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

Relationships between changes in levels of catechols and directly recorded sympathetic nerve activity were examined using simultaneous measurements of renal sympathetic nerve activity and arterial and renal venous concentrations of norepinephrine (NE), dihydroxyphenylalanine (dopa), and dihyroxyphenylglycol (DHPG) during reflexive alterations in renal sympathetic nerve activity in anesthetized, adrenal-demedullated rats. Nitroprusside infusion increased renal sympathetic nerve activity by 90%, arterial levels of dopa by 96%, NE by 326%, and DHPG by 141%. Phenylephrine infusion increased arterial DHPG levels by 81% and decreased renal sympathetic nerve activity by 37% and NE levels by 26%; arterial dopa levels were unchanged. Ganglionic blockade by chlorisondamine (with concomitant phenylephrine infusion to maintain MAP) decreased renal sympathetic nerve activity by 65% and NE concentrations by 37%; arterial dopa concentrations were unchanged, and DHPG concentrations increased by 60%. Proportionate responses of arterial levels of NE were strongly related to proportionate changes in renal sympathetic nerve activity. Clearance of DHPG from arterial plasma was prolonged by phenylephrine-induced hypertension and by nitroprusside-induced hypotension. The results suggest that changes in arterial NE levels reflect changes in sympathetic activity; changes in dopa levels reflect changes in catecholamine biosynthesis; and changes in DHPG levels depend on reuptake of released NE and on hemodynamic factors affecting DHPG clearance.
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PMID:Plasma levels of catechols during reflexive changes in sympathetic nerve activity. 250 66

Phenylephrine (Phe) is frequently administered as an intravenous (IV) bolus to increase blood pressure, yet the acute time course and hemodynamic effects of bolus Phe in patients with myocardial disease have not been reported. Therefore 50 randomized IV bolus doses of Phe (50, 100, 150, or 200 micrograms) were given to 18 patients during anesthesia for elective coronary artery surgery. Esophageal Doppler techniques were used to continuously monitor cardiac output (CO); mean arterial pressure (MAP), CO, and calculated systemic vascular resistance (SVR) were recorded every 5 seconds for a total of 2 minutes. The hemodynamic changes (mean +/- SEM) for each of the four doses of Phe (50, 100, 150, 200 micrograms) were maximal at about 42 seconds after the drug was given. They consisted of an increase in MAP (11.6 +/- 2.1, 15.6 +/- 2.4, 14.7 +/- 2.4, 18.0 +/- 1.5 mm Hg); increase in SVR (766 +/- 190, 930 +/- 310, 950 +/- 344, 1732 +/- 824 dynes.sec.cm-5); and a decrease in CO (-.58 +/- .11, -.68 +/- .13, -.73 +/- .20, -.77 +/- .18 L.min-1). Hypertension, increased age, low preoperative ejection fraction, high baseline CO, and low baseline SVR significantly (P less than 0.05) decreased hemodynamic responses to Phe (see text). In conclusion, bolus IV Phe in patients with myocardial disease increases MAP and SVR and simultaneously decreases CO; these peak hemodynamic events occur approximately 42 seconds after Phe administration.
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PMID:Time course and hemodynamic effects of alpha-1-adrenergic bolus administration in anesthetized patients with myocardial disease. 254 37

Catechol and indole metabolism in rostral ventrolateral medulla (RVLM or C1) was studied in response to changes in blood pressure across different rat strains. Sprague-Dawley, Wistar Kyoto normotensive and spontaneously hypertensive rats were anesthetized with urethane and had a 250 mu carbon paste in vivo electrochemical electrode implanted in RVLM area. Two electrochemical peaks were detected in this region. The first was at 0.12 V and the second at 0.28 V. To identify the electrochemical peaks, inhibitors of monoamine metabolism were administrated. alpha-Methylparatyrosine (tyrosine hydroxylase inhibitor), fusaric acid (dopamine-beta-hydroxylase inhibitor), pargyline (monoamine oxidase inhibitor) and LY 134046 (phenylethanolamine-N-methyltransferase inhibitor) showed that the first peak measured in the RVLM is likely to have multiple components including epinephrine, norepinephrine and 3,4-dihydroxyphenylacetic acid. The second peak most likely represents 5-hydroxyindole acetic acid. Phenylephrine or nitroprusside was infused to increase or decrease the blood pressure. Phenylephrine-induced hypertension reduced the catechol peak and increased the indole peak. By contrast, nitroprusside-induced hypotension produced reciprocal results. Hypotension led to an increase in the catechol peak and a reduction in the indole peak. The same pattern was observed in all three rat strains. We conclude that catechol and serotonin metabolism in RVLM changes in close relation to changes in blood pressure.
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PMID:Catechol and indole metabolism in rostral ventrolateral medulla change synchronously with changing blood pressure. 272 47

Induced systemic arterial hypotension by intravenous nitroprusside administration and by acute arterial occlusion in sheep have been found to reduce lymphocyte traffic as mirrored in the output of lymphocytes into the efferent lymph of peripheral lymph nodes. In the present series of experiments in sheep with chronically cannulated efferent lymphatics of peripheral lymph nodes, induced and monitored systemic arterial hypertension with intravenous pump infusions of phenylephrine or dopamine both produced sharp increases in the output of lymphocytes into efferent lymph in all of 27 studies. The increases in lymphocyte output with dopamine were more sustained and less associated with evidence of lymphoid tissue damage than with phenylephrine. Phenylephrine infusions were attended by a high incidence of gross bleeding into the efferent lymph, of increased coagulability of efferent lymph in the absence of gross bleeding and of prolonged depression of lymphocyte outputs after the cessation of intravenous infusion.
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PMID:Increased outputs of lymphocytes in lymph efferent from the lymph nodes of sheep during systemic arterial hypertension induced by phenylephrine or dopamine. 344 45

Acute hypertension induced by adrenergic agents opens up the blood-CSF barrier (choroid plexus) to nonelectrolyte and protein tracers. Sprague-Dawley adult rats anesthetized with ketamine were given an intravenous bolus of either epinephrine (10 micrograms/kg), phenylephrine (100 micrograms/kg), isoproterenol (10 micrograms/kg), or D,L-amphetamine (2 mg/kg). Tracers were injected simultaneously with test agents, and the animals killed 10 min later. Epinephrine raised MABP by 57 mm Hg, to a peak pressure of 160 mm Hg; and it increased the volume of distribution (Vd) of urea, mannitol, and 125I-bovine serum albumin in CSF by 1.5-, 2.7-, and 30-fold, respectively. There was enhanced uptake by lateral and fourth ventricle choroid plexuses, cerebral cortex, cerebellum, medulla, and thalamus. Phenylephrine also elevated MABP to 160 mm Hg, but it increased permeation of tracers into CSF (and several brain regions) to a lesser extent than epinephrine, attributable to protective vasoconstriction associated with alpha-agonist activity. Ratio analysis of Vd data provides evidence that augmented permeation of nonelectrolyte tracers in acute hypertension occurs predominantly by diffusion rather than vesicular transport. It is postulated that elevated MABP distends the central cores of choroid plexus villi and cerebral capillaries, with resultant stretching and opening of tight junctions in both barrier systems; with less hindrance to diffusion, urea and mannitol are cleared at rates closer to free diffusion. Neither isoproterenol (decreased MABP by 40 mm Hg) nor amphetamine (did not alter MABP) significantly opened the choroid plexus or blood-brain barrier to tracers.
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PMID:Adrenergic-induced enhancement of brain barrier system permeability to small nonelectrolytes: choroid plexus versus cerebral capillaries. 392 38

Most cold preparations contain sympathomimetic decongestants in combination with antihistamines, anticholinergics or expectorants. All of the sympathomimetic decongestants have the potential to elevate blood pressure, yet little information has been reported on their use in patients with hypertension. Phenylephrine and phenylpropanolamine stimulate alpha-adrenergic receptors, causing elevation of blood pressure and a reflex decrease in heart rate. Ephedrine and pseudoephedrine stimulate both alpha and beta receptors, elevating blood pressure with an increase or no change in heart rate. Because little is clinically known, these agents should probably be avoided in hypertensives.
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PMID:Drugs for cough and cold symptoms in hypertensive patients. 397 59

Phenylephrine, a strong alpha-adrenergic receptor-stimulating agent, was compared with adrenaline in 65 patients with out-of-hospital cardiac arrest, in a double-blind study. The resuscitation was performed by the physician-staffed Prehospital Emergency Care Unit of Helsinki University Central Hospital. The patients received either 1.0 mg of phenylephrine or 0.5 mg of adrenaline i.v. in the treatment of fine ventricular fibrillation, asystole or electromechanical dissociation. If two doses of either drug did not restore circulation, 0.5 mg of known 0.01% adrenaline was given i.v., maximally twice. In the adrenaline group, which consisted of 36 patients with a mean age of 61 years, 10 patients (28%) were successfully resuscitated. The phenylephrine group consisted of 29 patients with a mean age of 62 years. In this group nine patients (31%) were successfully resuscitated. The two groups were comparable regarding their apnoea-times, and there was no difference in the need for extra adrenaline between the groups. No adverse effects, such as hypertension or bradycardia, were noted in the patients treated with either adrenaline or phenylephrine, nor did the overall rate of successful resuscitation fall during the test period. It is concluded that phenylephrine seems as effective as adrenaline in the treatment of cardiac arrest, but further studies seem warranted.
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PMID:Comparison of adrenaline and phenylephrine in out-of-hospital cardiopulmonary resuscitation. A double-blind study. 406 Oct 4

The value of plasma norepinephrine measurement in assessing baroreceptor-mediated changes in sympathetic vasomotor activity was studied in seven healthy normotensive volunteers. Blood pressure was decreased by graded steady-state infusions of sodium nitroprusside (25-100 micrograms/min) and increased by infusions of phenylephrine (25-100 micrograms/min) at rates producing a 10% to 20% change in diastolic blood pressure. Sodium nitroprusside produced significant decreases in diastolic blood pressure (p less than 0.01) and calculated mean arterial blood pressure (p less than 0.005), and increases in heart rate (p less than 0.001) and plasma norepinephrine (p less than 0.001). Phenylephrine administration produced increases in systolic (p less than 0.005), diastolic (p less than 0.005), and mean blood pressure (p less than 0.001). Heart rate (p less than 0.001) and plasma norepinephrine (p less than 0.05) fell. The absolute changes in diastolic and mean pressure and heart rate were not significantly different for the two drugs, but were of opposite sign; however, the increase in plasma norepinephrine during hypotension was greater than the decrease during hypertension (p = 0.02). We conclude that plasma norepinephrine changes appropriately in response to altered blood pressure and that the response is greater to a given fall than to a rise in blood pressure, consistent with known changes in sympathetic vasomotor outflow.
Hypertension
PMID:Plasma norepinephrine in the evaluation of baroreceptor function in humans. 715 32

1. Whole body trans-section at the level of the first or second lumbar vertebra of stress-susceptible or normal Poland China swine provided a preparation of isolated perfused caudal muscle that was without nervous or hormonal influences. Metabolic responses to halothane anaesthesia were exaggerated in the susceptible preparation. 2. Carbachol (10(-4) M) increased O2 consumption threefold and elevated blood lactate levels from 3 to 8 mumole/ml. in susceptible but not in normal muscle preparations. 3. Isoprenaline in a continuous infusion (2.5 micrograms/kg caudal wt. per min for 12 min, subsequently diminished to 1.2 microgram/kg per min) did not increase O2 consumption of susceptible or normal muscle but did increase blood lactate by 2 mumole/ml. in both. 4. Simultaneous administration of carbachol and isoprenaline resulted in additive increases in blood lactate. 5. Incremental increases in temperature above 41 degrees C initiated exaggerated increases in O2 consumption and blood lactate in susceptible but not normal muscle; these were similar to whole body responses. 6. Phenylephrine (0.2-25 micrograms/kg per min continuous) produced (i) hypertension, (ii) no observed effects upon aerobic or anaerobic metabolism and (iii) progressive tissue oedema; these effects were similar in susceptible and normal muscle. 7. Skeletal muscle from stress-susceptible swine is evidently inherently capable of metabolic responses to cholinergic agonists and increased temperature; these responses are greater than those in normal muscle. This suggests that initiation of stress responses in intact swine is related to somatic motor and sympathetic stimulation of abnormal skeletal muscle, and not to a disorder of the somatic or sympathetic nervous system.
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PMID:Porcine muscle responses to carbachol, alpha- and beta-adrenoceptor agonists, halothane or hyperthermia. 720 67

Phenylephrine hydrochloride is a potent, effective, relatively safe drug with few ocular side effects. Side effects from topical instillation are uncommon but include severe systemic cardiovascular effects with elevated blood pressure and stroke. Ten percent phenylephrine should be used with caution in patients with known cardiac disease, hypertension, aneurysms, long-standing insulin-dependent diabetes, or advanced arteriosclerosis. A 2.5% concentration is generally indicated for ophthalmic examination as well as for use in infants and in the elderly. Phenylephrine should not be used in patients with narrow-angle glaucoma, and it is also contraindicated in patients taking monoamine oxidase inhibitors or tricyclic antidepressants.
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PMID:3. Phenylephrine hydrochloride. 724 10


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