Ischemic Left Ventricular Failure Research Articles

Left ventricular diastolic relaxation and pressure-diameter relations during ischaemic left ventricular failure in the dog.

The significance of severe ischaemic left ventricular (LV) failure on the LV isovolumic relaxation process and diastolic chamber stiffness has been investigated in nine open-chest pentobarbital-anaesthetized dogs. LV failure was induced by bolus injections of 50 micron microspheres into left coronary vascular bed until LV minor axis diameter had increased about 25% and end-diastolic pressure about 20 mmHg. Such ischaemic LV failure did not shift the relation between diastolic LV pressure and minor axis diameter compared with pressure-diameter curves obtained before induction of failure. Neither inotropic nor chronotropic stimulation evoked such shifts. Assuming exponential pressure decline, LV relaxation was significantly slower during failure, but proceeded in all experimental conditions at rates which indicated complete relaxation in late diastole. Analysis of the pressure decline during LV relaxation demonstrated that this process proceeded faster than assumed by an exponential function both before and during LV failure.

Ventricular diastolic pressure-volume shifts during acute ischemic left ventricular failure in dogs

Ischemic left ventricular failure was produced in eight acutely instrumented, anesthetized dogs to study the contribution of changing myocardial compliance and pericardial pressure to shifts in right and left ventricular diastolic pressure-volume relations. Right and left ventricular and pericardial volumes were measured by ungated computed tomography. Cardiac volumes were manipulated by infusion of saline solution, hemorrhage, phenylephrine infusion and, during failure only, nitroglycerin administration. During both control and failure periods, these interventions shifted the left and right ventricular pressure-volume relations by changing pericardial pressure only; that is, these interventions caused no change in the ventricular transmural pressure-volume relation. The induction of failure as such increased pericardial pressure only minimally and did not change the left ventricular or right ventricular transmural pressure-volume relations significantly. Volume loading during the control period caused an apparent pericardial creep which attenuated the pericardial effect on ventricular pressure-volume relations. During failure, volume loading caused an increase of right ventricular volume, but tended to decrease left ventricular volume; this was associated with a leftward displacement of the interventricular septum. In conclusion, in the presence of ischemic left ventricular failure as well as normally, changes in preload, afterload and circulating blood volume shift ventricular diastolic pressure-volume relations by stretching or relaxing the pericardium, thus changing pericardial pressure. In these circumstances, there were no consistent changes in myocardial compliance.

Haemodynamic and metabolic consequences of elevated plasma free fatty acids during acute ischaemic left ventricular failure in dogs

Haemodynamic and metabolic effects of elevated plasma concentrations of free fatty acids (FFA) were studied during acute ischaemic left ventricular failure in closed-chest anaesthetized dogs. Embolization of the left main coronary artery with 50 micron plastic microspheres induced severe depression of left ventricular performance as indicated by a marked increase in left ventricular end-diastolic pressure (LVEDP), and marked reductions in LVdP/dtmax, cardiac output and myocardial oxygen consumption (MVO2). When stable conditions were reached, eight dogs received a triglyceride emulsion and heparin to raise plasma FFA. This was associated with increased MVO2 and further elevation of LVEDP. In two dogs receiving the triglyceride emulsion but no heparin, plasma FFA was not elevated, and MVO2 and LVEDP were unchanged. In conclusion, elevation of plasma FFA was associated with increased myocardial oxygen requirement and further depression of LV function in dogs with acute ischaemic LV failure.

Inosine infusion in dogs with acute ischaemic left ventricular failure: favourable effects on myocardial performance and metabolism.

Haemodynamic and metabolic effects of inosine were examined during acute left ventricular (LV) failure in closed-chest anaesthetised dogs. Embolisation of the left main coronary artery with 50 microm plastic microspheres induced severe depression of LV function, and the dogs remained in stable failure throughout the experimental period as shown in the untreated control dogs (n = 4). Intravenous infusion of inosine 3.8 to 7.5 mg . min-1 . kg-1 caused an increase in maximum LVdP/dt from 290 +/- 32 (mean +/- SEM, n = 8) to 376 +/- 39 kPa . s-1 and a decrease in LV end-diastolic pressure from 3.6 +/- 0.2 to 2.5 +/- 0.1 kPa. Total peripheral resistance decreased from 10.2 +/- 1.0 to 7.4 +/- 0.7 kPa . litre-1 min, and cardiac output increased from 1.64 +/- 0.17 to 2.27 +/- 0.23 litre . min-1 during inosine infusion. Myocardial blood flow increased from 65 +/- 10 to 94 +/- 16 cm3 . min-1 . 100 g-1 with no change in myocardial oxygen consumption. Inosine markedly decreased arterial concentrations and myocardial uptake of FFA. Arterial concentrations of glucose were moderately decreased while myocardial uptake of glucose showed a non-significant increase. Inosine markedly increased myocardial uptake of lactate. These metabolic changes were associated with increased plasma concentrations of insulin. In conclusion, inosine improved myocardial performance and increased myocardial uptake of carbohydrates relative to FFA during acute ischaemic LV failure in dogs.

Effects of the β-adrenergic receptor agonist pirbuterol on cardiac performance during acute ischaemic left ventricular failure in dogs

The effects of the β-adrenergic receptor agonist pirbuterol on left ventricular (LV) performance were examined during acute ischaemic LV failure in anaesthetized dogs. Plastic microspheres (50 μm) were injected into the left main coronary artery, and the dogs developed severe LV failure. The stability of the heart failure model was demonstrated in a group of untreated control dogs (n = 5). Administration of pirbuterol 7 μg·kg −1 i.v. during failure caused an increase in cardiac output from 1.52 ± 0.14 (mean ± S.E.M., n = 7) to 2.56 ± 0.32 1· min −1 (P < 0.01) at 30 min after drug administration. The LV end-diastolic pressure (LVEDP) decreased from 24.6 ± 1.1 to 21.0 ± 1.9 mmHg (P < 0.05) and maximum LV dP/dt was increased from 2012 ± 124 to 2602 ± 119 mmHg · s −1 (P<0.01). The LVEDP-stroke work relation (n = 2) shifted markedly upward. Heart rate was not significantly changed by pirbuterol. Mean aortic blood pressure and total peripheral resistance decreased from 103 ± 3 to 85 ± 5 mmHg (P < 0.05) and from 68 ± 6 to 34 ± 4 mmHg·1 −1·min (P<0.01), respectively. Pirbuterol increased plasma free fatty acid concentrations from 264 ± 45 (n = 4) to a maximum value of 956 ± 169 μmol·1 −1. In conclusion, by a combination of inotropic stimulation and systemic vasodilation, pirbuterol markedly improved cardiacperformance in dogs with acute ischaemic LV failure.

Regional blood flow during acute heart failure in dogs. Role of adipose tissue perfusion in regulating plasma-free fatty acids

The effect of acute ischaemic left ventricular failure on regional blood flow and the possible role of adipose tissue perfusion in the regulation of plasma FFA during failure were examined. Left ventricular failure was induced in closed-chest anaesthetized dogs by injection of 50 micrometer plastic microspheres into the left main coronary artery. Regional blood flow, measured with tracer microspheres, showed a redistribution of cardiac output after the induction of failure. Adipose cardiac output (P less than 0.05), while skeletal muscle and pancreatic blood flow decreased about in proportion to the decrease in cardiac output. There was only a moderate decrease in renal blood flow and in left ventricular myocardial blood flow. In the free wall of the right ventricle blood flow was unchanged. There was a marked decrease in plasma FFA during failure (P less than 0.05), which could not be attributed to enhanced FFA turnover rate nor to inhibition of adipose tissue lipolysis, as plasma glycerol tended to increase. The marked decrease in adipose tissue blood flow during failure suggests that plasma FFA decreased due to trapping of FFA in adipose tissue.

A reproducible and stable model of acute ischaemic left ventricular failure in dogs.

A model of acute ischaemic left ventricular (LV) failure is presented. In closed-chest anaesthetized dogs 50 micrometer plastic microspheres were injected repeatedly into the left main coronary artery over a period of about 40 min. The injections effected stepwise elevations of LV end-diastolic pressure (LVEDP). Thus, LVEDP could be increased to a desired level, about 20 mmHg, in a very controlled manner. All dogs developed signs of markedly depressed LV performance. Haemodynamic conditions stabilized about 60 min after embolization. The maximum LVDP/dt decreased from 2696 +/- 169 to 1823 +/- 98 mmHg . x-1, cardiac output decreased from 2.81 +/- 0.20 to 1.98 +/- 0.14 l . min-1 and mean aortic blood pressure decreased from 144 +/- 4 to 127 +/- 3 mmHg, while total peripheral resistance increased from 56 +/- 3 to 69 +/- 3 mmHg . l-1 . min. Myocardial blood flow decreased from 103 +/- 7 to 79 +/- 6 ml . min-1 . 100 g-1 and myocardial oxygen consumption decreased from 12.5 +/- 0.9 to 8.3 +/- 0.8 ml . min-1. 100 g-5. Myocardial uptake of lactate and free fatty acids decreased markedly. Electrocardiography showed signs of acute ischaemia. There were no deaths due to ventricular fibrillation. Morphological studies showed multiple small infarcts throughout the entire LV. In conclusion, repeated coronary embolization with 50 micrometers plastic microspheres, guided by the rise of LVEDP represents a simple and reproducible method for induction of uniform and stable acute LV failure.

Immediate and sustained haemodynamic effects of prazosin during upright exercise in man.

To ascertain the immediate pharmacodynamic and long-term haemodynamic effects of prazosin in chronic ambulant heart failure, measurements were made during sitting, standing, and walking in 12 patients with severe ischaemic left ventricular failure before and after their first dose of prazosin (2 mg) and in six of these patients after a further 12 weeks of sustained treatment (2 mg tds). When first added to treatment with digoxin and frusemide, prazosin was followed within an hour by substantial reductions in systemic arterial, pulmonary arterial, and pulmonary venous pressures in both postures at rest and also during walking. These changes were significantly attenuated after continued treatment. Cardiac output while sitting and standing at rest was reduced in both instances but the response to exercise was unchanged. The pharmacodynamic effects of prazosin in heart failure are explicable in terms of blockade of alpha1 adrenoceptors in arterial resistance and venous capacitance vessels augmented perhaps by lessening of reflex vasoconstriction secondary to the reduction in pulmonary venous pressure. The cause of the attenuation of the acute haemodynamic effects of the drug during sustained treatment is unknown.

Haemodynamic and metabolic effects of the antiarrhythmic drug melperone during acute left ventricular failure in dogs

Haemodynamic and metabolic effects of the new antiarrhythmic drug melperone were studied during acute ischaemic left ventricular failure in closed-chest anaesthetized dogs. Embolisation of the left main coronary artery with 50 micrometer plastic microspheres induced severe depression of left ventricular performance as evidenced by a marked increase in left ventricular end-diastolic pressure and a marked reduction in the maximum rate of left ventricular pressure rise (LVdP/dtmax), cardiac output, and stroke volume. Six dogs received intravenous melperone 1.0 and 2.5 mg . kg-1 (cumulative dose) 90 and 115 min after the embolisation, respectively. Six other dogs received no treatment and served as controls. Melperone effected a marked reduction in left ventricular end-diastolic pressure, a slight but transient increase in LVdP/dtmax, a moderate reduction in heart rate, a moderate reduction in mean aortic blood pressure and total peripheral resistance and a moderate increase in stroke volume. Melperone moderately decreased myocardial O2-consumption, while myocardial lactate uptake remained unchanged. In conclusion, in contrast to commonly used antiarrhythmic drugs which may all induce cardiodepression, melperone improved left ventricular function in dogs with acute ischaemic left ventricular failure.

Cardiocirculatory and myocardial energetic effects of prostaglandin E 1 in severe left ventricular failure due to chronic coronary heart disease

The cardiocirculatory actions of brief (69 ± 5 minutes) infusions of prostaglandin E 1 were evaluated in nine chronic coronary heart disease patients with severe left ventricular (LV) failure caused by previous myocardial infarction. Prostaglandin E 1 infusion did not alter heart rate (HR) and produced modest declines in mean systemic blood pressure (BP) (85 ± 6 to 76 ± 5 mm Hg, p < 0.025) and LV filling pressure (19 ± 3 to 15 ± 2 mm Hg, p < 0.01). Simultaneously, prostaglandin E 1 augmented LV pump function raising cardiac index from 1.9 ± 0.2 to 2.5 ± 0.2 L/min/m 2 ( p < 0.005), elevating stroke index from 28 ± 2.4 to 35 ± 2.9 ml/beat/m 2 ( p < 0.01), and increasing stroke work index from 26 ± 4.3 to 30 ± 4.4 gm·m/m 2 ( p < 0.02). Additionally, total systemic vascular resistance decreased from 1862 ± 192 to 1282 ± 100 dynes-sec-cm −5 ( p < 0.02) and double product LV aerobic index of HR · systolic BP diminished from 9492 ± 666 to 8278 ± 493 ( p < 0.02). Concomitantly, in the forearm, vascular resistance fell, blood flow rose, and venous tone remained unchanged. These results indicate that prostaglandin E 1 is a potent systemic arteriolar dilator with markedly beneficial effects on cardiac function in chronic coronary patients having severe ischemic LV failure refractory to conventional therapy.

Haemodynamic and metabolic effects of inosine during acute ischaemic left ventricular failure in dogs: O.A. Smiseth and O.D. Mjøs. Institute of Medical Biology, University of Tromsø, Tromsø, Norway

Haemodynamic and metabolic effects of inosine during acute ischaemic left ventricular failure in dogs: O.A. Smiseth and O.D. Mjøs. Institute of Medical Biology, University of Tromsø, Tromsø, Norway

Beneficial effect of amrinone on myocardial oxygen consumption during acute left ventricular failure in dogs

In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction In cardiac output and a left ventricular end-dlastolic pressure of 18 mm Hg or more was produced by proximal occlusion of the left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. Administration of amrlnone In an Intravenous bolus injection followed by a constant Infusion produced Improvements in cardiac output (from 1.62 ± 0.50 to 2.19 ± 0.52 Itters/min [ mean ± standard deviation], p <0.05), left ventricular end-dlastolic pressure (from 21.6 ± 3.5 to 11.0 ± 5.4 mm Hg, p <0.05) and peak positive rate of rise of left ventricular pressure [dP/dt](from 1,264 ± 241 to 1,800 ± 458 mm Hg· −1, p <0.05). These Improvements were maintained throughout the 20 minute period of therapy. No significant alteration in heart rate or arterial pressure was noted. In parallel with the hemodynamic improvement myocardial oxygen consumption improved to 0.094 ± 0.05 and 0.092 ± 0.04 vol· −1⋗ −1 after 2 and 20 minutes; respectively, of amrinone compared with 0.124 ± 0.05 during left ventricular failure (both <0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodllatation. The reduction in myocardial oxygen consumption during amrlnone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an Increase in contractility.

Blood circulation in adipose tissue

articleBlood circulation in adipose tissueS. Rosell, and E. BelfrageS. Rosell, and E. BelfragePublished Online:01 Oct 1979https://doi.org/10.1152/physrev.1979.59.4.1078MoreSectionsPDF (4 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByInhibition of α-adrenergic tone disturbs the distribution of blood flow in the exercising human limbIlkka Heinonen, Maria Wendelin-Saarenhovi, Kimmo Kaskinoro, Juhani Knuuti, Mika Scheinin, and Kari K. Kalliokoski15 July 2013 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 305, No. 2Role of Uncoupling Proteins in Cancer16 April 2010 | Cancers, Vol. 2, No. 2Renin dynamics in adipose tissue: adipose tissue control of local renin concentrationsJason D. Fowler, Stacy B. Krueth, David A. Bernlohr, and Stephen A. Katz1 February 2009 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 296, No. 2β-Adrenergic Receptors and Regulation of Energy Expenditure: A Family AffairAnnual Review of Pharmacology and Toxicology, Vol. 44, No. 1Human Adipose Tissue Cells Keep Tight Control on the Angiotensin II Levels in Their VicinityJournal of Biological Chemistry, Vol. 277, No. 50Prediction of the volume of distribution of a drug: which tissue-plasma partition coefficients are needed?18 February 2010 | Journal of Pharmacy and Pharmacology, Vol. 54, No. 9Analyte flux through chronically implanted subcutaneous polyamide membranes differs in humans and ratsN. Wisniewski, N. Rajamand, U. Adamsson, P. E. Lins, W. M. Reichert, B. Klitzman, and U. Ungerstedt1 June 2002 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 282, No. 6Model predictions and comparisons for three toxicokinetic models for the systemic transport of trichloroethyleneMathematical and Computer Modelling, Vol. 35, No. 9-10Lipolysis in human adipose tissue during exercise: comparison of microdialysis and a-v measurementsKai Henrik Wiborg Lange, Jeanne Lorentsen, Fredrik Isaksson, Lene Simonsen, Jens Bülow, and Michael Kjær1 March 2002 | Journal of Applied Physiology, Vol. 92, No. 3Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors2 August 2001 | International Journal of Obesity, Vol. 25, No. 8Lipid metabolism during endurance exerciseThe American Journal of Clinical Nutrition, Vol. 72, No. 2Intraneural stimulation elicits an increase in subcutaneous interstitial glycerol levels in humans7 September 2004 | The Journal of Physiology, Vol. 521, No. 2Insulin- and glucagon-independent effects of calcitonin gene—related peptide in the conscious dogMetabolism, Vol. 48, No. 5Application of Physiologic Models to Predict the Influence of Changes in Body Composition and Blood Flows on the Pharmacokinetics of Fentanyl and Alfentanil in PatientsAnesthesiology, Vol. 88, No. 3Physiological and metabolic consequences of obesityMetabolism, Vol. 44β-adrenergic stimulation and abdominal subcutaneous fat blood flow in lean, obese, and reduced-obese subjectsMetabolism, Vol. 44, No. 2Adipose tissue metabolismClinics in Dermatology, Vol. 7, No. 4The nervous system and adipose tissueClinics in Dermatology, Vol. 7, No. 4Beta-adrenoceptor sensitivity of brown and white adipocytes after chronic pretreatment of rats with reserpineBiochemical Pharmacology, Vol. 36, No. 1Patterns of hyperphagia in the Zucker obese rat: A role for fat cell size and number?Brain Research Bulletin, Vol. 14, No. 6Circulatory implications of exercise and heat stressPharmacology & Therapeutics, Vol. 31, No. 1-2Effects of the β-adrenergic receptor agonist pirbuterol on cardiac performance during acute ischaemic left ventricular failure in dogsEuropean Journal of Pharmacology, Vol. 87, No. 4Sympatho-adrenal regulation of adipose tissue blood flow in dog and manGeneral Pharmacology: The Vascular System, Vol. 14, No. 1In vivo α2-adrenoceptor-mediated inhibition of isoproterenol of isoproterenol-stimulated free fatty acid output in dog bone marrow adipose tissueEuropean Journal of Pharmacology, Vol. 76, No. 4Obesity and the heartCurrent Problems in Cardiology, Vol. 5, No. 3 More from this issue > Volume 59Issue 4October 1979Pages 1078-1104 Copyright & PermissionsCopyright © 1979 the American Physiological Societyhttps://doi.org/10.1152/physrev.1979.59.4.1078PubMed386395History Published online 1 October 1979 Published in print 1 October 1979 Metrics

Metabolism of glucose by the ischemic dog heart.

ARTICLESMetabolism of glucose by the ischemic dog heartN Brachfeld, and J ScheuerN Brachfeld, and J ScheuerPublished Online:01 Mar 1967https://doi.org/10.1152/ajplegacy.1967.212.3.603MoreSectionsPDF (992 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDecreased interstitial glucose and transmural gradient in lactate during ischemiaBasic Research in Cardiology, Vol. 89, No. 5Changes in myocardial metabolism as a diagnostic tool and therapeutic measureJournal of Cardiothoracic and Vascular Anesthesia, Vol. 6, No. 1Case conferenceJournal of Cardiothoracic Anesthesia, Vol. 4, No. 2Positron Emission Tomography in Clinical CardiologyCardiology Clinics, Vol. 7, No. 3Sustained nonoxidative glucose utilization and depletion of glycogen in reperfused canine myocardiumJournal of the American College of Cardiology, Vol. 13, No. 3Positron 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positron-emission computed tomographyAmerican Heart Journal, Vol. 103, No. 4Post-anoxic recovery of myocardial performance in senescent miceExperimental Gerontology, Vol. 16, No. 3Fundamental Validity and Clinical Usefulness of Myocardial Lactate Balance During Ischaemia A comparison with Other Biochemical MarkersEffects of glucose and glucose-insulin-potassium on haemodynamics and enzyme release after acute myocardial infarction.Heart, Vol. 39, No. 7FACTORS MODIFYING ISCHEMIC ALTERATIONS OF VENTRICULAR FUNCTION AND METABOLISM IN THE INTACT WORKING SWINE HEART24 April 2009 | Acta Medica Scandinavica, Vol. 199, No. S587Effect of coronary blood flow on glycolytic flux and intracellular pH in isolated rat hearts.Circulation Research, Vol. 37, No. 6Changes in intramyocardial ST segment voltage and gas tensions with regional myocardial ischemia in the dog.Circulation Research, Vol. 37, No. 4Study of Daily Caloric Intake of Patients in the Coronary Intensive Care Unit2 July 2016 | Angiology, Vol. 26, No. 4Heart Rate and Myocardial Substrate Preference During Normal and Hypoxic Perfusion of the Heart in Vivo27 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 83, No. 1Zur Wirkung von Insulin auf den Glukosestoffwechsel und die Hämodynamik des isolierten Rattenherzens bei HypoxieBasic Research in Cardiology, Vol. 68, No. 6Function of the hypoxic myocardiumThe American Journal of Cardiology, Vol. 32, No. 4Comparison of the Effects of Anoxia and Whole Heart Ischemia on Carbohydrate Utilization in Isolated Working Rat HeartsCirculation Research, Vol. 32, No. 6Substrate Preference and Metabolic Activity of the Aerobic and the Hypoxic Turtle HeartCirculation Research, Vol. 31, No. 3Effect of Glucose-Insulin-Potassium Infusion on Myocardial Infarction following Experimental Coronary Artery OcclusionCirculation, Vol. 45, No. 6Regional metabolic changes in the myocardium following coronary artery ligation in dogsAmerican Heart Journal, Vol. 83, No. 2Metabolic Response during Impending Myocardial InfarctionCirculation, Vol. 45, No. 2Glucose Extraction by the Human Myocardium during Pacing StressCirculation, Vol. 45, No. 1Myocardial Metabolism in Patients with Ischemic Heart DiseaseComparison between metabolic changes in local venous and coronary sinus blood after acute experimental coronary arterial occlusionThe American Journal of Cardiology, Vol. 25, No. 5Biochemical aspects of early myocardial ischemiaThe American Journal of Cardiology, Vol. 24, No. 6RELATIVE CHANGES IN FREE-FATTY-ACID AND GLUCOSE UTILISATION BY ISCHÆMIC MYOCARDIUM AFTER CORONARY-ARTERY OCCLUSIONThe Lancet, Vol. 293, No. 7607Beta adrenergic blockadeThe American Journal of Cardiology, Vol. 21, No. 6Limitation of Myocardial Function by Reduced Coronary Blood Flow during Isoproterenol ActionCirculation Research, Vol. 21, No. 1 More from this issue > Volume 212Issue 3March 1967Pages 603-606 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.212.3.603PubMed6020533History Published online 1 March 1967 Published in print 1 March 1967 Metrics

Left heart bypass in left ventricular failure due to experimental coronary artery ligation

Summary and conclusions 1. A study of left heart bypass in ischemic left ventricular failure in anesthetized mongrel dogs has been presented. A difference in right and left ventricular end- diastolic pressures suggests that isolated left ventricular failure is present. Functional mitral insufficiency has been observed during the late stages of left ventricular failure due to serial coronary artery ligation. 2. The value of peripheral arterial pressure and central venous pressure as early indications of left ventricular failure is in doubt. 3. The arteriovenous oxygen difference or, by extension, the central venous oxygen saturation is a clinically useful estimate of the effectiveness of the cardiac output in the presence of left ventricular failure and this value becomes abnormal long before arterial hypotension or elevation of the central venous pressure occurs. 4. Hypovolemia, ventricular fibrillation, and inadequate drainage of the left atrium all influence directly the effectiveness of left heart bypass and, when left heart bypass is inadequate in the presence of left ventricular failure, an inadequate tissue perfusion results.

Protracted Shock in the Closed-Chest Dog Following Coronary Embolization With Graded Microspheres

Protracted Shock in the Closed-Chest Dog Following Coronary Embolization With Graded Microspheres