Differential cardiac sympathetic activity during acute myocardial ischemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1534-H1541 ◽  
Author(s):  
B. H. Neely ◽  
G. R. Hageman
Keyword(s):  
Sympathetic Activity ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Ischemic Myocardium ◽  
Neural Responses ◽  
Ischemic Region ◽  
Innervation Patterns ◽  
Anesthetized Dogs ◽  
Increased Activity ◽  
Cardiac Nerves

Efferent sympathetic activities were simultaneously recorded from two thoracic cardiac nerves in 33 chloralose-anesthetized dogs. Efferent innervation patterns were determined by electrical stimulation prior to recording in each animal. One of the nerves selected for recording was shown to innervate the proposed ischemic region, whereas the other nerve was selected because it was shown to innervate nonischemic regions. Left ventricular ischemia was produced by occlusion of a branch of either the left anterior descending (LAD) or left circumflex (LCX) coronary arteries. Heart rate was paced. Cardiac postganglionic sympathetic efferent activities were recorded during a 30-min coronary occlusion in 22 animals. Thirty minutes after LAD occlusion (n = 10), postganglionic sympathetic activity to ischemic myocardium was decreased (84 +/- 5% of control; P less than 0.05) while activity to nonischemic myocardium was unchanged. Thirty minutes after LCX occlusion (n = 12), postganglionic sympathetic activity to ischemic myocardium was also decreased (87 +/- 3% of control; P less than 0.01); however, sympathetic activity to nonischemic myocardium was increased (159 +/- 10% of control; P less than 0.001). Thus, in the anesthetized canine, regional left ventricular ischemia elicits differential sympathetic neural responses that are dependent on the location of the ischemic myocardium as well as the efferent destinations of the nerves. Changes in cardiac postganglionic sympathetic efferent activities are characterized by decreased activity to ischemic regions, with either no change or increased activity to nonischemic regions.

Effects of deafferentation or sequential occlusions on cardiac sympathetic activity during ischemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1542-H1549 ◽  
Author(s):  
B. H. Neely ◽  
G. R. Hageman
Keyword(s):  
Coronary Occlusion ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Reflex Response ◽  
Acute Ischemia ◽  
Ischemic Region ◽  
Small Branch ◽  
Afferent Fibers ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy

In 39 anesthetized dogs, we compared the effects of selective afferent sympathectomy, vagotomy, epicardial phenol painting, or a previous coronary occlusion on cardiac sympathetic activities recorded during 30 min of acute myocardial ischemia. Efferent innervation patterns were verified by electrical stimulation, and cardiac efferent activities were simultaneously recorded from two thoracic sympathetic nerves. One nerve was selected for recording because it was shown to innervate the proposed ischemic region, whereas the other nerve was selected because it was shown to innervate nonischemic regions. Left ventricular ischemia was produced by occlusion of a small branch of either the left anterior descending (LAD) or left circumflex (LCX) coronary arteries. Heart rate was paced. Reflex changes in sympathetic activities to ischemic regions were prevented by elimination of afferent fibers with either phenol or bilateral vagotomy. Ablation of sympathetic afferents prevented ischemia-induced reflex changes to nonischemic regions but did not prevent reflex changes to ischemic regions. Reflex changes in cardiac sympathetic activities during a second coronary occlusion of 30 min were vastly different from the initial occlusion but were similar to those observed after local deafferentation. Our findings indicate that 1) differential reflex changes in cardiac sympathetic activities during 30 min of left ventricular ischemia are due to afferent signals originating from the ischemic region, 2) both sympathetic and vagal afferent fibers participate in the ischemia-induced cardio-cardiac reflex, and 3) the nature of the sympathetic reflex response to acute ischemia is influenced by a previous ischemic insult.

Myocardial and interstitial matrix metalloproteinase activity after acute myocardial infarction in pigs

2001 ◽  
Vol 281 (3) ◽  
pp. H987-H994 ◽  
Author(s):  
Takuma Etoh ◽  
Cassandra Joffs ◽  
Anne M. Deschamps ◽  
Jennifer Davis ◽  
Kathryn Dowdy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Remote Region ◽  
Circumflex Artery ◽  
Disease States ◽  
Ischemic Region ◽  
Activity Measurements ◽  
Acute Mi ◽  
Structural Event

A structural event during the evolution of a myocardial infarction (MI) is left ventricular (LV) remodeling. The mechanisms that contribute to early changes in LV myocardial remodeling in the post-MI period remain poorly understood. Matrix metalloproteinases (MMPs) contribute to tissue remodeling in several disease states. Whether and to what degree MMP activation occurs within the myocardial interstitium after acute MI remains to be determined. Adult pigs ( n = 15) were instrumented to measure regional myocardial function and interstitial MMP levels within regions served by the circumflex and left anterior descending arteries. Regional function was measured by sonomicrometry, and interstitial MMP levels were determined by selective microdialysis and zymography as well as by MMP interstitial fluorogenic activity. Measurements were performed at baseline and sequentially for up to 3 h after ligation of the obtuse marginals of the circumflex artery. Regional fractional shortening fell by over 50% in the MI region but remained unchanged in the remote region after coronary occlusion. Release of soluble MMPs, as revealed by zymographic activity of myocardial interstitial samples, increased by 2 h post-MI. The increased zymographic activity after MI was consistent with MMP-9. Myocardial interstitial MMP fluorogenic activity became detectable within the ischemic region as early as 10 min after coronary occlusion and significantly increased after 1 h post-MI. MMP fluorogenic activity remained unchanged from baseline values in the remote region. The present study demonstrated that myocardial MMP activation can occur within the MI region in the absence of reperfusion. These unique results suggest that MMP release and activation occurs within the ischemic myocardial interstitium in the early post-MI period.

A new method to measure regional myocardial time-varying elastance using minute vibration

1998 ◽  
Vol 274 (4) ◽  
pp. H1404-H1415 ◽  
Author(s):  
Toshiaki Shishido ◽  
Masaru Sugimachi ◽  
Osamu Kawaguchi ◽  
Hiroshi Miyano ◽  
Toru Kawada ◽  
...  
Keyword(s):  
Young’S Modulus ◽  
Coronary Occlusion ◽  
Young's Modulus ◽  
Equations Of Motion ◽  
Left Ventricular ◽  
Time Varying ◽  
Ventricular Elastance ◽  
Ischemic Region ◽  
A New Technique ◽  
Measured Displacement

We developed a new technique to evaluate regional myocardial elastance using minute vibration. In 13 isolated cross-circulated canine hearts, we applied small sinusoidal vibrations of displacement to the left ventricular surface at various frequencies (50–100 Hz). Using the measured displacement and force between the vibrator head and myocardium, we derived myocardial elastance on the basis of the equation of motion for a given moment of the cardiac cycle. Simultaneous solution of the equations of motion at different frequencies yielded a unique value of elastance. Time-varying myocardial elastance increased from diastole (0.028 ± 0.211 × 106 dyn/cm) to systole (0.833 ± 0.391 × 106 dyn/cm). The end-systolic elastance ( e es) linearly correlated with end-systolic left ventricular elastance ( r = 0.717, P < 0.001) and also with the end-systolic Young’s modulus ( r = 0.874, P < 0.0001). We also measured e es at both ischemic and nonischemic regions during coronary occlusion. Young’s modulus, estimated by normalizing e es by the wall thickness and by the estimated mass, did not change significantly at the nonischemic regions, whereas it decreased significantly from 2.303 ± 0.556 to 1.173 ± 0.370 × 106dyn/cm2 at the ischemic region after coronary occlusion ( P < 0.005). We conclude that this technique is useful for the quantitative assessment of regional myocardial elastance.

Effects of yohimbine and desipramine on cardiac noradrenaline release and ventricular arrhythmias during acute coronary artery occlusion and reperfusion in anesthetized dogs

1987 ◽  
Vol 65 (11) ◽  
pp. 2244-2253 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Daniel Lamontagne ◽  
Ghislain Boudreau ◽  
Reginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Coronary Artery ◽  
Nerve Stimulation ◽  
Left Ventricular Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Neuronal Uptake ◽  
Ischemic Region ◽  
Anesthetized Dogs ◽  
Na Release

Effects of yohimbine (YHMB, an α2-antagonist) and desipramine (DMI, a neuronal uptake inhibitor) were compared on cardiac noradrenaline (NA) release either upon left ansa subclavia nerve stimulation during acute occlusion of the left anterior descending coronary artery (LAD) or upon subsequent LAD reperfusion without stimulation in anesthetized dogs. In control dogs, before LAD occlusion, coronary sinus (CS) NA output increased from 5.4 ± 1.0 to 26.8 ± 4.0 ng/min (p < 0.05) upon stimulation (2 Hz, 30 s). The response to stimulation remained unchanged 25 min after LAD occlusion. During reperfusion 60 min after occlusion, the output of CS-NA and lactate increased from 6.1 ± 0.8 to 51.3 ± 19.4 ng/min (p < 0.05) and from 2.7 ± 0.5 to 6.7 ± 1.3 mg/min (p < 0.05), respectively. In dogs treated with YHMB, the stimulation-induced increase in NA output was potentiated at least fourfold (p < 0.05) either before or during LAD occlusion, but not during reperfusion. In dogs receiving DMI, stimulation-induced CS-NA output was enhanced to a similar extent (approximately twofold, p < 0.05) either before or during occlusion, while reperfusion-induced NA output was markedly potentiated by approximately ninefold (p < 0.05). Maximum dP/dt of left ventricular pressure remained unchanged upon reperfusion in all groups. The total arrhythmic ratio in the drug-treated groups did not significantly differ from the ratio in control dogs upon either stimulation or reperfusion. The data suggest that an abrupt increase in NA output upon reperfusion may result from a washout of NA locally accumulated in the ischemic and (or) peri-ischemic region during the preceding occlusion period, and that N A thus released does not have substantial hemodynamic effects. The results indicate that in the presence of YHMB or DMI, the potentiated increase in NA release in response to either nerve stimulation during LAD occlusion or to reperfusion without stimulation did not aggravate ventricular arrhythmia, most probably owing to the antiarrhythmic properties of these substances.

Integrated regional work equals total left ventricular work in regionally ischemic canine heart

1988 ◽  
Vol 254 (5) ◽  
pp. H894-H904 ◽  
Author(s):  
Y. Goto ◽  
Y. Igarashi ◽  
Y. Yasumura ◽  
T. Nozawa ◽  
S. Futaki ◽  
...  
Keyword(s):  
Coronary Occlusion ◽  
Left Ventricular ◽  
Canine Heart ◽  
Stroke Work ◽  
Wall Tension ◽  
Ischemic Region ◽  
Regional Area ◽  
Before And After ◽  
Regional Work ◽  
Force Equilibrium

To assess left ventricular (LV) regional work with physically correct dimensions, wall tension-regional area (T-A) loops were analyzed before and after coronary occlusion in the excised cross-circulated canine LV (n = 11) connected to a volume-servo pump. Wall tension was calculated with the force equilibrium equation for a sphere, and regional areas were determined from pairs of orthogonal sonomicrometers in ischemic and nonischemic regions. LV and regional stroke work were simultaneously assessed from the pressure-volume and T-A loops during one cardiac cycle at various end-diastolic and stroke volumes. After coronary occlusion, regional work of the ischemic region markedly decreased to near or even below zero. Although regional work of the nonischemic region moderately decreased at constant LV end-diastolic and stroke volumes, the contribution of the nonischemic region to LV stroke work increased. Globally integrated regional work calculated from regional work/unit area and estimates of the extent of ischemia closely agreed with measured LV stroke work either before (n = 119; r = 0.92) or after coronary occlusion (n = 141; r = 0.93) despite the marked changes in regional work in both regions. We conclude that the global integral of regional work equals the total LV work and that regional work of the LV can be reliably assessed from the T-A loop with the same dimensions as energy in both normal and regionally ischemic hearts.

Quantification of Area at Risk during Coronary Occlusion and Reperfusion by Means of MR Perfusion Imaging

1997 ◽  
Vol 38 (4) ◽  
pp. 479-488 ◽  
Author(s):  
Dieter H. Szolar ◽  
M. Saeed ◽  
M. Wendland ◽  
H. Sakuma ◽  
M. A. Stiskal ◽  
...  
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Perfusion Imaging ◽  
Coronary Occlusion ◽  
Ischemic Myocardium ◽  
Post Mortem ◽  
Mr Perfusion ◽  
Area At Risk ◽  
Ischemic Region ◽  
Mr Perfusion Imaging

Purpose: Considerable clinical interest has focused on the size of ischemic myocardium. Fast MR imaging in conjunction with MR contrast media has the potential to identify hypoperfused and infarcted myocardium. This study used MR perfusion imaging to detect and quantify reperfused ischemic myocardium during a brief coronary occlusion and reperfusion, and to characterize the spatial extent of ischemic and reperfused ischemic myocardium relative to the “true” size of the area at risk as defined in histochemical morphometry at post mortem. Material and Methods: The left circumflex (LCX) coronary artery in 8 dogs was occluded for 15 min followed by reperfusion in order to produce regional reversible myocardial ischemia. Perivascular Doppler probes were used to measure blood flow in the left anterior descending (LAD) and LCX coronary arteries. Fast inversion recovery-prepared gradient-recalled-echo images were acquired to delineate the ischemic area during occlusion, and the area of reversible ischemic injury at 1 and 30 min of reperfusion. The size of ischemic and reperfused ischemic myocardium were compared with the area at risk as determined by histochemical morphometry at post mortem. Results: During LCX occlusion, LCX flow decreased from 16±1 to 0.2± 0.1 ml/min. On contrast-enhanced images, ischemic myocardium was evident as a zone of relatively low signal intensity (SI) compared to normal myocardium. The size of the ischemic region was significantly smaller (30± 2%) than at post mortem (36± 3%; p<0.05). Immediately after reperfusion, LCX flow increased to 83±11 ml/min and the contrast medium caused greater enhancement in the reperfused ischemic region than in the normal myocardium (69± 3 vs 42± 3 arbitrary units; p<0.05). The increase in regional SI correlated closely with the increase in regional blood flow (r=0.73). At 1 min of reperfusion, the size of the reperfused ischemic myocardium was larger (48± 3%, p<0.05) than the area at risk measured at post mortem. At 30 min of reperfusion, when the flow returned to baseline values (16± 2 ml/min), contrast bolus produced no differential enhancement between the 2 myocardial territories. Conclusion: MR perfusion imaging has the potential to detect and quantify the size of ischemic myocardium and the region of post-occlusive hyperemia in the early reperfusion period. There is a significant direct linear relationship between the regional contrast enhancement of reperfused ischemic myocardium and the blood flow during post-occlusive hyperemia. The difference in the size of the area at risk at MR perfusion imaging and at histochemical morphometry may reflect an influence of coronary collateral circulation.

Activation of cardiac KATP channels: an endogenous protective mechanism during repetitive ischemia

1993 ◽  
Vol 264 (2) ◽  
pp. H495-H504 ◽  
Author(s):  
Z. Yao ◽  
I. Cavero ◽  
G. J. Gross
Keyword(s):  
Katp Channel ◽  
Coronary Occlusion ◽  
Arterial Occlusion ◽  
Katp Channels ◽  
Similar Rate ◽  
Monophasic Action Potential ◽  
Protective Mechanism ◽  
Ischemic Region ◽  
Voltage Dependent ◽  
Anesthetized Dogs

The role of KATP channels in myocardial stunning produced by repetitive coronary occlusions was studied in barbital-anesthetized dogs. Regional percent segment function (%SS) was measured by sonomicrometry, and the monophasic action potential (MAP) in the ischemic region was measured by an epicardial probe. Under control conditions, six 5-min periods of coronary occlusion, interspersed with 10-min periods of reperfusion, and ultimately followed by 2 h of reperfusion produced regional segment dysfunction and a similar rate and amount of shortening of the MAP measured at 50% repolarization duration (MAPD50) during each successive ischemic period. Pretreatment with glibenclamide (0.3 mg/kg iv), a KATP channel antagonist, significantly prevented the reduction of MAPD50, particularly during the first occlusion period, and it worsened postischemic dysfunction. In contrast, pretreatment with aprikalim (10 micrograms/kg bolus +/- 0.1 microgram.kg-1.min-1 iv), a KATP channel opener, accelerated the rate and extent of shortening of MAPD50 during each occlusion and markedly improved %SS throughout reperfusion. Pretreatment with d-sotalol (2 mg/kg iv), an antagonist of voltage-dependent K+ channels, significantly prolonged MAPD50 of the ischemic region before coronary occlusion but did not alter the rate of shortening of MAPD50 during ischemia and did not affect the recovery of %SS. These results indicate that activation of KATP channels during ischemia with the resultant shortening of the MAPD50 is an endogenous adaptive mechanism that affords functional myocardial protection during repetitive, brief periods of coronary arterial occlusion.

Acid-induced excitation of afferent cardiac sympathetic nerve fibers

1975 ◽  
Vol 228 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Y Uchida ◽  
S Murao
Keyword(s):  
Sympathetic Nerve ◽  
Coronary Occlusion ◽  
Nerve Fibers ◽  
Left Ventricular ◽  
Minimum Concentration ◽  
Unmyelinated Fibers ◽  
Myelinated Fibers ◽  
Sympathetic Nerve Fibers ◽  
Anesthetized Dogs ◽  
Upper Thoracic

The effect of acids on activity of afferent sympathetic nerve fibers from the left ventricle has been examined. Action potentials were derived from the upper thoracic communicating rami of the left side of anesthetized dogs. Application of a solution of lactic acid to the left ventricular surface caused excitation in both myelinated and unmyelinated fibers. The minimum concentration required for excitation was 7.5-75 mug/ml for the unmyelinated fibers and 375-750 mug/ml for the myelinated fibers. Excitation of the unmyelinated fibers induced by coronary occlusion was suppressed by pretreatment with sodium bicarbonate, 500 mg/kg. However, excitation of the myelinated fibers was influenced little by the agent. Pretreatment with a large dose of Trasylol failed to suppress excitation induced by coronary occlusion. The result suggests that acidosis plays a role in excitation of the unmyelinated fibers induced by myocardial ischemia, but not in excitation of the myelinated fibers.

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