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

The anesthetic management of a 5-month-old male with norepinephrine-secreting neuroblastoma was described. Partial excision of the tumor was carried out under general anesthesia induced with enflurane, fentanyl and succinylcholine, and maintained with enflurane, nitrous oxide and oxygen. In this case, hypertension was observed intraoperatively and prostaglandin E1 was continuously infused at a rate of 0.1-0.5 micrograms.kg-1.min-1 to control blood pressure. Severe hypotension after removal of the tumor was not observed. Continuous administration of prostaglandin E1 was useful in this patient with norepinephrine-secreting neuroblastoma.
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PMID:[Anesthetic management of a patient with norepinephrine-secreting neuroblastoma by using prostaglandin E1]. 156 May 86

In recent years, the number of elderly patients who require operation has been increasing. We experienced three patients with perioperative brain infarction, occurring respectively, during the preoperative period, just after operation, and three days after operation. All three patients had more than one of the common risk factors for cerebrovascular accidents, including hypertension, advanced age, hyperfibrinogenemia, diabetes mellitus, and past history of cerebrovascular accident. On the basis of our experience with these three patients, we suggest the following: (1) Waiting period of elective surgery should be reconsidered in some cases with a past history of stroke. (2) Some high-risk patients may benefit from anticoagulative or antiaggregative drugs (e.g. low-molecular dextran or prostaglandin E1) to prevent brain ischemia. (3) Abrupt control of hypertension or diabetes mellitus status undoubtedly adversely affects the patient's general condition; and (4) A practical monitoring system to detect regional brain ischemia during operation under general anesthesia should be developed.
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PMID:[Three cases of perioperative brain infarction]. 156 May 89

We had five cases of surgical removal of pheochromocytoma by continuous intravenous injection of prostaglandin E1. During anesthesia, we used Swan-Ganz catheter for circulatory monitoring and measured plasma catecholamines. When PGE1 dose was increased from 0.05 to 0.1 and 0.15 microgram.kg-1.min-1, total systemic vascular resistance and mean arterial pressure were decreased but heart rate and cardiac output were not significantly altered from the preanesthetic values. Plasma catecholamines were also similar to the preanesthetic values. Therefore, the results suggest that the mechanism of suppression of hypertension by PGE1 is by affecting vascular beds directly rather than by diminishing catecholamine excretion from sympathetic nerve and adrenal medulla. During manipulation of pheochromocytoma, mean arterial blood pressure increased extremely. Although PGE1 was injected at a rate of 0.3 to 0.5 microgram.kg-1.min-1 in some cases, we could not suppress the elevation of blood pressure. PGE1 alone could not normalize blood pressure and heart rate, and other cardiovascular agents were necessary.
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PMID:[Anesthetic management of pheochromocytoma by continuous intravenous injection of prostaglandin E1]. 187 45

Misoprostol (Cytotec) is a recently released prostaglandin E1 analog approved for use in prevention of nonsteroidal anti-inflammatory drug-induced gastropathy. We report one of the first known examples of toxicity in an acute ingestion since the drug was first released in international markets in 1984. After an accidental ingestion of 3 mg misoprostol (approximately 15 times the maximum recommended therapeutic dose), a 71-year-old woman exhibited fever, tremor, tachycardia, hypertension, nausea, and abdominal cramping. Recovery ensued with standard supportive care. The physiology of this unique drug and implications for management of acute toxicity are summarized.
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PMID:Acute misoprostol toxicity. 190 33

The intravascular distribution of 0.2 mu lipid microspheres (LM) containing prostaglandin E1 (lipo-PGE1) injected intravenously in spontaneously hypertensive rats (SHR) and arteriosclerotic rabbits was investigated by electron microscopic observation and quantification of radiolabelled compounds. LM were observed under an electron microscope to concentrate in subendothelial space of vascular walls, particularly in vascular lesions associated with hypertension or arteriosclerosis. Radiolabelled lipo-PGE1 accumulated more densely in the vascular walls than did free PGE1, and the difference was more conspicuous in vascular lesions. This indicates that lipo-PGE1 penetrates vascular endothelium and then accumulates in blood vessels to result in augmentation of the pharmacological action of prostaglandin. These findings suggest the usefulness of LM as a carrier of prostaglandin to vascular lesions.
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PMID:Distribution of lipid microspheres incorporating prostaglandin E1 to vascular lesions. 207 41

In this study we investigated the effects of right atrial infusion of PGE1 (RAIPGE1) in doses from 40 to 500 ng/kg/min on sepsis-induced pulmonary artery hypertension (SIPAH). Thirteen pigs were randomized into a time-course group (n = 6) and a PGE1-treated group (n = 7). Pulmonary hypertension (PAH) was induced with the infusion of Pseudomonas Aeruginosa (PsAr) at a concentration of 2 X 10(8) CFU/20 kg/min in both groups. The infusion of PsAr caused a significant and persistent rise in mean pulmonary artery pressure (MPA), pulmonary vascular resistance (PVRI), right ventricular compliance (RVC), RV dp/dt, and right ventricular stroke work index (RVSWI), 30 min after the onset of infusion (P less than 0.05 vs baseline). Systemic hemodynamics and gas exchange were not affected throughout the 3-hr period of infusion (P = NS); however, left ventricular compliance (LVC) was depressed at a MPA greater than 35 mm Hg. The RAIPGE1 following SIPAH caused a concentration-dependent reduction above 40 ng/kg/min of MPA, PVRI, RVSWI, and RV dp/dt (P less than 0.05, 120 and 500 ng/kg/min vs PAH). RVC returned to baseline values during the infusion of PGE1. Systemic hemodynamics, including oxygen delivery and extraction, were unaffected by the infusion of PGE1, but LVC was improved (P less than 0.05, PGE1 500 vs PAH). The infusion of PGE1 caused a concentration-dependent rise in shunt fraction (Qs/Qt) and alveolararterial oxygen gradients which reached statistical significance during the infusion of 500 ng/kg/min. Our data show that RAIPGE1 is effective in ameliorating RV and pulmonary hemodynamics, but at the largest dose it negatively affects gas exchange.
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PMID:Efficacy of right atrial infusion of PGE1 in sepsis-induced pulmonary hypertension. 212 41

Various physiological changes of platelets and the vascular smooth muscle cell are intimately related. For this reason, in addition to the number of features in common between platelets and vascular smooth muscle and the increased risk for thromboembolic complication in essential hypertension, the platelet was used as an experimental model for the investigation of calcium-dependent functional anomalies associated with hypertension. It is demonstrated, by a sequential analysis of receptor and postreceptor events, that platelets in hypertension exhibit (a) a greater adenylate cyclase-activation and c-AMP-accumulation response to PGE1, (b) an enhanced epinephrine-induced phosphorylation response, and (c) an increased shape change sensitivity to serotonin and epinephrine. The anomalies in these calcium-dependent processes are linked to elevated free calcium concentrations in platelets from hypertensive subjects.
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PMID:Platelets and hypertension. 241 69

Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandin E1 and nitroglycerin reduce pulmonary capillary pressure but worsen ventilation-perfusion distributions in patients with adult respiratory distress syndrome. 249 9

Various abnormalities in platelet metabolism, including increased sensitivity to several aggregating agents, have been described in essential hypertension. Platelet response is controlled by Ca2+ and cyclic AMP-dependent mechanisms (stimulatory and inhibitory, respectively) which oppose one another. In the present study, the cyclic AMP contents of unstimulated platelets were measured by radio-immunoassay and observed to be lower in hypertensive than in normotensive subjects, either in the basal state or after prostaglandin E1 (PGE1) stimulation. In the presence of 7-bromo-1,5,dihydro-3,6-dimethylimidazo [2,1-b] quinazolin-2(3H)-one (Ro 15-2041), a specific inhibitor of phosphodiesterase, the increases in cyclic AMP content were similar in platelets from both groups, indicating that this enzyme was not responsible for the alterations in cyclic AMP metabolism observed in hypertension. Low external Ca2+ reduced basal and PGE1-stimulated cyclic AMP content in both normotensive and hypertensive groups but cyclic AMP levels remained lower in hypertensive patients than in normotensive subjects, indicating that Ca2+ influx is not responsible for this altered metabolism of cyclic AMP in hypertension. These data suggest that the reduced platelet cAMP content may participate in the hyperreactivity to various aggregating agents previously reported to accompany essential hypertension.
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PMID:Platelet cyclic AMP in essential hypertension. 255 May 42

We have shown earlier that abnormal platelet aggregation in spontaneously hypertensive rats (SHR) is not caused by prostaglandins. In this study platelets from SHR and normotensive (Wistar Kyoto, WKY) rats were used to examine the role of phosphoinositides and phosphorylation of 47,000 and 20,000 Dalton proteins in abnormal platelet activation in hypertension. Thrombin (0.05 U/ml) induced a rapid decrease in (32P)-P04 labelled phosphatidylinositol-4, 5-bisphosphate (PIP2), phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol (PI) in washed rat platelets. However, significantly greater loss of PIP2 and PI was seen in SHR platelets than in WKY platelets. For example the level of PIP2 declined by 32% in SHR platelets and only by 13% in WKY platelets at five seconds of incubation with thrombin. The loss of PI was similar in SHR and WKY platelets for the first five seconds of incubation with thrombin. However, by 15 seconds SHR platelets showed a significantly greater loss (24%) in PI than in WKY platelets (8%). Thrombin induced a 14% and 18% decrease in PIP at three seconds in WKY and SHR platelets respectively. In SHR platelets PIP level returned to the baseline in five seconds and then rose to 20% above the baseline by 30 seconds. In contrast PIP level in WKY platelets slowly reached the basal value by 30 seconds. Thrombin also produced a two- to three-fold greater accumulation of (32P)-phosphatidic acid (PA) in SHR platelets than in WKY platelets. Thrombin (0.05 U/ml) induced rapid phosphorylation of 47,000 Dalton (P47) and 20,000 Dalton (P20) proteins in both WKY and SHR platelets. Thrombin induced a four-fold greater increase in phosphorylation of P47 in SHR platelets than in WKY platelets in the first five seconds. Thrombin produced significantly greater increase in phosphorylation of P20 in SHR platelets (34% and 41%) than in WKY platelets (18% and 28%) at 5 and 15 seconds. Phosphorylation of P20 was followed by dephosphorylation in both WKY and SHR platelets. Aspirin (500 microM) did not affect phosphorylation of either P47 or P20 in SHR or WKY platelets. In other experiments prostaglandin E1 (0.5 microM), which stimulates adenylate cyclase via a guanine nucleotide regulatory protein termed Gs, caused an eighteen-fold increase in cyclic AMP level in SHR platelets as compared to a six-fold increase in WKY platelets. These data lead us to suggest that increased turnover of phosphoinositides and increased phosphorylation of P47 and P20 are involved in abnormal platelet activation in SHR platelets.
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PMID:Thrombin-induced abnormal platelet activation in spontaneously hypertensive rats is linked with phosphoinositides turnover and phosphorylation of 47,000 and 20,000 dalton proteins. 283 38


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