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Biomedical subjects

M V Cohen

Publications and source records attributed to M V Cohen.

160 records · Page 9Linked to original sources
PubMed1973

The effects of nitroglycerin on coronary collaterals and myocardial contractility.

Nitroglycerin (TNG) causes a prolonged dilatation of coronary collaterals. To demonstrate a functional significance of this dilatation we measured the effect of TNG on myocardial contractile force in dogs 2(1/2)-4 wk after the left anterior descending coronary artery (LAD) had been embolized in closed-chest animals. Development of collaterals was documented by angiography. Via a left thoracotomy the main left coronary artery (LCA) and LAD distal to the embolized plug were cannulated. Coronary flow and perfusion pressure were recorded. Contractile force was measured with gauges sutured to epicardial areas supplied by the left circumflex coronary artery (LCf) and occluded LAD. Coronary perfusion pressure in the LCA was gradually decreased until the contractile force recorded by the LAD gauge diminished while the LCf gauge was unaffected. Under these conditions, with coronary perfusion pressure held constant with the aid of a Starling resistance, TNG (18 mug) injected into the LCA increased peripheral LAD pressure by 3-12 mm Hg and contractile force in the LAD region by 36% (range 20-90%), returning it to near-normal levels, while having minimal effect in the LCf area. These changes persisted for 5 min. When LCf and LAD areas were both ischemic, intracoronary TNG had minimal effect on peripheral LAD pressure and contractile force. Thus, TNG causes prolonged dilatation of coronary collaterals and presumed increased collateral flow with subsequent enhancement of myocardial contractile force in ischemic areas. This effect is seen only when ischemia is limited to an area supplied by the collaterals. When the whole heart is ischemic, collaterals are unresponsive to TNG, suggesting that these collaterals dilate fully when the regions from which they originate become ischemic.

Adenosine↗
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Clinical and hemodynamic correlation in patients with pericardial effusion and swinging heart by echocardiography.

The clinical and hemodynamic findings in 13 consecutive patients with "swinging heart" on M-mode echocardiography were analyzed. In these patients the anterior right ventricular and posterior left ventricular walls and interventricular septum moved almost parallel to each other throughout the cardiac cycle, often with exaggerated excursion. In 10 of 13 patients right heart catheterization revealed the hemodynamic profile of cardiac tamponade, while one additional patient was found to have evidence of cardiac compression at the time of surgery. In the remaining two patients no acute invasive diagnostic procedures were performed. During the same observation period cardiac tamponade was observed in five patients without echocardiographic evidence of a swinging heart, and four of these had large clots in the pericardial space. Thus, the swinging heart pattern appears to be a reliable marker of cardiac tamponade, except in those patients with intrapericardial lesions which mechanically limit cardiac motion.

Adult↗
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Effects of anesthesia and K+ ATP channel blockade on interstitial adenosine accumulation in ischemic rabbit myocardium.

Glibenclamide, a K+ ATP channel antagonist, blocks the anti-infarct effect of ischemic preconditioning in rabbits, but only when the latter are anesthetized with ketamine-xylazine. Furthermore, the protection triggered by pinacidil, a K+ ATP channel opener, can be aborted by treatment with the adenosine antagonist 8-(P-sulfophenyl)theophylline. This study tests whether either the anesthetic regimen or glibenclamide affects infarct size by modulating interstitial adenosine levels. Interstitial adenosine and total purine concentrations were assessed in open-chest rabbits by the microdialysis technique. Dialysis fibers were inserted into myocardium served by a coronary artery branch surrounded by a snare. All animals sustained a 30-min coronary occlusion and then 120-min reperfusion. Rabbits were anesthetized with either sodium pentobarbital or a ketamine-xylazine mixture. Half of the latter animals also received glibenclamide. The control levels of adenosine in the dialysate were comparable in the three groups, as were those of total purines, and the infusion of glibenclamide caused no change. Ischemia led to 10- to 20-fold increases in interstitial adenosine and 10- to 40-fold rises in total purine concentrations. These increases were equivalent in all groups. Further-more, infarct size as a percentage of the myocardium at risk was also comparable in the three groups. Neither the anesthetic agent nor glibenclamide appears to modulate interstitial adenosine release from ischemic tissue.

Adenosine↗
PubMedDate not supplied

Mast cell degranulation does not contribute to ischemic preconditioning in isolated rabbit hearts.

Preconditioning the heart with a short period of ischemia makes it resistant to infarction from a subsequent ischemic insult. We have proposed that preconditioning is triggered by the release of endogenous substances including adenosine which activate protein kinase C through receptormediated cell signaling pathways. However, it has also been proposed that the initial brief ischemia may result in mast cell degranulation without significant myocardial damage, making it less likely that the toxic granule contents could be released to irreversibly damage vulnerable myocardial cells during the subsequent prolonged ischemia. To study the role of mast cells in ischemic preconditioning (PC) isolated rabbit hearts were subjected to 30 min of regional ischemia followed by 120 min of reperfusion. Infarct size was measured with triphenyltetrazolium chloride. In control hearts infarction was 31.9 +/- 2.6% of the risk zone. Preconditioning with 5 min of global ischemia and 10 min of reperfusion reduced infarct size to 5.6 +/- 6.1% (p < 0.01). When disodium cromoglycate (DSCG)(10 microM), a mast cell stabilizer, was infused shortly before the long ischemia it did protect the heart (12.8 +/- 2.9% infarction, p < 0.01 vs control) which supports the mast cell theory. However, a mast cell degranulating agent, compound 48/80 (24 mg/L), added to the perfusate prior to the 30 min ischemic period could not mimic PC (39.7 +/- 5.6% infarction). Mast cell granules are rich in histamine, and the latter was assayed in myocardium by immunoassay as a marker of intact granules. In homogenized left ventricle from normal rabbit hearts and those following a standard PC protocol of 5-min global ischemia/10-min reperfusion, histamine contents were 9.3 +/- 1.4 and 8.9 +/- 1.4 ng/g wet tissue, respectively. Compound 48/80 reduced histamine levels to 2.9 +/- 0.6 ng/g (p < 0.05 vs control). Although baseline histamine contents were 10-fold higher in rats, PC also had no effect, but compound 48/80 reduced content by 91%. Therefore, histamine tissue content and presumably mast cell granules were unaffected by a PC protocol which successfully protected ischemic myocardium, while pharmacological myocardial histamine depletion was not associated with protection. Hence, mast cells do not appear to be important in ischemic preconditioning. Although a mast cell stabilizer such as DSCG can protect ischemic myocardium, it may do so by one of its other properties, e.g., membrane stabilization.

Animals↗
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Coronary collaterals: role in restoration of blood flow and preservation of cardiac function during exercise.

Chronically instrumented dogs were studied at rest and during exercise on two occasions 10--12 weeks apart. The left circumflex coronary artery (LCf) was initially constricted in all dogs. By the time of the second study the LCf was still patent in 9 dogs and had become occluded in 6. In the dogs with chronic coronary occlusion, collaterals restored myocardial flow to normal both at rest and during exercise, and there were no adverse hemodynamic effects when running. Conversely, in dogs with constricted but patent LCfs collateral development was inadequate to return ischemic flows to normal following transient coronary occlusion, and occlusion during exercise produced significant myocardial failure. Thus coronary collaterals can compensate for decreased antegrade coronary flow.

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Cardiac tamponade in dogs with normal coronary arteries. I. Effect of changing intravascular volume on hemodynamics and myocardial blood flow.

Intravascular volume expansion has been shown to improve cardiac output in experimental cardiac tamponade. To determine the limitations of intravascular volume manipulation, acute tamponade was created in 20 anesthetized, spontaneously breathing dogs. The intrapericardial volume causing tamponade was determined for each animal, and kept constant. Hemodynamics were recorded with and without tamponade at multiple levels of intravascular volume. During cardiac tamponade, intravascular volume expansion increased cardiac output only in animals which were initially volume-depleted. Volume expansion of normovolemic or hypervolemic animals caused minimal changes in cardiac output, but increased atrial and aortic pressures. Intravascular volume depletion of the normovolemic animal caused a significant decline in cardiac output, in contrast to the trend towards an increased output following phlebotomy of the volume-expanded animals. In general, the benefit of intravascular volume expansion during cardiac tamponade could only be demonstrated when atrial pressures were below 12 mm Hg.

Animals↗
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Cardiac tamponade in dogs with normal coronary arteries. II. Myocardial flow and metabolism with moderate and severe hemodynamic impairment.

To determine the effects of cardiac tamponade on myocardial blood flow and its distribution, dogs were prepared with indwelling pericardial catheters. Hemodynamic, myocardial blood flow, and myocardial metabolic data were collected in 5 closed-chest, spontaneously breathing animals with normal blood volumes and hemoglobin concentrations and 6 with acute anemia. Instillation of an average of 89.0 +/- 14.9 ml of modified Normosol into the pericardial space in dogs with normal hemoglobin levels produced mild tamponade with a modest decline in aortic pressure (119.5 +/- 14.3 to 96.8 +/- 12.1 mm Hg) and significant rises in left and right atrial and pericardial pressures to 7-8 mm Hg. Increasing the pericardial volume to 124.0 +/- 13.6 ml produced hypotension (mean aortic pressure 86.2 +/- 10.5 mm Hg) and rises in the left and right ventricular filling pressures and pericardial pressure to 10-11 mm Hg. Total myocardial blood flow fell from 1.19 +/- 0.18 to 0.73 +/- 0.17 ml/min/g (p less than 0.02) during mild tamponade, and fell further to 0.56 +/- 0.17 ml/min/g (p less than 0.05) with more severe tamponade. Despite these declines, the left ventricular wall inner/outer flow ratio and left ventricular flow as a proportion of total cardiac output were unchanged. In dogs with anemia more severe tamponade was created, with consequently more marked hemodynamic abnormalities. However, the relative changes in myocardial blood flow and inner/outer flow ratio were similar. Myocardial metabolic parameters could be evaluated only in the dogs with less severe tamponade.(ABSTRACT TRUNCATED AT 250 WORDS)

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The effects of intracoronary Renografin injection on coronary flow and distribution in dogs following coronary occlusion.

To study the effects of a contrast agent commonly used in coronary angiography (Renografin) on myocardial flow distribution, the main left coronary arteries of 9 dogs were cannulated and perfused from the carotid arteries. The left anterior descending coronary artery (LAD) was ligated and cannulated to monitor peripheral coronary pressure (PCP). Myocardial blood flow and distribution were determined with radioactive microspheres before Renografin administration and after resolution of the brief period of hypotension following injection of 2-3.5 cm3 of the contrast agent directly into the coronary perfusion tubing. Renografin significantly increased blood flow to normal myocardial regions (0.90 to 1.51 cm3 . g-1 . min-1, p less than 0.001). Despite this flow augmentation and normal aortic and coronary perfusion pressures. PCP decreased from 28.0 +/- 3.4 to 24.4 +/- 2.8 mm Hg (p less than 0.001), and myocardial blood flow to the central ischemic LAD area halved from 0.17 +/- 0.04 to 0.09 +/- 0.03 cm3 . g-1 . min-1 (p less than 0.025). The inner/outer left ventricular wall blood flow ratio in the central ischemic region increased from 0.28 to 0.39 (p less than 0.05). Thus the contrast agent causes a coronary steal or redistribution of coronary flow away from already ischemic regions, and the endocardium appears to be less affected than the epicardium.

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