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

Abdominal aortic aneurysmectomy is being performed with progressively lower operative mortality and morbidity. Three hundred thirty seven patients have had elective aneurysm repair since 1954. Factors affecting mortality and morbidity in the last 108 cases are analyzed. Seventy-four per cent of patients had pre-existing disease, either cardiac, pulmonary, renal, cerebrovascular, diabetes mellitus, or hypertension. Six patients died following operation, a mortality rate of 5.5%. One died of pulmonary and 5 of cardiac causes. No patient died of renal failure or required dialysis. A signficant feature of management is the regimen of fluid therapy using dextrose in lactated Ringer's solution during and after operation to minimize hypotensive and renal complications. No patient developed a wound infection, graft infection, wound dehiscence, stroke, or intestinal ischemia. Serious postoperative complications were largely cardiac or pulmonary. Despite recent liberalization of indications for operation, comparative figures show continued reduction in operative mortality from 17% during 1954-1961, or 7.4% during 1962-1967, to 5.5% in the 1968-1974 era. This declining mortality is related to earlier diagnosis using non-invasive methods (sonogram), simplified operative techniques, improvement in fluid management, innovations in cardiopulmonary therapy, and recognition and proper handling of unusual manifestations of aortic aneurysms.
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PMID:Surgical management of abdominal aortic aneurysms: factors influencing mortality and morbidity--a 20-year experience. 12 60

Neurochemical changes in the extracellular fluid of the rostral ventrolateral medulla (RVLM) were produced by changes in arterial blood pressure. Blood pressure was raised or lowered with systemic infusions of phenylephrine or nitroprusside and neurochemicals were recovered from RVLM by in vivo microdialysis. A dialysis probe 300 microns in diameter and 500 microns in length was stereotaxically implanted in the RVLM of the urethane-anesthetized rat. Sterile physiological Ringer's solution was perfused at a rate of 1.5 microliter/min. The perfusate was collected under ice-cold conditions every 15 min for the assay of epinephrine, dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA), ascorbic acid, and uric acid. After stable baseline neurochemical concentrations were achieved, animals were infused with phenylephrine or nitroprusside intravenously to raise or lower the blood pressure. Increasing blood pressure 50 mm Hg above the baseline value by phenylephrine led to a significant reduction in heart rate and a reduction in extracellular epinephrine and DOPAC concentrations. The 5-HIAA concentration was increased during the hypertensive drug infusion. There were no changes in the concentrations of ascorbic acid or uric acid. Hypotension produced by nitroprusside (-20 mm Hg) led to neurochemical changes which were the reciprocal of those seen during hypertension. During hypotension, heart rate increased as did the extracellular fluid epinephrine concentration. The 5-HIAA concentration fell with hypotension and remained depressed following the nitroprusside infusion. Ascorbic acid and uric acid concentrations did not change during hypotension but ascorbic acid did increase after the nitroprusside infusion stopped. These data provide direct evidence that epinephrine release in RVLM is linked to changes in systemic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Drug-induced changes in blood pressure lead to changes in extracellular concentrations of epinephrine, dihydroxyphenylacetic acid, and 5-hydroxyindoleacetic acid in the rostral ventrolateral medulla of the rat. 137 44

In a search for factors contributing to the sustained blood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringer's solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in hemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 +/- 3 to 128 +/- 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretic factor, urine volume, and urinary sodium excretion were identical in the two groups, and natriuresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping infusion in both groups, but this potentiation was not correlated with the increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretic factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.
Hypertension 1988 Jul
PMID:Vasoconstriction and hypersensitivity to vasoactive substances after acute volume expansion in dogs. 245 68

To evaluate possible roles of endogenous Na+-K+-ATPase inhibitors in vasoconstricted blood pressure elevation produced by acute volume expansion, we administered ouabain (Na+-K+-ATPase inhibitor) intravenously (30 micrograms/kg) for 10 min to dogs, 3 h after volume expansion with dextran in lactated Ringer's solution (20 ml/kg, for 1 h). Acute volume expansion resulted in the elevation of blood pressure associated with an increase in cardiac output. In some dogs the blood pressure remained elevated with gradual increase in total peripheral resistance (Group I) or with sustained high cardiac output (Group II), and in other dogs (Group III) it returned to the control level. Ouabain administration elevated the blood pressure and total peripheral resistance in these groups and sham dogs which did not have volume expansion. And these effects of ouabain were not correlated with the degree of blood pressure or vasoconstriction produced by volume expansion. Thus, it is not likely that endogenous Na+-K+-ATPase inhibitors increased to produce vasoconstricted hypertension after acute volume expansion.
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PMID:Effect of ouabain on hemodynamics in acute volume expanded hypertensive dogs. 254 71

Dextran in lactated Ringer's solution (20 ml/kg) was infused for 1 hour into anesthetized dogs with sinoaortic denervation and vagotomy (deafferentation; n = 10) and dogs treated with hexamethonium (de-efferentation; n = 13) to compare with our previous observation in dogs with an intact autonomic nervous system (control, n = 34). During the infusion, increase in blood pressure associated with increase in cardiac output was observed in all three groups. The increases in blood pressure were larger in the two groups with an impaired autonomic nervous system. In the recovery period, the control dogs and the hexamethonium-treated dogs showed gradual increases in total peripheral resistance and in vasoconstricted hypertension 3 hours after stopping the infusion. In contrast, the dogs with sinoaortic denervation and vagotomy did not show any increase in total peripheral resistance. The vasoconstricted groups showed peaks of natriuresis soon after the infusion, not 3 hours after the infusion when vasoconstriction was observed, although the dogs with deafferentation did not show a significant increase in natriuresis. Norepinephrine (0.5 micrograms/kg) was administered intravenously before and after volume expansion, and the pressor responses in the three groups after volume expansion were enhanced similarly (143%, 128%, and 136%, respectively). These results indicate that the afferent signals from peripheral vessels to the brain contribute to the production of vasoconstricted hypertension after acute volume expansion and that the vasoconstriction is independent of pressor hypersensitivity and is dissociated in time from the natriuresis.
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PMID:Contribution of the baroreflex afferent nerves to the production of vasoconstricted hypertension in volume-expanded dogs. 257 37

Ten pregnant ewes were alternated in a study of the blocking effect of parenteral magnesium on the catecholamine response to cocaine. Indirect blood pressures were recorded at 1-minute intervals for 12 minutes before and after a bolus of 2 mg/kg of cocaine. Fetal heart rates were continuously recorded from skin electrodes. Platelet counts were performed before and 12 minutes after cocaine. Control ewes received lactated Ringer's solution, and test animals had 5 mg/kg of elemental magnesium in the form of MgSO4-7H2O in a rapid infusion. A semicrossover was also performed. Platelet counts fell precipitately in controls and rose after magnesium infusions. Fetal heart rates rose in controls at 5-minute intervals and were unchanged in magnesium-treated mothers. Because of disparity of the baseline mean arterial pressure, direct comparisons were not significant before and after cocaine. Alterations from the baseline were different in magnesium-treated versus control animals, with values in the latter rising by 28 +/- 10 mm Hg with lactated Ringer's solution plus cocaine and falling by 3 +/- 5 mm Hg with magnesium pretreatment. Values in test animals originally treated with magnesium rose 4 +/- 11 mm Hg for an overall significance of p less than 0.05. Low beginning serum magnesium levels were associated with ovine hypertension and reduced fetal weight and survival.
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PMID:Effect of magnesium on cocaine-induced, catecholamine-mediated platelet and vascular response in term pregnant ewes. 258 60

The present study was undertaken to determine the specificity of the vasoconstrictor activity to angiotensin II (AII) and arginine vasopressin (AVP) on the microcirculation in normal and renovascular hypertensive states. Ten to fourteen days after the induction of hypertension, Syrian hamsters were anesthetized with pentobarbital sodium, the cheek pouch was exposed, and a plastic chamber was placed in situ so the membrane could be suffused with bicarbonate-buffered Ringer's solution (5% CO2, 95% N2, pH 7.4). Third order arterioles (30-45 micron) were identified for study and vessel diameter was measured using a shearing device. In one group of normotensive and hypertensive hamsters, AII was microapplied to the arteriole before and after adding an AVP antagonist to the suffusate. In a second group of similar hamsters, AVP was microapplied to the arteriole before and after adding an angiotensin II blocker, saralasin acetate, to the suffusate. AVP and AII receptor blockade was documented by observing whether the vasoconstrictor effect of either AVP or AII was abolished. Dose-response curves for either peptide were not altered in the presence of the antagonist to the other peptide; however, they were shifted to the left in the RHT hamsters. Neither AVP nor AII receptor blockade altered control resting arteriolar diameters. Thus, it can be concluded that the microvascular response to both AII and AVP are potentiated in RHT and there are no interactions between either AII or AVP with the receptors of the other peptide in these microvessels in normal or RHT hamsters, indicating a high specificity for each peptide to its vascular receptor.
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PMID:Specificity of arginine vasopressin and angiotensin II for microvessels in the hamster cheek pouch after the induction of renovascular hypertension. 334 41

The effects of hypotension, hemodilution, and their combination on the relationship between concurrent brain electrical activity and resulting brain injury were studied in anesthetized monkeys. The authors compared changes in the electroencephalogram and somatosensory and auditory evoked potentials with eventual neuropathologic outcome. Our goals were: 1) to define the margin of safety for the monkey brain during hemodilution and hypotension under several simulated clinical conditions; and 2) to determine whether noninvasive measurements of brain electrical activity can predict ischemic brain cell damage. Forty-one monkeys were anesthetized with halothane (0.8 vol % inspired) and ventilated mechanically. Arterial hypotension was induced with trimethaphan (25 +/- 8 mmHg mean arterial blood pressure [MABP] for 30 min). Hemodilution was induced by replacing blood with lactated Ringer's solution (14 +/- 2% hematocrit for 1 h). Combined hemodilution and hypotension consisted of 30 min of hemodilution alone followed by superimposing hypotension for 30 min (16 +/- 3% hematocrit and 29 +/- 5 mmHg MABP). Ten monkeys died following severe hypotension alone or combined hemodilution and hypertension as a consequence of cardiac arrest or undetermined (possibly neurologic) causes. No histologic evidence of ischemic brain cell injury was found in surviving monkeys subjected to hemodilution or hypotension alone. Neuropathologic alterations in the cerebral cortex, cerebellum, hippocampus and globus pallidus as well as neurologic and behavioral deficits were found in seven of 16 surviving monkeys subjected to both hemodilution and hypotension. These findings resulted from combinations of hematocrit less than 20% and MABP below 40 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys. 378 33

Hypertonic saline (2400 mOsm/L) has been used successfully for fluid resuscitation of dogs subjected to severe hemorrhagic shock. This study compared the effects of resuscitation with hypertonic saline vs. lactated Ringer's solution on intracranial pressure (ICP) in dogs subjected to 30 min of sustained hypovolemic shock. Hypotension was produced by rapid withdrawal of blood until mean arterial pressure was 50 mm Hg, maintained at that level by withdrawal or infusion of blood over the next 30 min as necessary. Eight animals were resuscitated with hypertonic saline solution and nine with lactated Ringer's solution. Both solutions restored systolic blood pressure and cardiac output to control values. However, diastolic blood pressure and mean arterial pressure did not return to control values. The most prominent difference between the two groups was in ICP measured after resuscitation. ICP was lower in dogs resuscitated with hypertonic saline than in dogs resuscitated with lactated Ringer's solution (p = .029). Hypertonic saline fluid resuscitation may represent a potential alternative when aggravation of intracranial hypertension during resuscitation would place a patient at greater risk.
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PMID:Effects on intracranial pressure of resuscitation from hemorrhagic shock with hypertonic saline versus lactated Ringer's solution. 398 19

The role of the baroreceptor mechanism in determining the relationship between fluid volume and arterial pressure is not clear. Therefore, the effects of the baroreflex on the arterial pressure and fluid volume of conscious, anephric dogs were studied after a sustained 10% increase in blood volume. The animals were equipped with long-term indwelling arterial and venous catheters, and arterial pressure was monitored 24 hours a day. The increase in blood volume was achieved by intravenous infusion of 50 ml/kg of lactated Ringer's solution in 30 minutes. After volume loading arterial pressure increased rapidly to hypertensive levels (130.8 +/- 7.5% of control) in a baroreceptor denervated group. The initial increase in arterial pressure in a group of normally innervated dogs was smaller (118.8 +/- 1.8% of control), but by 24 hours postinfusion the arterial pressure of both groups had reached the same level. The innervated group had probably experienced baroreceptor resetting by this time. Blood volume both before and after infusion was not different in the denervated and innervated groups; however, sodium space was markedly higher before the infusion in the denervated dogs (431.8 +/- 13.8 ml/kg vs 344.8 +/- 19.0 ml/kg in the innervated dogs), and the volume load caused parallel increases in this space in the denervated and innervated groups. The present study shows that the blood volume of anephric dogs was unchanged after baroreceptor denervation while the extracellular fluid volume of denervated dogs was elevated. Furthermore, a small sustained increase in blood volume in either conscious, innervated dogs or conscious, baroreceptor denervated dogs, in contradistinction to the effects in anesthetized dogs, resulted in significant increases in arterial pressure (p less than 0.05).
Hypertension
PMID:Effects of baroreceptor denervation on volume loading hypertension in anephric dogs. 400 91


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