Positive Functional Effects of Milrinone and Methylene Blue Are Not Additive in Control and Hypertrophic Canine Hearts

Leone, Richard J.; Weiss, Harvey R.; Scholz, Peter

doi:10.1006/jsre.1998.5321

Cited by 8 publications

(3 citation statements)

References 25 publications

(5 reference statements)

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“…The mechanism of this effect differs from those of other vasoactive agents (epinephrine, dopamine, norepinephrine, and isoproterenol), which exert inotropic effects by increasing intracellular cyclic adenosine monophosphate (cAMP) [10][11][12]. In contrast, MB acts through a reduction in intracellular cGMP [13][14][15][16][17][18][19][20]. Because of its unique mechanism of action, MB has been investigated across different clinical scenarios involving treatment-refractory hypotension associated with low SVR such as that occurring during and after cardiopulmonary bypass, sepsis, and liver transplantation [4][5][6][7][8][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

The effect of methylene blue during orthotopic liver transplantation on post reperfusion syndrome and postoperative graft function

Fukazawa

Pretto

2010

J Hepato Biliary Pancreat

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Section: Introductionmentioning

confidence: 99%

The effect of methylene blue during orthotopic liver transplantation on post reperfusion syndrome and postoperative graft function

Fukazawa

Pretto

2010

J Hepato Biliary Pancreat

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“…cGMP has been shown to shorten action potential duration, decrease O 2 consumption, and cause negative inotropy (14,23,24,30). cAMP has been shown to cause positive inotropy and also increase myocardial metabolic function (2,8,12,15,21). Increased cAMP causes positive inotropy through increased calcium current, the inward influx of calcium responsible for the initiation of cardiac contraction (8,15,18).…”

mentioning

confidence: 99%

“…There is experimental evidence suggesting that cAMP not only increases the mean open time of each calcium channel but also increases the number of open channels (25). It has also been demonstrated that alterations in cGMP can affect the level of cAMP in the heart and myocytes (10,12). This has suggested that an interaction exists between the second messenger systems mediated by cAMP and cGMP in the regulation of myocardial function.…”

mentioning

confidence: 99%

Negative metabolic and coronary flow effects of decreases in cAMP and increases in cGMP in control and renal hypertensive rabbit hearts

Rodríguez

Molino²,

Weiss³

et al. 2004

Journal of Applied Physiology

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The interaction during stimulation of cGMP and inhibition of cAMP was investigated in control and renal hypertensive hearts. Control and hypertensive [1 kidney, 1 clip (1K1C)] rabbits were used. The anesthetized open-chest groups were vehicle, 8-bromo-cGMP (8-Br-cGMP; 10(-3)M), propranolol (Prop; 2 mg/kg), and Prop + 8-Br-cGMP. O(2) consumption levels (Vo(2)) in the subepicardium (Epi) and subendocardium (Endo) were determined from coronary flow (microspheres) and O(2) extraction (microspectrophotometry). Wall thickening and cAMP levels were also determined. In control, no significant change in Vo(2) was seen for the 8-Br-cGMP group, but Vo(2) was decreased from Epi (9.7 +/- 1.5 ml O(2) x min(-1) x 100 g(-1)) and Endo (10.5 +/- 0.4 ml O(2) x min(-1) x 100 g(-1)) to 6.8 +/- 0.6/7.8 +/- 0.5 ml O(2) x min(-1) x 100 g(-1) in the control Prop group. Control Prop + 8-Br-cGMP did not cause a further fall in Vo(2) but lowered Endo flow. In 1K1C, Vo(2) decreased from Epi/Endo (10.8 +/- 1.3/11 +/- 1.0 ml O(2).min(-1).100 g(-1)) to 7.8 +/- 1.1/8.7 +/- 0.5 ml O(2) x min(-1) x 100 g(-1) in the 1K1C 8-Br-cGMP group and to 7 +/- 0.5/8.1 +/- 0.5 ml O(2) x min(-1) x 100 g(-1) in the 1K1C Prop group. 1K1C Prop + 8-Br-cGMP did not cause a further fall in Vo(2) but lowered blood flow. No significant changes in cAMP levels were present with 8-Br-cGMP in control or 1K1C rabbits, but significant decreases were seen with Prop in both control and 1K1C rabbits. No further change was seen in Prop + 8-Br-cGMP for either control or 1K1C. Thus the negative metabolic effect of stimulating cGMP was seen only in the hypertensive rabbit heart. The negative metabolic effect of inhibiting cAMP was seen in both the control and the hypertensive rabbit heart. However, the negative metabolic effects of cGMP and cAMP were nonadditive.

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On the genesis of myocardial ischemia

Sroka¹

2004

Z Kardiol

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About three quarters of myocardial ischemic events are triggered by the autonomic nervous system. The pathognomonic constellation is a combination of an almost complete withdrawal of tonic vagal activity with increased sympathetic activity. The reduction of tonic vagal activity, which is characteristic for ischemic heart disease, and the acute withdrawal of vagal drive preceding the onset of ischemia are not dependent on coronary artery disease. In this paper, the pathophysiological steps that lead from sympathetic-parasympathetic imbalance to myocardial ischemia shall be discussed. A considerable increase of aerobic glycolysis within the myocardium as a result of the autonomic imbalance is of special importance in this process.

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Positive Functional Effects of Milrinone and Methylene Blue Are Not Additive in Control and Hypertrophic Canine Hearts

Cited by 8 publications

References 25 publications

The effect of methylene blue during orthotopic liver transplantation on post reperfusion syndrome and postoperative graft function

The effect of methylene blue during orthotopic liver transplantation on post reperfusion syndrome and postoperative graft function

Negative metabolic and coronary flow effects of decreases in cAMP and increases in cGMP in control and renal hypertensive rabbit hearts

On the genesis of myocardial ischemia

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