Protective Effects of Estradiol on Myocardial Contractile Function Following Hemorrhagic Shock and Resuscitation in Rats

Resuscitation following hemorrhagic shock result in myocardial contractile dysfunction and injury. We examined the protective effects of non-selective inhibitor of nitric oxide synthase N(G)-nitro-L-arginine methylester (L-NAME) on myocardial contractile function in the isolated perfused hearts, after ex vivo as well as in vivo treatment with L-NAME and resuscitation following one hour of hemorrhagic shock.Male Sprague Dawley rats (300-350 gm) were assigned to 2 sets of experimental protocols: ex vivo and in vivo treatment and resuscitation. Each set has 3 experimental groups (n= 6 per group): normotensive (N), hemorrhagic shock and resuscitation (HS-R) and hemorrhagic shock rats treated with L-NAME and resuscitated (HS- L-NAME-R). Rats were hemorrhaged over 60 min to reach a mean arterial blood pressure of 40 mmHg. In the ex vivo group, hearts were harvested and ex vivo treated and resuscitated by perfused in the Langendorff System. In the L-NAME treated group, L-NAME was added for the first 5 min . Cardiac function was measured Left ventricular generated pressure and +dP/dt were calculated. In the in vivo group, rats were treated with L-NAME intra-arterially after 60 min hemorrhagic shock. Resuscitation was performed in vivo by the reinfusion of the shed blood for 30 min to restore normo-tension. Inhibition of nitric oxide synthase using L-NAME before resuscitation in ex vivo treated and resuscitated isolated hearts and in in vivo treated and resuscitated rats following hemorrhagic shock improved myocardial contractile function. Left ventricular generated pressure and + dP/dt max was significantly higher in L-NAME treated rats compared to the untreated group.Treatment with L-NAME improved left ventricular generated pressure following hemorrhagic shock in the ex vivo as well as the in vivo treated and resuscitated rats. The results indicate that L-NAME protects the myocardium against dysfunction by inhibiting NOS.

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Effect of alkali therapy with NaHCO3 or THAM on cardiac contractility

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.270.5.r955 ◽

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.

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Myocardial contractile function and vulnerability to ischemia ex vivo can be worsened by prior experimental ischemic stroke in rats

Archives of Cardiovascular Diseases Supplements ◽

10.1016/s1878-6480(17)30391-9 ◽

2017 ◽

Vol 9 (2) ◽

pp. 158

Author(s):

A. Méloux ◽

E. Rigal ◽

C. Brenière ◽

Y. Cottin ◽

L. Rochette ◽

...

Keyword(s):

Ischemic Stroke ◽

Contractile Function ◽

Ex Vivo ◽

Myocardial Contractile

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Glucose-6-Phosphate Dehydrogenase and NADPH Redox Regulates Cardiac Myocyte L-Type Calcium Channel Activity and Myocardial Contractile Function

PLoS ONE ◽

10.1371/journal.pone.0045365 ◽

2012 ◽

Vol 7 (10) ◽

pp. e45365 ◽

Cited By ~ 17

Author(s):

Dhwajbahadur K. Rawat ◽

Peter Hecker ◽

Makino Watanabe ◽

Sukrutha Chettimada ◽

Richard J. Levy ◽

...

Keyword(s):

Calcium Channel ◽

Cardiac Myocyte ◽

Contractile Function ◽

Channel Activity ◽

Myocardial Contractile ◽

Glucose 6 Phosphate Dehydrogenase

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Viscerosomatic interaction induced by myocardial ischemia in conscious dogs

Journal of Applied Physiology ◽

10.1152/japplphysiol.00495.2006 ◽

2007 ◽

Vol 103 (2) ◽

pp. 511-517 ◽

Cited By ~ 2

Author(s):

Patricia A. Gwirtz ◽

Jerry Dickey ◽

David Vick ◽

Maurice A. Williams ◽

Brian Foresman

Keyword(s):

Myocardial Ischemia ◽

Contractile Function ◽

Muscle Tone ◽

Muscle Tension ◽

Left Ventricular ◽

Diagnostic Potential ◽

Myocardial Contractile ◽

Muscle Groups ◽

The Right ◽

Somatic Response

Studies tested the hypothesis that myocardial ischemia induces increased paraspinal muscular tone localized to the T2–T5 region that can be detected by palpatory means. This is consistent with theories of manual medicine suggesting that disturbances in visceral organ physiology can cause increases in skeletal muscle tone in specific muscle groups. Clinical studies in manual and traditional medicine suggest this phenomenon occurs during episodes of myocardial ischemia and may have diagnostic potential. However, there is little direct evidence of a cardiac-somatic mechanism to explain these findings. Chronically instrumented dogs [12 neurally intact and 3 following selective left ventricular (LV) sympathectomy] were examined before, during, and after myocardial ischemia. Circumflex blood flow (CBF), left ventricular contractile function, electromyographic (EMG) analysis, and blinded manual palpatory assessments (MPA) of tissue over the transverse spinal processes at segments T2–T5 and T11–T12 (control) were performed. Myocardial ischemia was associated with a decrease in myocardial contractile function and an increase in heart rate. MPA revealed increases in muscle tension and texture/firmness during ischemia in the T2–T5 segments on the left, but not on the right or in control segments. EMG demonstrated increased amplitude for the T4–T5 segments. After LV sympathectomy, MPA and EMG evidence of increased muscle tone were absent. In conclusion, myocardial ischemia is associated with significant increased paraspinal muscle tone localized to the left side T4–T5 myotomes in neurally intact dogs. LV sympathectomy eliminates the somatic response, suggesting that sympathetic neural traffic between the heart and somatic musculature may function as the mechanism for the interaction.

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Preconditioning and Myocardial Contractile Function

Developments in Cardiovascular Medicine - Ischemic Preconditioning: The Concept of Endogenous Cardioprotection ◽

10.1007/978-1-4615-2602-5_3 ◽

1994 ◽

pp. 41-60 ◽

Cited By ~ 3

Author(s):

Michel Ovize ◽

Robert A. Kloner ◽

Karin Przyklenk

Keyword(s):

Contractile Function ◽

Myocardial Contractile

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ALTERED CONTRACTILE FUNCTION IN DOGS AFTER CLINICAL DEATH FOLLOWING ACUTE MIOCARDIAL INFARCTION AND INTACT HEART

Complex Issues of Cardiovascular Diseases ◽

10.17802/2306-1278-2018-7-2-121-128 ◽

2018 ◽

Vol 7 (2) ◽

pp. 121-128 ◽

Cited By ~ 1

Author(s):

G. V. Lisachenko ◽

A. V. Budaev ◽

S. V. Bannih

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Contractile Function ◽

Clinical Death ◽

Postresuscitation Period ◽

Systemic Hemodynamics ◽

Cardiac Contractile Function ◽

Cardiac Contractile ◽

Circulatory Insufficiency ◽

Myocardial Contractile

Aim. To assess myocardial contractile function in dogs after clinical death following acute myocardial infarction and to determine its role in the development of hemodynamic derangements after cardiopulmonary resuscitation. Methods. 180 dogs included in the experiment received pentobarbital anesthesia to assess contractile function and systemic hemodynamics after a 5-min clinical death caused by myocardial infarction. Results Dogs had phase changes in the myocardial contractile function with its initial increase, subsequent depression and normalization in the early postresuscitation period after myocardial infarction. Depressed cardiac contractile function was accompanied by a decrease in the myocardial functional reserve. A similar tendency was found in the restoration of systemic hemocirculation. Conclusion. Similar phase alterations in the myocardial contractile function and systemic hemodynamics developed in the postresuscitation period of acute myocardial infarction. Immediately after recovery, the parameters of systemic hemoperfusion increased due to the activation of the cardiac contractile function. The subsequent initial (3 – 60 min) decrease in the volumetric perfusion parameters was mainly caused by the depressed cardiac contractile function. Rhythm disturbances affected on-going circulatory insufficiency 4 - 5 hours after the recovery. The subsequent progressive decrease in the volumetric perfusion was caused by the extracardiac factors.

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