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At present, a practical method for continuous monitoring of the state of tissue metabolism in the individual patient's heart during cardiac operations is not available. We have explored the use of miniature electrode measurements of myocardial interstitial pH to provide this monitoring capability, making comparisons with intracellular pH in left ventricular biopsy specimens and with tissue PCO2 measured by mass spectrometry. The electrode system consisted of a hydrogen ion-sensitive glass miniature electrode, housed in the beveled end of a 21 gauge (0.8 mm diameter) hypodermic needle, and a 2 mm diameter reference electrode, with an internal silver-silver chloride electrode coupled to tissue through a saline bridge (150 mM/L sodium chloride) saturated with silver chloride. Accuracy in blood at 37 degrees C was compared with conventional instrumentation (Radiometer BMS-3 MK-2 Blood Micro System) over a pH range of 7.4 to 6.4 with linear regression analysis (n = 26) revealing a high correlation (r = 0.997) and a mean difference in paired observations of only 0.01 +/- 0.004 (mean +/- SEM) pH units. In two groups of dogs on cardiopulmonary bypass, the pH needle and reference electrodes were inserted into the anterior wall of the left ventricle. Ischemic arrest of the heart at 37 degrees C was used to vary myocardial pH. In Group 1 (n = 8), intracellular pH was estimated from left ventricular biopsy specimens (400 mg each) taken over a microelectrode pH range of 7.37 to 6.37, snap frozen, and homogenized. In Group II (n = 6), tissue PCO2 in the anterior wall of the left ventricle was determined by mass spectrometry (sampling catheter 1.3 mm diameter). Miniaturized electrode (interstitial) pH exceeded biopsy (intracellular) pH under control conditions by 0.28 +/- 0.025 pH units (p less than 0.001), but below an electrode pH of 6.8 the results of the two techniques did not differ significantly. The tissue PCO2 rose from 69 +/- 2 mm Hg to a final plateau of 419 +/- 25 mm Hg, which was similar to the predicted value of 427 +/- 28 mm Hg calculated from the pH change (7.37 +/- 0.01 to 6.01 +/- 0.07), providing a further independent check on the pH electrode technique. These data indicate that our intramyocardial pH measurements do reflect intracellular metabolism during elective arrest of the heart and may have potential for clinical use.
J Thorac Cardiovasc Surg 1979 Sep
PMID:Intramyocardial pH as an index of myocardial metabolism during cardiac surgery. 3 64

Antiarrhythmic concentrations of disopyramide in canine plasma and myocardium were determined by gas chromatography. Ventricular tachycardia was incuded in anesthetized dogs by the intravenous administration of ouabain. Disopyramide phosphate was then administered by a two-stage continuous infusion method. A rapid infusion of disopyramide (9.08 mg/kg/hr) was administered for 30 min, followed by a slow infusion (2.18 mg/kg/hr) to maintain steady-state plasma levels of 1.98-2.21, mean +/- SEM = 2.1 +/- 0.02 microgram/ml at the end of 2 hr. Myocardial tissue levels of disopyramide at steady-state plasma levels were four times those of plasma (atrial tissue, 8.91 +/- 0.10; right ventricular free wall, 8.93 +/- 0.13; left ventricular free wall, 9.11 +/- 0.16 microgram/gm wet tissue). The intravenous administration of 80 units crystalline zinc insulin produced both hypokalemia (3.78 +/- 0.22 reduced to 2.36 +/- 0.18 mEq potassium/liter plasma) and a reappearance of ventricular tachycardia despite no change in plasma and myocardial tissue concentrations of disopyramide from those which had been effective in establishing and maintaining sinus rhythm. The observations demonstrate a relationship between plasma and myocardial disopyramide concentrations such that the former can be used in assessing patient therapy. In addition, this study suggests the important of plasma potassium in determining the therapeutic effectiveness of disopyramide.
J Cardiovasc Pharmacol
PMID:Disopyramide plasma and myocardial tissue concentrations as they relate to antiarrhythmic activity. 9 10

Phasic left circumflex coronary artery and aortic blood flow were monitored in six awake dogs during a control period and at several degrees of cardiac tamponade. A mean pericardial pressure of 24 plus or minus 3 mm Hg (mean plus or minus SEM) was attained at the maximum tamponade level. Total left circumflex coronary blood flow decreased 51% while the systolic portion of this flow became negative or retrograde. Following acute relief of the tamponade, a coronary hyperaemic response was noted. It it suggested that myocardial ischaemia may be partially responsible for the depressed cardiac function seen in this condition and that extravascular compression of the epicardial vessels may limit the coronary blood flow during systole.
Cardiovasc Res 1975 Jan
PMID:The effect of cardiac tamponade on coronary haemodynamics in the awake dog. 12 83

In order to evaluate the cardiac sympathetic nerve tone in cardiomyopathies, plasma norepinephrine concentration in the coronary sinus (NE(CS)) and artery (NE(A)) was measured by THI method in five patients with the hypertrophic type (HCM) and in seven with the congestive type (CCM); six patients with functional murmur served as controls. NE(CS) was 182 +/- 39 ng/liter (SEM) in HCM, 288 +/- 47 in CCM, and 306 +/- 65 in controls. The NE(CS) - NE(A) difference (delta NE) was 9 +/- 22 ng/liter in HCM, -57 +/- 34 in CCM, and 81 +/- 29 in controls. Norepinephrine overflow into the coronary sinus,which was calculated by multiplying coronary sinus plasma flow by delta NE, was 0.54 +/- 0.86 ng/min/100gm, -2.81 +/- 1.47, and 3.73 +/- 1.77, respectively. Norepinephrine overflow and delta NE were significantly lower in CCM than in controls. The results suggest than an excessive sympathetic discharge does not exist in HCM and that cardiac sympathetic activity is reduced in CCM.
Cathet Cardiovasc Diagn 1978
PMID:Plasma norepinephrine concentration in the coronary sinus in cardiomyopathies. 15 72

Serum creatine kinase (CK) isoenzyme MB and total CK activity concentrations in 11 patients with acute myocardial infarction (AMI) were compared with the corresponding enzyme activities in 25 patients after coronary bypass surgery, not complicated clinically by AMI. Peak CK-MB occurred 2 +/- 0 (mean +/- SEM) hours after the end of surgery (mean duration of operation 6 hours), but 17 +/- 1 hours from the onset of symptoms in AMI. The plasma half"life for CK-MB was 11 +/- 1 hours under both conditions. Peak total CK was found after about 20 hours in both series of patients. Total CK half-life was 17 +/- 2 hours in AMI, but 30 +/- 3 hours following surgery. CK kinetics were thus different in these two situations, indicating different mechanisms for the elevations of serum CK-MB activity. In conclusion, the time course for the transient CK-MB elevation following bypass surgery should be considered in the diagnosis of peri operative infarction.
Scand J Thorac Cardiovasc Surg 1979
PMID:Serum CK-MB kinetics in acute myocardial infarction and after coronary bypass operations. 31 44

An unselected, consecutive cohort of 125 patients underwent operative repair of acute and chronic aortic dissections with tubular graft interposition over a 16 year span. The absence of remote geographical referral biases and the unselected nature of this series provided a patient population that was representative of the disease process (as assessed heretofore only from autopsy series). Furthermore, this enabled high-risk subsets to be defined by retrospective analysis. Patients were classified according to whether the ascending aorta was involved (type A with involvement, type B without), irrespective of the site of intimal tear, and according to age of the dissection: Fifty-three patients had acute type A (Ac-A), 29 had chronic type A (Ch-A), 20 had acute type B (Ac-B), and 23 had chronic type B (Ch-B) dissections. Fourteen percent (17/125) of the dissections had ruptured. Concomitant aortic valve replacement (AVR) was performed in 11% (6/53) for Ac-A cases and 38% (11/29) of the Ch-A cases. A total of 391 patient-years of follow-up was analyzed; follow-up averaged 4.5 years and extended to 13.7 years. Over-all operative mortality rate was 34% (18/53) for Ac-A, 14% (4/29) for Ch-A, 45% (9/20) for Ac-B, and 22% (5/23) for Ch-B; during the most recent 5 year interval these figures were lower: 27%, 8%, 20%, and 20%, respectively, N = 50. Multiple preoperative variables were found to correlate significantly with both operative death and long-term survival. Operative survivors generally experienced satisfactory functional benefit. Late attrition averaged 8% per year; 61% of all late deaths were related to cardiac or cerebral causes. Over-all actuarial survival (+/- SEM) for the entire cohort was 54% +/- 5% at 5 years and 26% +/- 7% at 10 years; for the 89 patients surviving operation, these figures were 76% +/- 5% and 37% +/- 10%, respectively. No significant differences in long-term survival were evident between the different subgroups. Whether the primary intimal tear had been resected or concomitant AVR had been performed had no statistically significant bearing on operative mortality, functional result, necessity for late reoperation, or late attrition. The long-term "natural" history of surgically treated patients with aortic dissections, as defined in this study, should facilitate comparison with other treatment modalities. Results of the present analysis support immediate operative intervention for patients with Ac-A dissections and probably for those with Ac-B dissections. Additionally, surgical treatment of patients with symptomatic or enlarging Ch-A and Ch-B dissections provides satisfactory rehabilitation and long-term survival. Finally, we re-emphasize our recommendation for simplified classification of aortic dissections, based solely upon the presence or absence of ascending aortic involvement. Pathophysiology and expected biologic behavior pivot on this feature, and appropriate clinical strategy can thereby be defined.
J Thorac Cardiovasc Surg 1979 Sep
PMID:Operative treatment of aortic dissections. Experience with 125 patients over a sixteen-year period. 47 Apr 17

Human iliac arteries, obtained at surgery, were examined at SEM. The ultrastructural aspects has evidenced pathological pictures, quite unexpected. The material observed resulted very adapt for scanning electron microscope.
J Cardiovasc Surg (Torino)
PMID:Morphological aspects of the human intimal surface at scanning electron microscope. A preliminary approach in surgical material (iliac arteries). 51 21

The role of angiotensin II in the pulmonary vasoconstriction induced by alveolar hypoxia was investigated with the competitive inhibitor of angiotensin, saralasin acetate. Unilateral alveolar hypoxia was induced in dogs by ventilation of one lung with 100% N2 through a double lumened endotracheal cannula while maintaining adequate systemic oxygenation by ventilating the other lung with 1oo% O2. Pulmonary perfusion was monitored with 133Xe and external detectors. In 8 dogs perfusion to the test lung on room air before N2 ventilation was 49.2% (SEM +/- 3.8) of total lung perfusion. After 7 min of nitrogen ventilation, perfusion to that lung was 35.6% (SEM +/- 2.9) of cardiac output (P less than 0.001), a reduction of 27.5% (SEM +/- 2.4). After infusion of 6--24 microgram.kg-1/min of saralasin acetate, beginning 2 min before the alveolar hypoxic challenge and continuing through it, unilateral alveolar hypoxia continued to reduce perfusion to that lung by 28.8% (P = 0.6 from control). In 2 dogs a higher infusion of 60 microgram.kg-1/min failed to reduce the alveolar hypoxic vasoconstriction and in 2 dogs a 15 min infusion of 6 microgram.kg-1 of saralasin acetate before alveolar hypoxia and continuing through it, still failed to inhibit alveolar hypoxic vasoconstriction. Thus, no role was demonstrated for angiotensin II in acute alveolar hypoxic vasoconstriction of the dog.
Cardiovasc Res 1977 Nov
PMID:Failure of saralasin acetate, a competitive inhibitor of angiotensin II, to diminish alveolar hypoxic vasoconstriction in the dog. 60 79

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.
Cardiovasc Res 1978 Jun
PMID:Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs. 69 89

The etiology of chest pain in patients with the anginal syndrome and normal coronary arteriograms has not been established. There has been no explanation for the association of electrocardiographic, hemodynamic, and myocardial metabolic abnormalities consistent with myocardial ischemia observed in some patients with this disorder. Historical, clinical, laboratory, and hemodynamic data of 45 patients (24 females, 21 males), mean age 47.5 years, with chest pain and normal coronary arteriograms are reviewed. Left ventriculograms were analyzed utilizing the single-plane cineangiographic measurement of left ventricular volume. Systolic ejection fractions for the 45 patients ranged from 0.66 to 0.91 (mean 0.80 +/- 0.01 SEM). Ventricular volumes determined angiographically revealed mean end-diastolic and end-systolic volumes of 83 +/- 5 ml and 18 +/- 2 ml, respectively. The mean changes in longitudinal and transverse segmental axis shortening that occurred during ventricular systole were 28.8% and 50.7%, respectively. These elevated values for ejection fraction, and reduced measurements of ventricular volumes, indicate that some patients with chest pain and normal coronary arteriograms may have small hearts with hyperdynamic ventricular contraction. These findings suggest that hyperdynamic ventricular contraction may play a causative role in the development of transient, angina-like chest pain in these patients. The etiology of the proposed hyperdynamic ventricle is unknown, but it may be attributable to increased beta-sympathetic stimulation of the myocardium.
Cathet Cardiovasc Diagn 1978
PMID:Elevated ejection fractions in patients with the anginal syndrome and normal coronary arteriograms. 73 29


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