Coronary metabolic adaptation restricted by endothelin in the dog heart

Fazekas, Levente; Kékesi, Violetta; Soós, Pál; Barát, Erzsébet; Huszár, Éva; Juhász‐Nagy, Alexander

doi:10.1556/aphysiol.88.2001.1.4

Cited by 5 publications

(4 citation statements)

References 32 publications

(51 reference statements)

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“…An experimental model was designed to induce myocardial ischaemia by coronary vasospasm provoked by endothelin-1 (ET-1) in the in situ canine heart. The ET-1 vasoconstrictor effect has certain characteristics that are uncommon in the coronary bed : the vascular effects of a high-dose bolus injection are usually long lasting, occlusive and uncompensated by the autoregulatory processes of the heart [15][16][17]. These features make this peptide the most likely candidate as an endogenous agent eliciting natural coronary spasm [18,19].…”

Section: Introductionmentioning

confidence: 99%

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

et al. 2002

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It has been shown that the adenosine concentration in the pericardial fluid of the normal heart is higher by one order of magnitude than that of the venous plasma. A further increase in the pericardial adenosine concentration was also demonstrated in myocardial ischaemia or hypoxia. It was proposed that pericardial nucleoside levels may represent the interstitial concentrations of the adenine nucleosides. An experimental model was designed to determine the intrapericardial concentrations of adenosine, inosine and hypoxanthine during coronary spasm provoked by intracoronary administration of endothelin-1 (ET-1; 0.08+/-0.02 nmol/g of myocardial tissue). In the in situ dog heart (n=10), adenosine, inosine and hypoxanthine concentrations were determined by HPLC in fluid samples collected from the closed pericardial sac before and after ET-1 administration, and from the systemic arterial blood. Systemic blood pressure, heart rate and standard ECG were registered continuously. We found that the nucleoside concentrations in the infusate samples increased significantly during coronary spasm [adenosine, 1.49+/-0.44 compared with 0.37+/-0.07 microM (P<0.05); inosine, 27.43+/-11.51 compared with 0.47+/-0.11 microM (P<0.05); hypoxanthine, 21.17+/-6.49 compared with 4.91+/-1.24 microM (P<0.05)], while a significant decrease in blood pressure and an elevation in ECG ST segments were observed. The levels of the purine metabolites did not change in the systemic blood. The data indicate that changes in adenine nucleoside levels measured in pericardial infusate samples reflect activation of coronary metabolic adaptation in this model of spastic ischaemia, and that pericardial nucleoside levels may characterize alterations in interstitial adenine nucleoside concentrations.

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Section: Introductionmentioning

confidence: 99%

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

et al. 2002

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“…The intrapericardial levels of these agents may be augmented further in pathophysiological conditions. Moreover, these levels may be interrelated, if augmented intapericardial concentrations of ET-1 induce myocardial ischaemia [14].…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1-induced elevations in purine metabolite concentrations — autoregulatory protection in the canine pericardium?

et al. 2002

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Pericardial fluid accumulates the cardioprotective purine metabolites, as well as the endogenous vasoconstrictor agent endothelin-1 (ET-1). The aim of the present study was to characterize the pericardial concentrations of the purine metabolites adenosine, inosine and hypoxanthine before and after intrapericardial administration of ET-1 to the in situ heart. The closed pericardial sac of anaesthetized dogs (n=9) was cannulated for ET-1 administration and for obtaining native pericardial fluid and control pericardial infusate samples (C1 and C2), as well as consecutive pericardial infusate samples (samples I, II and III) obtained 15 min after intrapericardial administration of 150 pmol/kg ET-1. In an additional five dogs, using the same protocol, ventricular epicardial and endocardial monophasic action potential recordings were performed to assess local ischaemic electrophysiological changes. Significant elevations of pericardial purine metabolite concentrations (measured by HPLC) were found in sample II compared with sample C2: adenosine, 4.5+/-1.7 compared with 0.5+/-0.1 microM (P<0.05); inosine, 18.3+/-2.8 compared with 0.9+/-0.2 microM (P<0.001); hypoxanthine, 38.1+/-8.0 compared with 13.4+/-2.6 microM (P<0.01). Systemic blood pressure, left ventricular pressure and contractility, and systemic plasma levels of the purine metabolites remained unchanged during the ET-1 effect, while significant ECG ST elevations (ST(max) 0.68+/-0.01 mV; P<0.001) were observed. In the five dogs analysed electrophysiologically, the left ventricular epicardial monophasic action potential duration and upstroke velocity decreased significantly at time point II compared with C2, while the endocardial monophasic action potential duration and upstroke velocity did not show ischaemia-related changes. The results suggest that intrapericardial administration of ET-1 induces subepicardial ischaemia, with parallel activation of coronary metabolic adaptive and cardiac self-protective mechanisms in the epimyocardial layer of the heart.

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“…This peptide is produced predominantly by the endothelium, but in pathophysiological states, other cell types such as leukocytes, macrophages, smooth muscle cells, cardiomyocytes and mesangial cells can also serve as sources of its release [12]. The increased plasma level of ET-1 could be responsible for the decreased coronary perfusion [32] and pulmonary hypertension. The activation of vasoconstrictor ET receptors can further play a decisive role in acute microcirculatory disorders of the peripheral cardiovascular system.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Activation after Experimental Cardiac Tamponade

Vass¹,

Süveges²,

Érces

et al. 2013

Eur Surg Res

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Background/Purpose: Cardiac tamponade is a medical emergency situation associated with a high rate of life-threatening complications, even after immediate interventions. Our aim was to characterize the acute inflammatory consequences of this event in a clinically relevant large animal model. Methods: Cardiac tamponade was induced for 60 min in anesthetized, ventilated and thoracotomized minipigs by intrapericardial fluid administration, the mean arterial pressure (MAP) being maintained in the interval of 40-45 mm Hg (n = 8). A further group (n = 7) served as sham-operated control. The global macrohemodynamics, including the right- and left-heart end-diastolic volumes (RHEDV and LHEDV), the pulmonary vascular resistance index (PVRI) and the superior mesenteric artery (SMA) flow, were monitored for 240 min, and the intestinal microcirculatory changes (pCO₂ gap) were evaluated by indirect tonometry. Blood samples were taken for the determination of cardiac troponin T and vasoactive inflammatory mediators, including histamine, nitrite/nitrate, big-endothelin, superoxide and high-mobility group box protein-1 levels in association with intestinal leukocyte and complement activation. Results: The cardiac tamponade induced significant decreases in MAP, cardiac output, LHEDV and SMA flow, while the PVRI and the pCO₂ gap increased significantly. After the removal of fluid from the pericardial sac, the MAP and the LHEDV were decreased, while the PVRI and the pCO₂ gap remained elevated when compared with those in the sham-operated group. In the posttamponade period, the abrupt release of inflammatory mediators was accompanied by a significant splanchnic leukocyte accumulation and complement activation. Conclusions: The macrocirculatory and splanchnic microcirculatory disturbances were accompanied by a significant proinflammatory reaction; endothelin and the complement system may be significant components of the inflammatory cascade that is activated in this porcine model of pericardial tamponade.

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Coronary metabolic adaptation restricted by endothelin in the dog heart

Cited by 5 publications

References 32 publications

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

Endothelin-1-induced elevations in purine metabolite concentrations — autoregulatory protection in the canine pericardium?

Inflammatory Activation after Experimental Cardiac Tamponade

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