Monitoring Cobalamin Inactivation During Nitrous Oxide Anesthesia by Determination of Homocysteine and Folate in Plasma and Urine

Ermens, A. A. M.; Refsum, Helga; Rupreht, J.; Spijkers, L. J. M.; Guttormsen, Anne Berit; Lindemans, Jan; Ueland, Per Magne; Abels, J.

doi:10.1097/00132586-199208000-00014

Cited by 3 publications

(6 citation statements)

References 12 publications

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“…The finding that tHcy levels did not change or slightly increased in patients who were randomly allocated to receive anaesthesia with N 2 O is compatible with the known inhibitory effect of N 2 O on cobalamin which acts as a cofactor of methionine synthase, the key enzyme in the remethylation pathway of homocysteine to methionine [1, 2]. Three previous studies have shown that tHcy increases after surgery [7–9]. In two of these, which were uncontrolled [8] or non‐randomised [7], the increase in tHcy after N 2 O anaesthesia was very marked, while in the third, randomised and controlled study, the tHcy increase was about 70% [9].…”

Section: Discussionmentioning

confidence: 61%

“…Three previous studies have shown that tHcy increases after surgery [7–9]. In two of these, which were uncontrolled [8] or non‐randomised [7], the increase in tHcy after N 2 O anaesthesia was very marked, while in the third, randomised and controlled study, the tHcy increase was about 70% [9]. The greater effect of N 2 O on tHcy in those studies compared to ours may be explained by differences in the patient populations studied and, most likely, in the duration of anaesthesia, because the inhibitory effect of N 2 O on cobalamin is time‐dependent [4, 19], being biologically relevant only for exposure times exceeding 2 h [4].…”

Section: Discussionmentioning

confidence: 99%

“…More recently, it has been demonstrated that the inhibition of methionine synthase by N 2 O causes an increase in the plasma levels of homocysteine, a sulphur aminoacid derived from methionine, which is transformed to cysteine through a vitamin B6‐dependent trans‐sulfuration pathway or remethylated to methionine by methionine synthase [5]. High levels of total homocysteine (tHcy) after exposure to N 2 O were described in leukaemia patients [6], or surgical patients undergoing otolaryngology surgery [7, 8] or neurosurgery [9]. The extent of the effect of nitrous oxide on tHcy seemed to be positively related to the duration of anaesthesia.…”

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confidence: 99%

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Effects of surgical stress and nitrous oxide anaesthesia on peri‐operative plasma levels of total homocysteineA randomised, controlled study in general surgery

et al. 2001

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SummaryAcute renal failure is a frequent complication of critical illness and optimal preventive therapy remains elusive. There is increasing evidence from animal models and some human studies that adenosine receptor antagonism by aminophylline may reduce the severity of renal impairment caused by a variety of aetiologies. We studied the renal effects of intravenous aminophylline in an unblinded, within-patient study of 20 patients admitted to a general intensive care unit following major surgery. We demonstrated that there were no adverse cardiovascular complications related to aminophylline therapy. Renal sodium and osmolar clearance increased with a non-significant trend towards increased diuresis during treatment. Creatinine clearance, however, was unchanged but the study was not designed and did not have the power to test whether aminophylline increased renal blood flow or glomerular filtration rate. We suggest the renal actions of aminophylline in critical illness merit further investigation. Acute renal failure is a frequent complication of critical illness, major surgery and in particular sepsis. Renal replacement therapy is associated with prolongation of intensive care and increased mortality. Factors that increase the risk of renal impairment include pre-existing renal impairment, insulin-and non-insulin-dependent diabetes, hypertension, atherosclerosis, particularly renal arterial disease, jaundice and increasing age [1].The pathophysiology of acute renal failure is not fully understood and hence optimum therapies for prevention of acute renal failure in patients at risk remain elusive. Animal-based research has suggested that adenosineinduced renal vasoconstriction may have an important role in the pathophysiology of acute renal failure and that adenosine receptor antagonists are protective.In major abdominal surgery and critical illness where ischaemic renal impairment may result, we hypothesised that theophylline, an adenosine A1 and A2 receptor antagonist, may have renal protective action. This was a study to investigate the renal actions of theophylline following major surgery. Methods Study designThe trial was an open, within-patient controlled study of 20 consecutive patients fulfilling the admission criteria. Patients were recruited at The Bristol Royal Infirmary general intensive care unit. The study had local ethics committee approval. Informed consent was obtained if possible, or assent was obtained from a near relative of those patients unable to give consent. Patients and methodsEligible patients were over 18 years of age and had undergone major abdominal surgery requiring admission to the ICU for postoperative management. Patients were haemodynamically stable, defined as in sinus rhythm with a pulse less than 120 beat.min 21 , systolic arterial blood pressure . 100 mmHg without the use of inotropic medication, central venous blood pressure . 8 mmHg and less than 20% variation in these parameters for 3 h before the start of the study. Patients had not received diuretics or dopamine for 6...

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of surgical stress and nitrous oxide anaesthesia on peri‐operative plasma levels of total homocysteineA randomised, controlled study in general surgery

et al. 2001

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“…20 Nitrous oxide alters cobalamine metabolism within 1 h of administration, resulting in increased Hcy concentrations that can remain elevated for longer than 1 week. 21 Fenofibrate, bezafibrate, and colestipol in combination with niacin result in hyperhomocysteinemia by yet to be defined mechanisms. 22,23 Tobacco and caffeinated coffee are also associated with increased Hcy concentrations.…”

Section: Etiology Of Hyperhomocysteinemiamentioning

confidence: 99%

The association of homocysteine and coronary artery disease

Gauthier¹,

Keevil²,

McBride³

2003

Clinical Cardiology

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Summary: Hyperhomocysteinemia has been associated with increased risk of atherosclerosis and myocardial infarction by a number of prospective case-control studies. A variety of genetic mutations, nutritional deficiencies, disease states, and drugs can elevate homocysteine concentrations. Treatment with folic acid with or without B-complex vitamins effectively lowers homocysteine levels. Whether therapy corresponds with decreased risk of coronary events is unknown, but may be promising. This article reviews the biochemistry of homocysteine metabolism, pathogeneisis, and etiology of hyperhomocysteinemia, along with its association with coronary artery disease, screening, and treatment.

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“…Agents interfering with vitamin B,, metabolism. Plasma H(e) increases within 90 min of exposure to nitrous oxide [64]. The amount of increase is related to the duration of anaesthesia and persists for at least 1 week.…”

Section: Hornocyst(e)inaemia and Pharmacological Agents Not Includingmentioning

confidence: 99%

Homocyst(e)ine and arterial occlusive diseases

Malinow

1994

Journal of Internal Medicine

230

105

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Homocysteine is a thiol-containing amino acid resulting from demethylation of methionine. The free and protein-bound forms of the amino acid and derived disulfides are called homocyst(e)ine [H(e)]. Multiple studies have shown elevated H(e) levels in patients with coronary, cerebrovascular, or peripheral arterial diseases; this association is frequent and independent of most other risk factors for atherosclerosis. In the 1993 Frontiers in Medicine Symposium investigators discussed the genetic, physiological, nutritional, and pharmacological mechanisms involved in the regulation of plasma H(e), the association of H(e) with arterial occlusive diseases, and the relationships of H(e) with nitric oxide and haemostasis. High plasma H(e) levels usually can be reversed with vitamin supplements. Whether vitamin supplements will affect the evolution of arterial occlusive diseases needs to be established in prospective, placebo-controlled, randomized, clinical trials.

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Monitoring Cobalamin Inactivation During Nitrous Oxide Anesthesia by Determination of Homocysteine and Folate in Plasma and Urine

Cited by 3 publications

References 12 publications

Effects of surgical stress and nitrous oxide anaesthesia on peri‐operative plasma levels of total homocysteineA randomised, controlled study in general surgery

Effects of surgical stress and nitrous oxide anaesthesia on peri‐operative plasma levels of total homocysteineA randomised, controlled study in general surgery

The association of homocysteine and coronary artery disease

Homocyst(e)ine and arterial occlusive diseases

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