Open heart surgery increases the levels of histamine in arterial and coronary sinus blood

Valen, Guro; Kaszaki, József; Nagy, S.; Vaage, Jarle

doi:10.1007/bf01986386

Cited by 13 publications

(12 citation statements)

References 35 publications

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“…The systemic histamine levels may have been increased before start of the procedure due to anaesthesia, as morphine, thiopental, and vancuronium induce release of histamine [23]. Before ventricular fibrillation the arterial histamine level was higher than that in the coronary sinus, confirming previous observations that histamine is taken up in the human coronary circulation [8], as in all other mammals investigated [7]. We do not have a good explanation for why arterial histamine decreased 5 rain after fibrillation.…”

Section: Inflamm Ressupporting

confidence: 82%

“…In previous experimental studies on cardiac histamine levels models of ischaemia-reperfusion have been employed, and the ischaemic episodes have lasted for a minimum of 10 minutes [5, 8-11, 19, 20]. Increased coronary sinus levels of histamine were found after ischaemia-reperfusion injury in dogs [9,19], guinea pigs [10,20], rats [5,11], and humans [8]. Histamine in the coronary circulation increased rapidly upon reperfusion of the ischaemic heart [5,8,9,11].…”

Section: Inflamm Resmentioning

confidence: 96%

“…Myocardial infarction increases plasma levels of histamine in humans [12,13]. Cold cardioplegia in open heart surgery releases histamine into the human coronary circulation [8]. Although histamine has potent effects on the cardiovascular system, it is presently ignored as a mediator of ischaemia-reperfusion injury [14].…”

Section: Introductionmentioning

confidence: 99%

“…Histamine is normally taken up by the heart [7,8], but is released after experimental ischaemia-reperfusion injury in several species [9,10,11]. Myocardial infarction increases plasma levels of histamine in humans [12,13].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD)

et al. 1995

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Histamine has inotropic, chronotropic, arrhythmogenic, and vasoactive effects, and is released from the heart in ischaemia-reperfusion injury. The effect of ventricular fibrillation (VF) and defibrillation (DEF) on histamine release was investigated in 9 anaesthetized patients undergoing transvenous implantation of ICD. Concomitant arterial and coronary sinus (CS) blood samples were drawn before induction of VF (duration 20 seconds), immediately after, and 2 and 5 min after DEF (18-24 Joules). Basal arterial histamine was 2.5 +/- 6 nmol/l, and did not increase after VF. The histamine level in CS was 1.1 +/- 0.2 nmol/l before VF (p < 0.008 compared to arterial), and increased to 2.5 +/- 0.6 nmol/l immediately after (p < 0.045 compared to basal), to 3 +/- 1.1 nmol/l 2 min after (p < 0.45), and to 2.4 +/- 0.8 nmol/l 5 min after VF. In the basal state there was an uptake of histamine across the coronary circulation. After VF/DEF the level of histamine increased in coronary venous blood, suggesting cardiac release of histamine.

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Section: Inflamm Ressupporting

confidence: 82%

Section: Inflamm Resmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD)

et al. 1995

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“…Some studies have reported that during myocardial ischemia and reperfusion, histamine is released from the heart of rats (9), dogs (10,11), guinea pigs (12,13), and humans (14,15). Histamine is known to be one of the chemical mediators with inotropic and chronotropic actions and is also a vasoactive and arrhythmogenic substance (16 -18).…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of H2-Receptor Activation Against the Duration of Myocardial Hypoxia/Reoxygenation-Induced Ventricular Fibrillation in Sensitized Guinea-Pig Hearts

Imajo¹,

Matsui²,

Yasui³

et al. 2005

J Pharmacol Sci

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Abstract. Patients with high serum immunoglobulin E levels were reported to be protected against sudden death during acute myocardial infarction. The protection mechanism might be attributed to the facilitation of histamine release from sensitized mast cells; however, this remains to be clarified. In this study, we examined the influence of sensitization on ventricular fibrillation (VF) induced by myocardial hypoxia / reoxygenation (H / R). Guinea pigs were actively sensitized by subcutaneous injection of ovalbumin in Bordetella pertussis vaccine. Hearts isolated from non-sensitized and sensitized guinea pigs were subjected to 30-min hypoxia / 30-min reoxygenation using a Langendorff apparatus. The amount of histamine released in the sensitized guinea-pig hearts was elevated, and the duration of VF was found to be reduced. The treatment with a histamine H 2 -receptor antagonist inhibited the reduction of VF duration. Treatment of the non-sensitized hearts with the histamine H 2 -receptor agonist resulted in the decrease of VF duration to the same level as that in the sensitized hearts. In conclusion, these results suggest that the risk of sudden death during myocardial H / R may be attenuated in the sensitized hearts and that histamine H 2 -receptor activation due to the released histamine may be involved in the protective effect.

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The effects of exogenous histamine in isolated rat hearts

1995

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The role of histamine in cardiac physiology and pathophysiology is not clarified, but is dependent on species. The effects of exogenous histamine in Langendorff-perfused rat hearts were investigated. 1 mM, 100, 10, 1 and 0.1 microM of histamine (n = 7 each) as 15 min infusions were employed in a dose-response study, and compared to control perfused hearts (n = 7). In another experimental series, 100 microM histamine (n = 15) was added during reperfusion after 25 min global ischemia, and compared to control ischemia-reperfusion (n = 15). The maximal response to histamine in the dose-response study (100 microM) was an increase of left ventricular developed pressure to 126 +/- 8% of initial value (mean +/- SEM, p < 0.04), and increase of coronary flow to 152+6% (p < 0.02) after 5 min infusion. 100 microM histamine did not significantly influence heart rate or rhythm. The lowest concentration (0.1 microM) did not have effects cardiac performance. Reperfusion with histamine for 2 min after ischemia reduced left ventricular developed pressure to 68 +/- 10% of initial value versus 116+17% in ischemic controls (p < 0.05), and increased left ventricular end-diastolic pressure to 24 +/- 8 mmHg compared to 6 +/- 2 mmHg in controls (p < 0.04). Left ventricular pressures were similar in hearts reperfused with histamine and in ischemic controls for the rest of the observation. Coronary flow increased during reperfusion in hearts given histamine. Histamine had a dose-dependent positive inotropic and vasodilatory effect in isolated rat hearts. Exogenous histamine had only minor effects on post-ischemic cardiac function.

show abstract

Open heart surgery increases the levels of histamine in arterial and coronary sinus blood

Cited by 13 publications

References 35 publications

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD)

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD)

The Protective Effect of H2-Receptor Activation Against the Duration of Myocardial Hypoxia/Reoxygenation-Induced Ventricular Fibrillation in Sensitized Guinea-Pig Hearts

The effects of exogenous histamine in isolated rat hearts

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