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Biomedical subjects

S Levitsky

Publications and source records attributed to S Levitsky.

At least 127 records · Page 7Linked to original sources
PubMed1987

The effect of cardioplegic oxygenation on the correlation between the linearized Frank-Starling relationship and myocardial energetics in the ejecting postischemic heart.

To ascertain whether oxygenated cardioplegia is beneficial during surgically induced global ischemia, 27 canine hearts underwent sonomicrometric determination of cardiac mechanics and energetics during volume loading on right heart bypass before and after 2 hr of potassium cardioplegic arrest with crystalloid, oxygenated crystalloid, or blood vehicles. The slope of the linear stroke work vs end-diastolic volume relationship, an index of contractility, was preserved by each vehicle. Similarly, oxygen utilization to perform external mechanical work during reperfusion was unaffected in all groups. However, there were significant 119% and 122% increases in basal oxygen utilization after both unoxygenated and oxygenated crystalloid cardioplegia (p less than .05) that were prevented by the blood-based vehicle. These data suggest that the salutary effects of blood cardioplegia on postischemic myocardial energetics may not be solely mediated by its oxygen-carrying capacity.

Animals↗
PubMed1986

Combined tracheal transection and innominate artery disruption from blunt chest trauma.

Both transection of the trachea and injury of the aorta and its arch vessels can occur after blunt chest trauma; however, the combination of these injuries in 1 patient is exceedingly rare. This report of a patient with distal trachea transection and proximal innominate artery disruption from blunt chest trauma reviews some of the important factors to be considered in managing these injuries. Management of the airway must be planned before the operative procedure is begun and can be facilitated by the use of a sterile anesthesia circuit passed on to the operative field. Exposure of tracheal injuries as low as the carina can be achieved through sternotomy incision if this approach is indicated for repair of the associated vascular injury. The use of prosthetic materials should be avoided in vascular injury repair due to contamination of the field from the associated airway disruption. Attention to postoperative bronchial hygiene is mandatory for successful outcome after tracheal anastomosis.

Adult↗
PubMed1986

Oxygen utilization during isovolumic pressure-volume loading: effects of prolonged extracorporeal circulation and cardioplegic arrest.

In canine hearts supported by cardiopulmonary bypass, isovolumic peak developed pressure (PDP, mm Hg) and myocardial oxygen consumption (MVO2, ml O2 X 10(-2)/beat/100 gm left ventricular [LV] weight) were determined at 5-ml increments of LV balloon inflation before and after either 2 hours of potassium cardioplegic arrest (ischemia, N = 7) or a comparable period of normothermic perfusion without ischemia (control, N = 6). The sensitivity of MVO2 as a marker of ischemic injury was compared with preservation of both adenosine triphosphate (ATP) stores and systolic pump function. Over a physiological range of end-diastolic volumes (5 to 35 ml) and end-diastolic pressures (0 to 18 mm Hg), the Frank-Starling curves were not depressed following both cardioplegic arrest and prolonged nonischemic perfusion. Although ATP stores decreased by 26% and 22% (ischemia and control groups, respectively; not significant), these levels did not distinguish the effects of cardioplegic arrest from prolonged perfusion. At the preinterventional measurement in both groups, PDP between 50 and 200 correlated with MVO2 from 3.0 to 10.0 (r = +0.84). Following cardioplegic arrest, postischemic MVO2 increased 137 +/- 6% when measured over the PDP range of 75 to 200 mm Hg (p less than 0.01). This change was not evident at a PDP of less than 75, in the empty beating heart, or in control hearts subjected to nonischemic extracorporeal perfusion. These data suggest that increased utilization of oxygen to develop physiological pressures may be a more sensitive indicator of ischemic injury than shifts in the pressure-volume relationship or depletion of adenine nucleotide stores.

Adenosine Triphosphate↗
PubMed1986

Nonoperative control of retroperitoneal hemorrhage secondary to placement of an inferior vena cava occluding device in a patient with recurrent pulmonary emboli.

A woman with multiple recurrent pulmonary emboli and iatrogenic inferior vena cava perforation caused by the Hunter-Sessions introducer was treated successfully by placement of a Hunter-Sessions balloon to control the ensuing retroperitoneal hemorrhage and interrupt the inferior vena cava. Full anticoagulation therapy was continued throughout the operation and postoperatively.

Catheterization↗
PubMed1986

Temperature-specific effects of adjuvant diltiazem therapy on myocardial energetics following potassium cardioplegic arrest.

Adjuvant slow calcium channel blockade theoretically minimizes the calcium influx attendant to potassium-induced cardioplegic arrest, particularly if clinically acceptable levels of cardiac hypothermia are not maintained. The present study assessed the efficacy of diltiazem therapy in ameliorating perturbations of myocardial oxygen consumption that could be attributable to postischemic intracellular calcium accumulation. In 30 canine hearts, myocardial oxygen consumption was determined during incremental isovolumic pressure-volume loading before and 30 minutes after 2 hours of either 20 or 28 degrees C potassium cardioplegic arrest. The intracoronary perfusate in randomized hearts was modified by the addition of diltiazem, 150 micrograms/kg. Although systolic performance (as defined by peak developed pressure as compared with balloon volume curves) was unchanged after 20 degrees C ischemia, adjuvant diltiazem therapy prevented the 44 +/- 2% (p less than .01) decrease in peak developed pressure after 28 degrees C arrest. Moreover, the 39% augmentation of postischemic myocardial oxygen consumption at specific peak developed pressure following both 20 and 28 degrees C ischemia was attenuated with diltiazem only after the warmer ischemic interval. This difference was characterized by a larger (35 +/- 2 vs. 26 +/- 2%; p less than .025) decrease in postischemic oxygen extraction despite a comparable hyperemia. These data suggest that adjuvant diltiazem therapy during potassium-induced cardioplegic arrest preserves energy-efficient pump function only after warmer ischemia, thereby limiting the clinical application of this myoprotective regimen.

Animals↗
PubMed1986

Flexible fiberoptic pericardioscopy for the diagnosis of pericardial disease.

Pericardiocentesis provides an etiologic diagnosis for pericardial effusions approximately 25% of the time. In seven patients with evidence of a large pericardial effusion of unknown origin without cardiac tamponade, a flexible fiberoptic bronchoscope was inserted through a subxiphoid incision after the effusion was drained. Pericardioscopy allowed visualization of all pericardial surfaces and made it possible to perform selective biopsy not limited to a subxiphoid window. It is a safe procedure that can permit distinction among benign, malignant and tuberculous origins of pericardial effusion.

Adolescent↗
PubMed1986

Direct effect of high-dose insulin on the depressed heart after beta-blockade or ischemia.

The direct cardiac effects of high-dose insulin (HDI) were assessed in 13 canine hearts supported by cardiopulmonary bypass. Isovolumic peak developed pressure (PDP, mmHg), coronary blood flow (CBF, ml/beat/100 g LV) and myocardial oxygen consumption (MVO2, ml O2/beat/100 g LV) were determined during incremental left ventricular balloon inflation before and after functional depression by beta-blockade (0.2 mg/kg propranolol) or 2 hours cardioplegic ischemia at 28 degrees C. The 2 regimens gave an overall functional reduction of 46 +/- 3% and 42 +/- 2%, respectively. The hearts were then challenged with an aortic root bolus of 1000 IU insulin. A glucose clamp was maintained at physiological levels. Insulin reversed the negative inotropic effect of propranolol to 80% of control function and normalized heart rate. Despite the significant amelioration of systolic function by HDI, MVO2 indexed for cardiac effort did not change. Neither systolic function nor heart rate was changed in the ischemically depressed hearts. In conclusion, HDI reverses the negative inotropic effect of beta-adrenergic receptor blockade without augmenting oxygen utilization. Apart from effects ascribable to systemic vasodilation and metabolic shifts, no direct cardiac inotropic stimulation can be expected on the post-ischemically depressed, nondiabetic myocardium unless there is a persistent negative effect of beta-blockers.

Animals↗
PubMed1986

The quiescent heart: excitability, compliance, and vascular resistance.

A rat heart, perfused via the aorta and fitted with a balloon in the left ventricle, was rendered quiescent by a local injection of lidocaine into the region of the atrioventricular node. Once quiescence was established it was extended by injection of formaldehyde into the same site via a coaxial needle. The quiescent heart (QH) was responsive to electrical stimulation and exhibited the same isovolumic pressure development as seen during spontaneous beating. Over a range of ventricular volume, slightly greater left ventricular pressures were found in the QH as compared with the diastolic pressure at the same ventricular volumes in the beating heart (BH). Left ventricular diastolic pressures in the QH were less than those found in the KCl-arrested heart. The QH perfused at constant flow rate with a syringe pump exhibited a constant perfusion pressure. Infusion of vasopressin induced a dose-related increase in perfusion pressure, whereas adenosine or sodium nitroprusside reduced the perfusion pressure. The QH appears to be a useful preparation for the study of vascular resistance free of cyclical intramyocardial pressure and relatively uninfluenced by vasoactive metabolites arising from contracting muscle.

Animals↗
PubMed1986

Myocardial energetics after thermally graded hyperkalemic crystalloid cardioplegic arrest.

Previous studies assessing the efficacy of myoprotective regimens have compared preischemic and postischemic myocardial oxygen consumption within a limited range of cardiac performance. However, recent data suggest that ischemia-induced perturbations in myocardial energetics may occur only when the left ventricle develops physiologic pressures. Therefore, in canine hearts supported by cardiopulmonary bypass, myocardial oxygen consumption (ml oxygen X 10(-2)/beat/100 gm left ventricular weight) was determined during incremental isovolumic pressure-volume loading before and 30 minutes after 2 hours of cardioplegic arrest. The ischemic insult was graded by maintaining myocardial temperature at 12 degrees C (Group I, n = 6), 20 degrees C (Group II, n = 7), or 28 degrees C (Group III, n = 6). Postischemic Starling curves were unchanged in Groups I and II but depressed 53% in Group III hearts (p less than 0.005). In Group I, postischemic myocardial oxygen consumption at specific peak developed pressures was similar to preischemic oxygen consumption. In contrast, postischemic Group II and III hearts consumed 39% more oxygen than preischemically when peak developed pressure exceeded 75 mm Hg (p less than 0.01). Postischemic hearts demonstrated reciprocal changes in arteriovenous oxygen content difference (24%, 30%, and 34% lower than preischemic values for Groups I, II, and III, respectively) and coronary blood flow (156%, 195%, and 192% higher than preischemic values for Groups I, II, and III, respectively). Only in Group II and III hearts did the increased coronary blood flow offset the defect in oxygen extraction such that myocardial oxygen consumption was increased. These data suggest that inefficient utilization of oxygen when the heart is developing physiologic pressures is a sensitive marker for myocardial injury after crystalloid cardioplegic arrest.

Animals↗
PubMed1986

Characterization of postischemic myocardial oxygen utilization.

To define the pertubations in myocardial oxygen consumption (MVO2) previously noted after potassium-induced arrest, MVO2 was determined in 19 canine hearts during isovolumetric pressure-volume loading before and serially after 2 hr of cardioplegic ischemia at 20 degrees C. Starling curves were initially unchanged after cardioplegic arrest, but postischemic propranolol (0.2 mg/kg) depressed peak developed pressure 36 +/- 4% and heart rate 24 +/- 1% (p less than .01, for both). MVO2 indexed per beat and for left ventricular weight at defined ranges of peak developed pressure was augmented postischemically by 40% (p less than .05) and this increased oxygen utilization persisted after attenuation of coronary hyperemia, normalization of oxygen extraction, 1 hr of reperfusion, and effective beta-adrenergic-receptor blockade. These data suggest that increased MVO2 to generate physiologic pressures is a sensitive biological marker for cardioplegic efficacy that is independent of coronary flow and oxygen uptake and is not solely attributable to increased beta-adrenergic stimulation.

Animals↗
PubMed1985

Effect of coronary artery occlusion on myocardial protection by retroperfusion of cardioplegic solutions.

Coronary artery stenoses impede delivery of cardioplegic solutions infused through the aortic root. Therefore, the efficacy of retroperfusion of cardioplegic solution through the coronary sinus was assessed in dogs subjected to cold, potassium cardioplegic arrest. Group I (N = 15) had the left anterior descending (LAD) coronary artery occluded throughout ischemia while Group II (N = 15) had a patent LAD. Transmural biopsies of both the left ventricular (LV) apex and right ventricle (RV) were assayed for adenosine triphosphate (ATP) and creatine phosphate (CP). Regional wall temperatures were sequentially monitored. The time from aortic cross-clamping to electrical arrest varied widely, but the mean arrest time of each group was similar (174 +/- 22 vs 175 +/- 28 sec). (table; see text) Comparable depletion of ATP stores (vs preischemia) occurred in each ventricle regardless of coronary artery patency. Similarly, CP stores were depleted 60-72% (P less than 0.01) during ischemia. Mean temperatures during arrest of the RV and LV (17.2-19.5 degrees C) did not differ and were not affected by LAD occlusion. Coronary venous resistance remained constant with repetitive infusions. These data suggest that myocardial protection with coronary sinus retroperfusion is independent of arterial patency, but is suboptimal, perhaps due to the prolonged time needed to induce ventricular arrest.

Adenosine Triphosphate↗
PubMed1985

Effect of carnitine on myocardial function and metabolism following global ischemia.

Carnitine has therapeutic potential for the postischemic heart by facilitating the oxidation of acylated fatty acid metabolites, the intracellular accumulation of which has a deleterious effect on myocardial function and metabolism. To test this hypothesis, two groups of dogs were given preischemic treatment with carnitine, 50 mg per kilogram of body weight (Group 1) or 100 mg/kg (Group 2), and were compared with untreated controls (N = 12 for all groups). The canine hearts underwent 30 minutes of global 37 degrees C ischemic arrest with reperfusion. Left ventricular systolic and diastolic function was assessed by an intracavitary balloon while metabolic derangements were quantitated by serial myocardial biopsies assayed for adenosine triphosphate (ATP). Comparable 49 to 53% (p less than 0.01) declines in preischemic ATP levels occurred during the study period in the controls and both experimental groups. However, postischemic systolic left ventricular function was better preserved in Group 2: these hearts generated 61 +/- 3% of preischemic peak developed pressure compared with 37 +/- 4% in the controls and 42 +/- 3% in Group 1 (p less than 0.01 for each), and 60 +/- 2% of preischemic maximum rate of rise of left ventricular pressure as opposed to 45 +/- 4% in the controls and 49 +/- 6% in Group 1 (p less than 0.02 for each).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1985

Gonococcal endocarditis during pregnancy: simultaneous cesarean section and aortic valve surgery.

Gonococcal endocarditis is a rare and potentially fatal consequence of disseminated gonococcal infection. Presented is the first known case of culture-proved gonococcal and serratia endocarditis in pregnancy. The case was further complicated by fetal distress at 30 weeks' gestation as a result of maternal decompensation from worsening congestive heart failure secondary to rapid destruction of her aortic valve. Consequently, cardiopulmonary bypass with subsequent aortic valve replacement and implantation of a left ventriculoaortic shunt was initiated immediately after an emergency cesarean section.

Adult↗
PubMed1985

Efficacy of crystalloid cardioplegic solutions in patients undergoing myocardial revascularization. Effect of infusion route and regional wall motion on preservation of adenine nucleotide stores.

The effect of varying the mode of cardioplegic delivery and the presence of regional wall motion abnormalities on myocardial protection by crystalloid cardioplegic solutions was assessed in 68 patients undergoing coronary artery bypass grafting. Serial transmural biopsy specimens from the left ventricular apex were assayed for adenosine triphosphate. All patients had more than 75% stenosis of the left anterior descending coronary artery. They were prospectively randomized into Groups I and II to receive (I) all cardioplegic solution infused via the aortic root or (II) reinfusions of cardioplegic solution given both centrally and through the completed distal left anterior descending anastomosis. Patients were also stratified as to the presence of normal (N) or impaired (Ab) apicoanterior regional wall motion. Inadequate delivery of cardioplegia during ischemia in Group I was manifested by a 41% (p less than 0.01) depletion of adenosine triphosphate stores in abnormally contracting myocardium distal to the left anterior descending stenosis that was not repleted after restoration of coronary flow and a 27% (p less than 0.05) decline in ATP stores during reperfusion in myocardium with normal preoperative wall motion. In contrast, nucleotide stores were preserved at preischemic levels throughout ischemia and reperfusion in Group II regardless of preoperative wall motion. Preservation of ATP did not correlate with duration of ischemia, highest recorded septal temperature, or volume of cardioplegic solution infused. Two patients in each group had a new perioperative infarction. However, 38% of patients in Group IAb required transient inotropic support versus 5% in Group IIAb (p less than 0.05). These data emphasize that reinfusion of cardioplegic solutions distal to coronary obstructions is mandatory for optimal myocardial protection during coronary revascularization.

Adenosine Triphosphate↗