Preservation of ischemic myocardium by pinane thromboxane A2

1980 ◽  
Vol 238 (1) ◽  
pp. H87-H92 ◽  
Author(s):  
K. Schror ◽  
E. F. Smith ◽  
M. Bickerton ◽  
J. B. Smith ◽  
K. C. Nicolaou ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Myocardial Ischemia ◽  
Thromboxane A2 ◽  
Acute Myocardial Ischemia ◽  
Ischemic Myocardium ◽  
Ischemic Region ◽  
Thromboxane Synthetase ◽  
Aggregation Inhibition ◽  
Premature Beats ◽  
Pinane Thromboxane A2

Pinane thromboxane A2 (PTA2), a thromboxane A2 analog has been shown to antagonize the vasoconstriction and platelet aggregation induced by thromboxane A2, in addition to specifically inhibiting thromboxane synthetase. Because thromboxane A2 generation would be detrimental in acute myocardial ischemia (MI) by both decreasing coronary blood flow and increasing platelet aggregation, inhibition of thromboxane production and action may be beneficial in myocardial ischemia. In pentobarbital-anesthetized cats, the left anterior descending coronary artery was ligated, and PTA2 (0.5 mumol . kg-1 . h-1) or a Na2CO3 vehicle was infused 30 min post-MI for 270 min. Compared to vehicle-treated MI cats, PTA2 prevented the increase in plasma thromboxane levels seen at 2 through 5 h (P less than 0.005 at 2 through 5 h) and prevented the large increase in plasma CK activities at 4 and 5 h (P less than 0.025). In addition, PTA2 treatment abolished the differences in myocardial CK activities between ischemic and nonischemic regions and prevented the decrease in percent-bound cathepsin D in the ischemic region. Moreover, ECG analysis revealed a decreased incidence of premature beats in PTA2-treated MI cats as compared to MI-vehicle cats. In summary, these data indicate that PTA2 protects the ischemic myocardium and provide further evidence that inhibition of thromboxane formation, in addition to antagonism of its activity, is beneficial during the early stages of acute myocardial ischemia.

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 High arrhythmic risk in antero-septal acute myocardial ischemia is explained by increased transmural reentry occurrence

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hector Martinez-Navarro ◽  
Ana Mincholé ◽  
Alfonso Bueno-Orovio ◽  
Blanca Rodriguez
Keyword(s):  
Myocardial Ischemia ◽  
High Performance ◽  
Acute Myocardial Ischemia ◽  
Border Zone ◽  
Apical Region ◽  
Efficacy Evaluation ◽  
Detailed Model ◽  
Subendocardial Ischemia ◽  
Ischemic Region ◽  
The Impact

AbstractAcute myocardial ischemia is a precursor of sudden arrhythmic death. Variability in its manifestation hampers understanding of arrhythmia mechanisms and challenges risk stratification. Our aim is to unravel the mechanisms underlying how size, transmural extent and location of ischemia determine arrhythmia vulnerability and ECG alterations. High performance computing simulations using a human torso/biventricular biophysically-detailed model were conducted to quantify the impact of varying ischemic region properties, including location (LAD/LCX occlusion), transmural/subendocardial ischemia, size, and normal/slow myocardial propagation. ECG biomarkers and vulnerability window for reentry were computed in over 400 simulations for 18 cases evaluated. Two distinct mechanisms explained larger vulnerability to reentry in transmural versus subendocardial ischemia. Macro-reentry around the ischemic region was the primary mechanism increasing arrhythmic risk in transmural versus subendocardial ischemia, for both LAD and LCX occlusion. Transmural micro-reentry at the ischemic border zone explained arrhythmic vulnerability in subendocardial ischemia, especially in LAD occlusion, as reentries were favoured by the ischemic region intersecting the septo-apical region. ST elevation reflected ischemic extent in transmural ischemia for LCX and LAD occlusion but not in subendocardial ischemia (associated with mild ST depression). The technology and results presented can inform safety and efficacy evaluation of anti-arrhythmic therapy in acute myocardial ischemia.

Ultrasound Characterization of Acute Myocardial Ischemia by Quantitative Texture Analysis

1986 ◽  
Vol 8 (4) ◽  
pp. 227-240 ◽  
Author(s):  
David D. McPherson ◽  
Philip E. Aylward ◽  
Boyd M. Knosp ◽  
Judy A. Bean ◽  
Richard E. Kerber ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Texture Analysis ◽  
False Positive ◽  
Image Data ◽  
Axial Direction ◽  
Acute Myocardial Ischemia ◽  
Depth Of Field ◽  
Acute Ischemia ◽  
Azimuthal Direction ◽  
Ischemic Region

In this study we tested the efficacy of quantitative texture analysis in the identification of acute myocardial ischemia using an ultrasound data acquisition system that digitizes and stores echocardiographic data in polar format. In nine closed-chest dogs, data were acquired before and after coronary occlusion using a 2.4 MHz echocardiographic system. Regions of interest were analyzed at end-diastole and end-systole from the ischemic area and normal area at the same depth of field. Ultrasound data were evaluated using previously reported quantitative gray level texture measures. After occlusion, texture changes indicative of ischemia were found in systolic images. The directional component of the data analysis was important; analysis in the azimuthal direction was more accurate than in the axial direction. Six texture measures exhibited significant changes in the ischemic region from control to occlusion when analyzing data in the azimuthal direction. One false positive result occurred (significant texture change in the normal region from control to occlusion) in the azimuthal direction. Several false positive alterations in the normal regions from control to occlusion were found when the texture was evaluated in the axial direction. For accurate assessment of ischemic changes, preocclusion image data were required. We conclude that quantitative echocardiographic texture analysis using polar format data can identify subtle changes in myocardial texture such as that due to acute ischemia, using data acquired through the Chest Wall.

Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

2007 ◽  
Vol 102 (2) ◽  
pp. 622-627 ◽  
Author(s):  
Toru Kawada ◽  
Hirotoshi Kitagawa ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Atsunori Kamiya ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Nerve Stimulation ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Myocardial Ischemia ◽  
Autonomic Nerves ◽  
Ach Release ◽  
Ischemic Region

Although hypothermia is one of the most powerful modulators that can reduce ischemic injury, the effects of hypothermia on the function of the cardiac autonomic nerves in vivo are not well understood. We examined the effects of hypothermia on the myocardial interstitial norepinephrine (NE) and ACh releases in response to acute myocardial ischemia and to efferent sympathetic or vagal nerve stimulation in anesthetized cats. We induced acute myocardial ischemia by coronary artery occlusion. Compared with normothermia ( n = 8), hypothermia at 33°C ( n = 6) suppressed the ischemia-induced NE release [63 nM (SD 39) vs. 18 nM (SD 25), P < 0.01] and ACh release [11.6 nM (SD 7.6) vs. 2.4 nM (SD 1.3), P < 0.01] in the ischemic region. Under hypothermia, the coronary occlusion increased the ACh level from 0.67 nM (SD 0.44) to 6.0 nM (SD 6.0) ( P < 0.05) and decreased the NE level from 0.63 nM (SD 0.19) to 0.40 nM (SD 0.25) ( P < 0.05) in the nonischemic region. Hypothermia attenuated the nerve stimulation-induced NE release from 1.05 nM (SD 0.85) to 0.73 nM (SD 0.73) ( P < 0.05, n = 6) and ACh release from 10.2 nM (SD 5.1) to 7.1 nM (SD 3.4) ( P < 0.05, n = 5). In conclusion, hypothermia attenuated the ischemia-induced NE and ACh releases in the ischemic region. Moreover, hypothermia also attenuated the nerve stimulation-induced NE and ACh releases. The Bezold-Jarisch reflex evoked by the left anterior descending coronary artery occlusion, however, did not appear to be affected under hypothermia.

Arachidonate Metabolism And Platelet Disaggregation (DA)-Reaggregation (RA)

1981 ◽  
Author(s):  
Gundu H R Rao ◽  
James G White
Keyword(s):  
Platelet Aggregation ◽  
Adrenergic Receptors ◽  
Thromboxane A2 ◽  
The Other ◽  
Inhibit Platelet Aggregation ◽  
Activated Platelets ◽  
Arachidonate Metabolism ◽  
Thromboxane Synthetase ◽  
Platelet Disaggregation ◽  
Refractory State

Previous work has shown that platelets irreversibly aggregated by ADP or thrombin (T) can be dissociated by various agents and that the refractory state of disaggregated cells can be reversed immediately by treatment with epinephrine (E). In the present study we have evaluated the influence of drugs which affect different steps in the process of prostaglandin (PG) synthesis on platelet DA-RA. Aspirin and indomethacin did not cause DA of platelets in the process of aggregation nor did they prevent reversal of the refractory state by E and subsequent RA of previously dissociated platelets. Imidazole, which inhibits conversion of endoperoxide to thromboxane A2, also failed to influence DA or restoration of sensitvity and RA of disaggregated platelets. On the other hand, chemicals which interfere with release of AA from the membrane of activated platelets, such as mepacrine, chlorpromazine and trifluoperazine, caused rapid DA. Products of PG synthesis, such as PGE1, PGD2 and PGI2, which usually inhibit platelet aggregation, also caused rapid DA. The refractory state of platelets dissociated from aggregates by most of these agents could be reversed by E treatment. However, trifluoperazine disaggregated platelets could be reaggregated only by the combination of E and AA. Agents which block the a-adrenergic receptors did not cause dissociation of aggregating platelets, but prevented correction of the refractory state of dissociated platelets by E. Thus interference with AA release, even after aggregation, can cause DA of clumped platelets, but blockade of peroxidase, cyclo-oxygenase and thromboxane synthetase do not cause reversal once it is in progress. A membrane linked mechanism associated with AA availability, but not metabolism, regulates DA and restoration of membrane sensitivity for RA.

Sign in / Sign up

Export Citation Format

Share Document