II. Validity and reliability of liquid chromatography with electrochemical detection for measuring plasma levels of norepinephrine and epinephrine in man

Goldstein, David S.; Feuerstein, Giora; Izzo, Joseph L.; Kopin, Irwin J.; Keiser, Harry R.

doi:10.1016/0024-3205(81)90139-9

Cited by 469 publications

(163 citation statements)

References 6 publications

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“…Plasma norepinephrine and epinephrine concentrations were assayed by HPLC with electrochemical detection [13], whole-blood propofol was assessed by an HPLC-fluorometric method [14], and plasma alfentanil by a radio-immunoassay [15]. Plasma dexmedetomidine concentrations were measured at Orion-Farmos Corporation using a GC-MS method [16].…”

Section: Methodsmentioning

confidence: 99%

The effect of intravenous dexmedetomidine premedication on the dose requirement of propofol to induce loss of consciousness in patients receiving alfentanil

Peden

Cloote

Stratford³

et al. 2001

Anaesthesia

119

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SummaryDexmedetomidine reduces the dose requirements for opioids and anaesthetic agents. We conducted a single-centre, open-label, noncomparative phase II study of the effect of intravenous dexmedetomidine on the dose requirement of propofol to induce loss of consciousness in 49 ASA I and II patients. The initial dexmedetomidine infusion scheme was reduced twice because of adverse events. Forty patients who received the final infusion scheme were randomly allocated to receive one of five stepped propofol infusions; loss of consciousness was assessed after 21 min. The ED 50 for the final infusion rate of propofol to suppress consciousness was 3.45 mg.kg 21 .h 21 (95% CL 2.7±4.2): ED 95 was 6.68 mg.kg 21 .h 21 (95% CL 5.1±19.1), EC 50 was 1.69 m g.ml 21 (95% CL 0.95±2.5) and EC 95 was 5.7 m g.ml 21 (95% CL 3.2 to . 10). Our final dose of dexmedetomidine of 0.63 m g.kg 21 caused a reduction in the overall concentration and dose of propofol required to produce loss of consciousness, but no significant shift in the dose±response curve compared with other studies. Drugs acting as agonists at a 2 -adrenoceptors may enhance anaesthesia by producing dose-related sedation, anxiolysis, decreased upper airway secretions, peri-operative haemodynamic stability and analgesia [1±3]. There is substantial evidence that the a 2 -agonists also exert an anaestheticsparing effect mediated in part through a decrease in central noradrenergic activity, but mainly through a direct effect on central a 2 -adrenoceptors in the locus coeruleus and other sites [4,5]. The a 2 -agonists also have activity at the imidazoline receptors involved in central blood pressure control [2,6,7].Dexmedetomidine, a specific, selective and potent a 2 -adrenoceptor agonist has been shown to have significant anaesthetic, sedative and analgesic-sparing effects in clinical studies [8±12]. Recently, the dose-dependent effects of dexmedetomidine on isoflurane [11] and sevoflurane [12] requirements have been assessed in humans. However, to date, no studies have explored the shift of a dose±response curve for intravenous agents in conjunction with the a 2 -agonists. We aimed to perform a descriptive dose-finding study to determine the effect of an infusion of dexmedetomidine on the dose and blood concentration of propofol required to suppress consciousness and motor activity during total intravenous anaesthesia with propofol and alfentanil.

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Section: Methodsmentioning

confidence: 99%

The effect of intravenous dexmedetomidine premedication on the dose requirement of propofol to induce loss of consciousness in patients receiving alfentanil

Peden

Cloote

Stratford³

et al. 2001

Anaesthesia

119

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“…On the sixth week rats were housed in individual Nalgene metabolic cages for 24 hours for habituation, after which, during the subsequent 24 hours, urine was collected for excretion of Na ϩ , K ϩ , creatinine, and NO urinary metabolites 15 and norepinephrine excretion. 18 In a subsequent experiment we added L-arginine 2 g/L to the drinking water of 28 rats to test whether it could prevent the effect of the L-NAME/insulin combination on blood pressure. Twentythree rats received L-NAME and insulin, as in the previous experiment, and were divided into 3 groups: L-NAMEϩinsulin combination (nϭ4); L-NAMEϩinsulinϩL-arginine (from day 1) (nϭ12); and L-NAMEϩinsulinϩlate L-arginine (from week 4) (nϭ9).…”

Section: Methodsmentioning

confidence: 99%

Subpressor Dose of L-NAME Unmasks Hypertensive Effect of Chronic Hyperinsulinemia

et al. 2000

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Abstract-We previously found that chronic exogenous hyperinsulinemia without sugar supplementation does not elevate blood pressure. This may be partially explained by the ability of insulin to release nitric oxide and cause vasodilatation.To test this hypothesis, we studied 4 groups of rats: 9 rats (body weight, 213Ϯ14 g) treated with a gradual increase of a sustained-release subcutaneous insulin pellet; 9 rats (body weight, 213Ϯ9 g) treated with N G -nitro-L-arginine methyl ester (L-NAME) in drinking water 50 mg/L; 19 rats (body weight, 217Ϯ11 g) treated with the combination of L-NAME and insulin; and 9 control rats (body weight, 218Ϯ11 g). Blood pressure was followed weekly for 6 weeks, and then rats were studied in metabolic cages. Weight gain was not different during the 6 weeks. Renal function did not differ between the 4 groups, but 24-hour urinary nitrite/nitrate excretion was lower (PϽ0.02) in L-NAME-treated and higher in insulin-treated rats. Plasma insulin doubled (PϽ0.002) in the insulin-treated rats, but there was no hypoglycemia and, by week 6, fructosamine levels were 2.1Ϯ0.2, 2.1Ϯ0.2, 2.3Ϯ0.1, and 2.3Ϯ0.2 mmol/L in control rats and rats treated with L-NAME, insulin, and L-NAME plus insulin, respectively. Systolic blood pressure, which did not differ at baseline, at week 3 was 122Ϯ17, 118Ϯ17, and 118Ϯ24 mm Hg in the control, L-NAME, and insulin groups and 136Ϯ14 mm Hg (PϽ0.03) in the combination group. At week 6, systolic blood pressure was 128Ϯ14, 127Ϯ15, and 118Ϯ13 mm Hg in the control, L-NAME, and insulin groups, respectively, and 150Ϯ14 mm Hg (PϽ0.0005) in the combination group. In a subsequent experiment, L-arginine 2 g/L abrogated the effects of L-NAME and insulin combination. In conclusion, chronic exogenous hyperinsulinemia does not affect blood pressure but may cause hypertension when endothelial function is compromised. Key Words: insulin Ⅲ nitric oxide Ⅲ sodium Ⅲ nitrites Ⅲ nitrates H yperinsulinemia was found to be common in essential hypertension even without obesity and is the foundation for the concept of the metabolic syndrome X. However, the manner in which insulin elevates blood pressure is unclear. Sympathetic activation, 1,2 sodium retention, 3 and vascular hypertrophy have been suggested 4 but never proven in a chronic model of hyperinsulinemia. Indeed, because of the vasodilatory effects of insulin, 2 it has been suggested the vasodilation may mask a prohypertensive effect. More recently it was found that, in part, insulin-induced vasodilation may be related to increase in nitric oxide synthase (NOS) activity. 5 There have been several attempts to produce hypertension in rats by way of chronic exogenous hyperinsulinemia. 6 -10 In most of these studies, increase in carbohydrate consumption (intravenous glucose or oral sucrose) was combined with insulin to prevent hypoglycemia. We previously devised a method for producing chronic exogenous hyperinsulinemia in normal rats, without sugar supplementation and without hypoglycemia, that did not affect blood pressure. 10 However, whe...

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“…Established methods were used to measure ADM (38), ET-1 (31), and catecholamines (15,17). ADM was measured by radioimmunoassay, as described by Lewis et al (38).…”

Section: Analytic Measurementsmentioning

confidence: 99%

“…For the catecholamine assay, plasma was extracted on alumina, and catecholamines were eluted with acetic acid using established techniques (15,17). The extracted catecholamines were separated and measured by reverse-phase high-performance liquid chromatography with electrochemical detection.…”

Section: Analytic Measurementsmentioning

confidence: 99%

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

Peebles

Richards²,

Celi

et al. 2008

Journal of Applied Physiology

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Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO 2), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O 2). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 Ϯ 18 and 150 Ϯ 36 mol/l at 4% and 8% CO 2, respectively (both P Ͻ 0.05). Release of cerebral CNP was also observed during changes in CO 2 (hypercapnia vs. hypocapnia, P Ͻ 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: Ϫ96 Ϯ 14 mol/l at 10% O 2 (P Ͻ 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO 2-induced CBF changes. cerebral circulation; nitric oxide; endothelium RESPIRATORY-INDUCED CHANGES in arterial PCO 2 (Pa CO 2 ) and, to a lesser extent, PO 2 (Pa O 2 ) play a major role in cerebral blood flow (CBF) regulation (9). Elevations in Pa CO 2 (hypercapnia) lead to vasodilation of cerebral arterioles in the downstream bed and a subsequent increase in CBF, whereas a reduction in Pa CO 2 (hypocapnia) leads to vasoconstriction and a subsequent decrease in CBF (28, 65). A fall in Pa O 2 (hypoxia) below a certain threshold (Ͻ40 Torr) also produces cerebral vasodilation (19). These arterial blood gas-induced changes in CBF are mediated through changes in cerebrovascular resistance via alterations in vascular smooth muscle diameter in response to changes in the level of intracellular calcium and/or calcium sensitivity (for review see Ref. 22). Cerebrovascular tone is influenced by several chemical substances, including nitric oxide (NO). NO, synthesized from the terminal guanidino nitrogen atom(s) of L-arginine in a two-step reaction that is catalyzed by the enzyme NO synthase (NOS) (48), is an important vasoactive factor that dilates the cerebral vasculature. Under normal conditions, two isoforms of NOS are expressed in the brain, endothelium-derived NOS (eNOS) and neuronal-derived NOS (nNOS) (61), although evidence for the role of eNOS vs. nNOS in the control of CBF is controversial (3). Vasodilation evoked by NO is initiated by an increase in cGMP (7).Pharmac...

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II. Validity and reliability of liquid chromatography with electrochemical detection for measuring plasma levels of norepinephrine and epinephrine in man

Cited by 469 publications

References 6 publications

The effect of intravenous dexmedetomidine premedication on the dose requirement of propofol to induce loss of consciousness in patients receiving alfentanil

The effect of intravenous dexmedetomidine premedication on the dose requirement of propofol to induce loss of consciousness in patients receiving alfentanil

Subpressor Dose of L-NAME Unmasks Hypertensive Effect of Chronic Hyperinsulinemia

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

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