A2 activity as a major pathway. When assessed in vitro in cell cytosolic fractions at identical calcium concentration, phospholipase A2 activity was lower in interstitial cells from salt-sensitive versus salt-resistant rats. Thus, both reduced cytosolic free calcium and phospholipase A2 activity of interstitial cells from salt-sensitive rats may contribute to the diminished capacity of these cells to liberate endogenous arachidonate for PGE2 synthesis.
Hypertension 1990 Apr
PMID:Decreased cytosolic calcium and prostaglandin synthesis in prehypertensive rats. 210 83

Three groups of eight dogs each were studied to evaluate the early evolution of the hyperamylasemia, hyperlipasemia, and acinar cell pathology at the light and electron microscopic levels during acute Diazinon-induced pancreatitis. Two more groups of five dogs each were evaluated for the effects of cholinergic receptor blockade with atropine and ductal decompression on the evolution of serum enzyme changes and acinar cell pathology. Group I dogs received a secretin infusion of 2 units/kg/hr, and a Diazinon infusion of 75 mg/kg, and demonstrated significant increases in serum amylase and lipase at one, two and three hours. Light microscopy revealed acinar cell vacuolization and progressive interstitial edema. Electron microscopy revealed the formation of large intracytoplasmic vacuoles filled with flocculent material, the fusion of these vacuoles with basolateral membrane, and the formation of interstitial edema. In both group II dogs (that received secretin alone) and Group III dogs (that received atropine, 200 micrograms/kg IV prior to secretin and Diazinon), the serum enzyme levels and histologic results were normal. In group IV dogs, pancreatic duct cannulation to prevent hypertension prevented the hyperamylasemia and hyperlipasemia, but not the acinar cell vacuolization and interstitial edema. This model for acute interstitial pancreatitis is apparently cholinergic-receptor mediated, the serum enzyme elevations are due primarily to ductal hypertension, and the acinar cell pathology is primarily due to cholinergic stimulation and occurs independent of ductal hypertension.
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PMID:The effect of atropine and duct decompression on the evolution of Diazinon-induced acute canine pancreatitis. 617 84

The aetiology of familial combined hyperlipidaemia remains obscure, with both genetic and environmental factors contributing to the phenotype, which is frequently associated with premature coronary heart disease. We have studied lipoprotein lipase (LPL) activity and hepatic lipase (HL) activity in patients with coronary heart disease to determine whether variation in lipase activities contributes to this phenotype. Forty-one patients (mean age 50 years; 30 male) were selected on the basis of cholesterol levels above 6.5 mmol/l and triglyceride levels above 2.2 mmol/l, with apoprotein B values over the 90th percentile. There was a family history of premature coronary heart disease in 78% and a personal history in 64%, at mean age 44, the patient group therefore predominantly corresponded to the common definition of familial combined hyperlipidaemia, appropriate in the absence of molecular markers. None of the patients was diabetic; hypertension and smoking were not over represented. Blood samples were taken following intravenous administration of heparin (100 IU/kg body wt), and LPL and HL activities were measured. Mean post-heparin LPL was significantly lower in patients than controls 10 min after heparin administration (2.98 +/- 1.04 and 3.86 +/- 0.93 mumol ml-1 h-1, respectively, P = 0.001), and 37% patients had values below the 10th percentile of controls. Both male and female patients had significantly higher HL activities than their respective controls at 5, 10, 20 and 30 minutes post-heparin. As expected, both female patients and controls had lower HL activities than males, although this sex difference did not reach statistical significance in the patient group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase activity in patients with combined hyperlipidaemia. 818 54

Cerebral and extracerebral effects of moderate hypothermia (core temperature 32.5 degrees C-33.0 degrees C) were prospectively studied in 10 patients with severe closed head injury (Glasgow Coma Scale score < 7) in the intensive care unit of a university hospital. Hypothermia was induced by cooling the patient's body surface with water-circulating blankets. Before cooling, a conventional intracranial pressure (ICP) reduction therapy was applied, which remained unchanged throughout the study. Cerebral blood flow (CBF), cerebral metabolic rates for oxygen (CMRO2) and lactate (CMRL), and ICP were simultaneously measured prior to inducing hypothermia, after obtaining hypothermia, after 24 hours of hypothermia, and after rewarming. With respect to extracerebral effects, supplemental investigations were conducted 24 and 72 hours after rewarming. The median delay between injury and induction of hypothermia was 16 hours. Hypothermia reduced CMRO2 by 45% (p < 0.01), whereas CBF did not change significantly. Before cooling, six patients had elevated CMRL indicating cerebral ischemia. Cooling normalized CMRL in all patients (p < 0.01). The intracranial hypertension present prior to cooling declined markedly during hypothermia (p < 0.01) without significant rebound effects after rewarming. Cardiac index decreased by 18% after hypothermia was reached (p < 0.05), recovered at 24 hours of hypothermia, and surpassed baseline values after rewarming. Platelet counts dropped continuously up to 24 hours after rewarming (p < 0.01). Plasma coagulation tests did not show significant worsening. Creatinine clearance decreased during cooling (p < 0.01) and recovered by 24 hours after rewarming. Twenty-four hours after cooling had begun, eight patients had elevated serum lipase activity (p < 0.01) and four of them acquired pancreatitis. Rewarming normalized both pancreatic alterations. Seven patients made a good recovery; one survived severely disabled; and two patients died. Moderate hypothermia is effective in preventing secondary brain damage while reducing cerebral ischemia. However, there are potentially hazardous side effects that require additional monitoring.
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PMID:Moderate hypothermia in patients with severe head injury: cerebral and extracerebral effects. 912 14

Until recently, obesity did not play a major role in considerations of physicians and public health authorities. The impact of health-threatening overweight was so far considered only as a risk factor for various other serious illnesses, such as hypertension, diabetes mellitus, hyperuricemia, elevated blood lipid levels and of vascular diseases of the heart, the brain and the kidneys. Recently however, obesity has been rated by the WHO as an unique disease, resulting in elevated morbidity and mortality. It is of constantly increasing importance because of the raising number of obese individuals in all industrial countries. In Austria an incidence of 8.5% of the adult population is estimated to be obese with a BMI > 30. Though the established concept for treatment of overweight consists of reduction of the caloric intake by diet, there is an obvious need for drugs making dieting easier acceptable to obese patients for prolonged periods. Orlistat is the first representative of a new class of such drugs, inhibiting intestinal acting lipase thus reducing the intestinal absorption of triglycerides; it contributes, therefore, to a reduced calorie intake. Preliminary results of treatment studies with Orlistat are presented, demonstrating its efficacy in inducing weight loss and improving metabolic parameters with tolerable intestinal side effects. After finalization of international studies, demonstrating efficacy and tolerability, orlistat has been registered in Austria in September 1998.
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PMID:[Reduction of obesity and improvement in metabolic parameters by inhibition of intestinal lipases: current results with orlistat]. 987 90

Cannabinoids, including the endogenous ligand anandamide, elicit pronounced hypotension and bradycardia through the activation of CB1 cannabinoid receptors. A second endogenous cannabinoid, 2-arachidonoyl glycerol (2-AG), has been proposed to be the natural ligand of CB1 receptors. In the present study, we examined the effects of 2-AG on mean arterial pressure and heart rate in anesthetized mice and assessed the role of CB1 receptors through the use of selective cannabinoid receptor antagonists and CB1 receptor knockout (CB1(-/-)) mice. In control ICR mice, intravenous injections of 2-AG or its isomer 1-AG elicit dose-dependent hypotension and moderate tachycardia that are unaffected by the CB1 receptor antagonist SR141716A. The same dose of SR141716A (6 nmol/g IV) completely blocks the hypotensive effect and attenuates the bradycardic effect of anandamide. 2-AG elicits a similar hypotensive effect, resistant to blockade by either SR141716A or the CB2 antagonist SR144528, in both CB1(-/-) mice and their homozygous (CB1(+/+)) control littermates. In ICR mice, arachidonic acid (AA, 15 nmol/g IV) elicits hypotension and tachycardia, and indomethacin (14 nmol/g IV) inhibits the hypotensive effect of both AA and 2-AG. Synthetic 2-AG incubated with mouse blood is rapidly (<2 minutes) and completely degraded with the parallel appearance of AA, whereas anandamide is stable under the same conditions. A metabolically stable ether analogue of 2-AG causes prolonged hypotension and bradycardia in ICR mice, and both effects are completely blocked by SR141716A, whereas the same dose of 2-AG-ether does not influence blood pressure and heart rate in CB1(-/-) mice. These findings are interpreted to indicate that exogenous 2-AG is rapidly degraded in mouse blood, probably by a lipase, which masks its ability to interact with CB1 receptors. Although the observed cardiovascular effects of 2-AG probably are produced by an arachidonate metabolite through a noncannabinoid mechanism, the CB1 receptor-mediated cardiovascular effects of a stable analogue of 2-AG leaves open the possibility that endogenous 2-AG may elicit cardiovascular effects through CB1 receptors.
Hypertension 2000 Feb
PMID:Cardiovascular effects of 2-arachidonoyl glycerol in anesthetized mice. 1067 17

Obesity is one of the pathologies with ever-increasing prevalence in modern societies. Its occurrence is strongly associated with increased risk of developing diabetes mellitus, atherosclerosis, hypertension, stroke, heart and respiratory failure, breast, prostate and gut cancer, gall stones, arthropathy. Obesity is common in Polish population. Obesity treatment is difficult and frustrating. It consists of several parts like diet, increased physical activity, lifestyle changes, drug therapy and surgery. However, obesity treatment is very often a failure, mostly because of discouraging long-term results and the necessity of intensive patient's involvement in the therapy. For many patients and doctors weight-decreasing agents look promising. The groups of anti-obesity drugs are presented in the article, with special reference to serotoninergic agents and intestinal lipase inhibitors. The prospects for new anti-obesity agents are discussed. Nevertheless, despite intensive research on obesity, we are still waiting for the development of an effective and safe drugs helping lose weight.
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PMID:[The role of pharmacotherapy for treatment of obesity in adults]. 1120 19

Orlistat (Xenical, Hoffmann-La Roche) is a powerful inhibitor of gastrointestinal lipase and as such, reduces fat absorption. Unlike other weight-reducing drugs it is minimally absorbed and has no effects in the CNS. Orlistat is indicated for patients with a body mass index (BMI) of at least 30 kg/m2 or 28 kg/m2 in the presence of obesity-associated complications, such as hypertension, diabetes mellitus, hyperlipidaemia and obstructive sleep apnoea. In clinical trials, orlistat (120 mg t.i.d.) in combination with life-style modification and a hypocaloric diet (30% of energy from fat) induced significantly more weight loss and improved health complications of obesity (diabetes, hypertension, hyperlipidaemia) compared to patients treated with diet alone. Side effects related to fat malabsorption, occurred in more than 20% of subjects during the first year of treatment and included oily faecal spotting, abdominal pain, flatus with discharge and fatty/oily stool. Side effects from orlistat diminished in the second year of treatment. Plasma concentrations of fat soluble vitamins decreased in orlistat-treated patients but did not usually fall below the normal range. No studies have evaluated the efficacy of orlistat or side effect profile beyond two years.
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PMID:Orlistat in the treatment of obesity. 2694 9

Some clinical cases published in literature show that angiotensin-converting enzyme (ACE)-inhibitor administration may cause acute pancreatitis. In this work, the authors report a case of a patient affected by hypertension. Upon admission, the authors started antihypertensive therapy using captopril, which caused an important amylase and lipase rise within 13 days. When the ACE-inhibitor therapy was stopped, a rapid decrease of the serum enzyme was observed within 3 days. The high levels of serum amylase and lipase were linked to neutrophilia but were not associated with relevant symptomatic findings or features of pancreatopathy. The absence of the usual conditions that may cause pancreatitis, such as biliary stasis, hypercalcemia, or alcohol abuse, and the rapid decrease of serum enzyme levels after drug suspension suggested an ACE-inhibitor-induced pancreatitis. This is the first clinical report of an ACE-inhibitor-induced pancreatitis in which captopril administration was found after hospitalization. The drug suspension probably prevented other complications. This case report suggests that, when ACE-inhibitor administration is started, serum amylase and lipase should be monitored in order to prevent acute pancreatitis without waiting for clinical evidence of a pancreatopathy.
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PMID:Angiotensin-converting-enzyme inhibitor administration must be monitored for serum amylase and lipase in order to prevent an acute pancreatitis: a case report. 1157 Jun 65


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