Mechanoelectric Feedback in the Ischemic Myocardium: An Interplay That Modulates Susceptibility to Fibrillation

2013 ◽  
Vol 66 (3) ◽  
pp. 168-170
Author(s):  
David Calvo ◽  
José Jalife
Keyword(s):  
Ischemic Myocardium ◽  
Mechanoelectric Feedback

Heparin from Intestine and Lung Source Administered in Large Dose to Dogs with Acute Myocardial Ischemia

1978 ◽  
Vol 40 (02) ◽  
pp. 407-417
Author(s):  
Michael J Saliba ◽  
Richard J Pavalec
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Adenosine Triphosphate ◽  
Intestinal Mucosa ◽  
Large Dose ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Atp Levels ◽  
Initial Control ◽  
The Difference

SummaryIntestinal mucosa heparin (IMH) and beef lung heparin (BLH) were infused into dogs subjected to myocardial ischemia by intermittent coronary artery occlusions. The IMH was from a mixture of beef, sheep, and pig intestinal mucosa. Initial control occlusion and recovery was followed by a second occlusion with 60,000 units of IMH or BLH added. Electrocardiographic S-T segment elevations (ST) were measured acutely. There were no significant differences in ST in non-ischemic myocardium before occlusions or with occlusions. In ischemic myocardium, IMH significantly lowered control ST 84% in amount (t = 6.1 p <0.00005), and 76% in number (t = 11.6 p <0.00001). BLH lowered control ST a significant, lesser, 36% in amount (t = 3.6 p <0.008), and 35% in number (t = 3.2 p <0.01). The difference between IMH and BLH in ischemic myocardium was a significant 48% in amount (t = 4.0 p <0.0007), and 41% in number (t = 2.0 p <0.06). Myocardial adenosine triphosphate (ATP) levels were assayed after 90 min. ATP levels were 31% higher in both ischemic and non-ischemic myocardium in IMH-treated dogs than in BLH- treated. It was concluded that IMH and BLH are functionally different, and IMH was significantly more effective.

scholarly journals Salvage of ischemic myocardium by nonsynchronized retroperfusion in the pig

1992 ◽  
Vol 104 (3) ◽  
pp. 619-625 ◽  
Author(s):  
Gloriarme V. Ropchan ◽  
Christopher M. Feindel ◽  
Gregory J. Wilson ◽  
Patty Boylen ◽  
Reena Sandhu
Keyword(s):  
Ischemic Myocardium

Effect of alkali therapy with NaHCO3 or THAM on cardiac contractility

1996 ◽  
Vol 270 (5) ◽  
pp. R955-R962
Author(s):  
C. D. Mazer ◽  
B. Naser ◽  
K. S. Kamel
Keyword(s):  
Myocardial Ischemia ◽  
Contractile Function ◽  
Venous Blood ◽  
Systolic Pressure ◽  
Ischemic Myocardium ◽  
Stroke Work ◽  
Length Relationship ◽  
Alkali Therapy ◽  
Myocardial Contractile ◽  
The Impact

We examined the impact of alkali therapy on myocardial contractility in a model of myocardial ischemia in dogs using direct measurements of myocardial contractile function. Myocardial ischemia in the left anterior descending (LAD) artery territory was induced using a perfusion circuit from the internal carotid artery to the LAD artery. Myocardial contractile function was assessed using sonomicrometry for measurement of percent systolic shortening (%SS), preload recruitable stroke work (PRSW) slope, and end-systolic pressure-length relationship (ESPLR) area. Because the blood flow in LAD artery was diminished by approximately 70%, there was a significant decrease in O2 delivery and uptake by the ischemic myocardium. Ischemia led to a significant fall in LAD regional contractile function with %SS decreasing from 15 +/- 2 to 7 +/- 2%, PRSW slope from 82 +/- 10 to 37 +/- 5 mmHg, and ESPLR area from 121 +/- 2 to 48 +/- 14 mmHg.mm (P < 0.05). In six dogs, the intracoronary administration of NaHCO(3) resulted in a significant increase in pH in LAD arterial and venous blood. There was, however, no significant increase in %SS (6 +/- 2), PRSW slope (43 +/- 10 mmHg), or ESPLR area (60 +/- 13 mmHg.mm). Since administration of NaHCO(3) resulted in a significant increase in PCO2 in LAD arterial and venous blood, similar experiments were carried out in five dogs, but with the intracoronary infusion of the amine buffer THAM [tris(hydroxymethyl)aminomethane (Tris) buffer; 2-amino-2-hydroxyl-1,3-propandiol] instead of NaHCO3. Although administration of THAM resulted in a significant increase in pH and a significant decrease in PCO2, in both LAD arterial and venous blood, there was no significant improvement in any of the parameters used to assess myocardial contractile function. In conclusion, administration of alkali (NaHCO3 or THAM) does not enhance the contractile function of the ischemic myocardium.

T1 mapping of the ischemic myocardium: Review of potential clinical use

2016 ◽  
Vol 85 (10) ◽  
pp. 1922-1928 ◽  
Author(s):  
Jan Baxa ◽  
Jiří Ferda ◽  
Milan Hromádka
Keyword(s):  
T1 Mapping ◽  
Ischemic Myocardium ◽  
Clinical Use

scholarly journals Hepatic cell mobilization for protection against ischemic myocardial injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shu Q. Liu ◽  
John B. Troy ◽  
Chi-Hao Luan ◽  
Roger J. Guillory
Keyword(s):  
Ischemia Reperfusion ◽  
Hepatic Cell ◽  
Ischemic Myocardium ◽  
Cell Nuclei ◽  
Protective Mechanisms ◽  
Specific Expression ◽  
Time Points ◽  
Hepatic Cells ◽  
Cell Mobilization ◽  
Myocardial Ischemia Reperfusion

AbstractThe heart is capable of activating protective mechanisms in response to ischemic injury to support myocardial survival and performance. These mechanisms have been recognized primarily in the ischemic heart, involving paracrine signaling processes. Here, we report a distant cardioprotective mechanism involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardial ischemia–reperfusion (MI-R) injury. A parabiotic mouse model was generated by surgical skin-union of two mice and used to induce bilateral MI-R injury with unilateral hepatectomy, establishing concurrent gain- and loss-of-hepatic cell mobilization conditions. Hepatic cells, identified based on the cell-specific expression of enhanced YFP, were found in the ischemic myocardium of parabiotic mice with intact liver (0.2 ± 0.1%, 1.1 ± 0.3%, 2.7 ± 0.6, and 0.7 ± 0.4% at 1, 3, 5, and 10 days, respectively, in reference to the total cell nuclei), but not significantly in the ischemic myocardium of parabiotic mice with hepatectomy (0 ± 0%, 0.1 ± 0.1%, 0.3 ± 0.2%, and 0.08 ± 0.08% at the same time points). The mobilized hepatic cells were able to express and release trefoil factor 3 (TFF3), a protein mitigating MI-R injury as demonstrated in TFF3−/− mice (myocardium infarcts 17.6 ± 2.3%, 20.7 ± 2.6%, and 15.3 ± 3.8% at 1, 5, and 10 days, respectively) in reference to wildtype mice (11.7 ± 1.9%, 13.8 ± 2.3%, and 11.0 ± 1.8% at the same time points). These observations suggest that MI-R injury can induce hepatic cell mobilization to support myocardial survival by releasing TFF3.

Metabolic changes in non-ischemic myocardium by coronary ligation

1992 ◽  
Vol 24 ◽  
pp. 199
Author(s):  
I. Yamasawa ◽  
N. Nakagawa ◽  
M. Aoki ◽  
S. Tiyotanda ◽  
N. Mibe ◽  
...  
Keyword(s):  
Metabolic Changes ◽  
Ischemic Myocardium ◽  
Coronary Ligation
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