Left Ventricular Function In Dogs Research Articles

Ranolazine, a partial fatty acid oxidation inhibitor, improves left ventricular function in dogs with heart failure through an increase in myocardial efficiency

Ranolazine, a partial fatty acid oxidation inhibitor, improves left ventricular function in dogs with heart failure through an increase in myocardial efficiency

The effects of high dose N G-nitro- l-arginine-methyl ester on myocardial blood flow and left ventricular function in dogs

Purpose: Nitric oxide (NO) synthase inhibition has been reported to cause elevation in mean arterial pressure (MAP) and a decrease in cardiac index (Cl), the cause of which is not completely understood. It has been shown that increased concentrations of NO synthase inhibitors cause a further drop in cardiac output without a corresponding increase in arterial pressure, prompting the conclusion that NO inhibition results in direct myocardial depression. However, myocardial ischemia was not completely ruled out as a cause for myocardial dysfunction in these studies. The purpose of this study was to examine the effects of 30 mg/kg of the NO synthase inhibitor N G-nitro- l-arginine-methyl ester (L-NAME) to those of 300 mg/kg and assess the effects on coronary ischemia and myocardial function. Materials and Methods: Eight anesthetized dogs underwent median sternotomy and pericardiectomy. L-NAME 30 mg/kg was administered and the effects were recorded at 5, 15, and 30 minutes. Thereafter, 300 mg/kg was administered and the effects were observed for 5, 15, and 30 minutes. We measured MAP, heart rate (HR), Cl, left ventricle (LV) end systolic and diastolic pressures, the first derivative of LV pressure (dP/dt), left anterior descending artery blood flow, regional LV contraction, gas tensions, and lactates. A coronary sinus catheter allowed for measurements of coronary sinus pressure, lactate, and gas tensions. Stroke volume, percent myocardial shortening (dL/dt) myocardial oxygen consumption, and net lactate myocardial production were calculated. Results: Whereas 30 mg/kg had minimal effects on coronary blood flow and LV function, 300 mg/kg resulted in profound hypotension, drop in Cl, and acidocis. Conclusions: L-NAME at 30 mg/kg caused a rise in MAP and systemic vascular resistance; however, it had no effect on ventricular function. High dose NO synthase inhibition causes myocardial depression not related to increased afterload, coronary vasoconstriction, or myocardial ischemia.

An anti-CD18 antibody limits infarct size and preserves left ventricular function in dogs with ischemia and 48-hour reperfusion

This study investigated whether an antibody against neutrophil adhesion protein CD18 could limit myocardial infarct size and preserve left ventricular function after prolonged reperfusion in a canine model. Myocardial reperfusion injury is mediated in part by accumulation of activated neutrophils. Although antibodies against CD18 have been shown to reduce neutrophil influx and infarct size after ischemia and 3 to 4 h of reperfusion, it is unknown whether protection is sustained beyond this time or whether there is meaningful preservation of ventricular function. Dogs undergoing 90-min circumflex coronary artery occlusion and 48-h reperfusion were randomized to receive 1 mg/kg bodyweight of R15.7 (an anti-CD18 antibody, n = 12) or saline (control, n =12) 10 min before reperfusion. Contrast left ventriculography was used to measure left ventricular ejection fraction and regional chord shortening at baseline, during occlusion and at 48 h. Microspheres injected during occlusion were used to measure collateral flow and risk region size. Postmortem infarct size was measured with triphenyltetrazolium chloride. In the dose administered, R15.7 bound to neutrophils in vivo, with >85% saturation of CD18 for >24 h, with sustained antibody excess in the plasma. R15.7 significantly reduced infarct size after adjusting for the effect of collateral flow (p = 0.0002, analysis of covariance). In a subgroup of dogs with collateral flow <30% of nonischemic flow, infarct size was reduced from 34.6 +/- 3.9% (mean +/- SE) of the region at risk in the control group to 19.5 +/- 3.3% in the antibody group (p = 0.008). Ejection fraction and regional chord shortening did not differ between the two groups at baseline or during occlusion, but after 48-h reperfusion, ejection fraction and inferior wall regional cord shortening (representing the infarct zone) were both higher in the R15.7 group than the control group (43.6 +/- 2.9% vs. 28.5 +/- 1.8%, p < 0.01; 2.55 +/- 0.29% vs. 1.06 +/- 0.18%, p < 0.05). A single injection of an anti-CD18 antibody given before reperfusion can limit myocardial infarct size by nearly 50% and preserve global and regional left ventricular function after 48 h of reperfusion.

F82. Improvement of left ventricular function in dogs with isovolumetric hemodilution at different times with acute myocardial infarction

F82. Improvement of left ventricular function in dogs with isovolumetric hemodilution at different times with acute myocardial infarction

Effect of disrupting the mitral apparatus on left ventricular function in dogs.

The importance of the mitral apparatus to left ventricular function has been suggested in clinical studies. The effect of disruption of the mitral apparatus on left ventricular diastolic and systolic properties has not been fully documented. We investigated the end-diastolic and end-systolic pressure-volume and stroke work-end-diastolic volume relations and measured the isovolumic relaxation time constant (tau infinity) during nonfilling beats before and after disruption of the mitral apparatus under different loading conditions in 14 dogs using our recently developed volume-clamping technique for the in situ left ventricle. Disruption of the mitral apparatus increased left ventricular diastolic equilibrium volume (V0d) without changing the slope of the end-diastolic pressure-volume relation (Sd) and increased end-systolic pressure-volume relation dead volume (V0s) and volume-axis intercept of stroke work-end-diastolic volume relation (V0sw) without changing the slopes of these relations (maximum elastance, Ees, and Ssw). Disruption of the mitral apparatus increased tau infinity. Disruption of the mitral apparatus increases the equilibrium volume without changing left ventricular diastolic stiffness or contractility and slows left ventricular relaxation. These results support and help explain the clinical observation that it is desirable to maintain the mitral apparatus during mitral valve replacement surgery.

Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs.

We used a load-insensitive index of systolic left ventricular (LV) function and an analysis of diastolic pressure-dimension relationships to test the hypothesis that recombinant human (rh) tumor necrosis factor-alpha (TNF alpha) impairs LV function in dogs. Animals were studied 7-10 d after aseptic implantation of instrumentation to monitor cardiac output, external anterior-posterior LV diameter, and LV and pleural pressures. Data were analyzed from seven dogs that received active rhTNF alpha (100 micrograms/kg over 60 min) and from five dogs that received heat-inactivated rhTNF alpha. At 24 h after infusion of active rhTNF alpha, the slope of the LV end-diastolic dimension-stroke work relationship decreased significantly, indicating a decrement in LV systolic contractility. Simultaneously, LV unstressed dimension increased significantly, suggesting diastolic myocardial creep. The end-diastolic relationship between LV transmural pressure and normalized LV dimension (strain) was markedly displaced to the left, suggesting increased diastolic elastic stiffness. Despite these changes in LV performance, cardiac index was maintained by tachycardia. The abnormalities in LV function were resolved by 72 h. We conclude that rhTNF alpha reversibly impairs LV systolic and diastolic function in unanesthetized dogs. Because dysfunction occurs greater than 6 h after the infusion of rhTNF alpha and persists for 24-48 h, the mechanism underlying this phenomenon may involve secondary mediators or a change in myocardial gene expression.

Effects of different dosage of dipyridamole on extent risk area and left ventricular function in dogs with quantitative myocardial ischemia

Effects of different dosage of dipyridamole on extent risk area and left ventricular function in dogs with quantitative myocardial ischemia

Left ventricular function in dogs 1 year after coarctectomy

Juxtaductal aortic coarctation was surgically created in beagle puppies at the age of 2 months and resected at the age of 10 months, after the development of good collateral circulation. Control dogs undergoing sham operations on each occasion were studied in the same environment. Cardiac catheterization was performed 1 year after the coarctectomy to evaluate the recovery of the heart. Cardiac output, heart rate, end-diastolic pressure, and Vmax were similar in both groups of seven dogs, but the systolic pressure gradient (SPG) over the operated area during isoproterenol infusion was significantly higher in the coarctectomized group, with a mean of 8.9 +/- 6.3 (SD) vs. 0.1 +/- 0.3 mmHg (p less than 0.05). The preejection period [PEP, 58 +/- 8 vs. 47 +/- 5 ms (p less than 0.01)], electromechanical delay [EMD, 18 +/- 3 vs. 13 +/- 3 ms (p less than 0.05)], and isometric contraction time [ICT, 39 +/- 7 vs. 32 +/- 4 ms (p less than 0.05)], were all significantly longer in the coarctation group after isoproterenol infusion. The results demonstrate that, even though cardiac output increased adequately during loading and mechanical pumping efficiency was preserved, excitation-contraction coupling was still prolonged. Thus, an anatomical successful coarctectomy, even at the age of 10 months, does not fully restore left ventricular function in dogs after chronic experimental coarctation.

Accuracy of gated equilibrium radioventriculography in measuring left ventricular function in dogs.

To assess the precision of gated equilibrium radioventriculography in measuring changes in left ventricular stroke volume (LVSV), we studied five dogs each with a chronically implanted electromagnetic flowmeter on the ascending aorta. Per cent changes in left ventricular stroke counts (LVSC) were compared to those in LVSV following acute changes induced by positive end respiratory pressure. We have compared LVSCs calculated in five different ways: (1) Manual outlining of LV region of interest (LVROI), either single fixed enddiastolic (ED) ROI or ED and endsystolic (ES) ROIs with the aid of functional images (first harmonic of Fourier analysis); (2-5) automatic outlining of LV ROI (the algorithm generated 30 profiles on which the maximum of second derivative delineated the LV edges) was performed either on ED image or both ED and ES images. For these four methods a crescent-shaped ROI for background correction was manually drawn at the border of the LV ROI. The fifth method used an automatically drawn single fixed LVED ROI with interpolative background substraction (IBS) between LV and RV edges. LVSC changes, calculated with the IBS method correlated better with LVSV changes than the other four methods. Thus assessment of small LVSC changes is highly processing-dependent.

Acute effects of doxorubicin (adriamycin) on left ventricular function in dogs

Although chronic doxorubicin (adriamycin) cardiotoxicity often is attributed to repeated episodes of acute myocardial injury, the acute effects of doxorubicin on in vivo left ventricular performance have not been studied in a carefully controlled setting. Accordingly, we recorded high-fidelity left ventricular pressures and segmental dimensions before and after either intravenous or intracoronary doxorubicin in twelve open-chest dogs. Propranolol was administered to prevent reflex sympathetic stimulation, and heart rate was held constant by atrial pacing. Intravenous doxorubicin (1.5 mg/kg) ( n = 6) caused significant decreases in all measured indices of myocardial contractility, in association with a large decrease in left ventricular systolic pressure (125 ± 28 and 81 ± 23 mm Hg before and 5 min after doxorubicin, respectively, P < 0.01). Intracoronary doxorubicin (0.075 to 0.3 mg/kg) ( n = 6) caused similar decreases in percent segment shortening (from 19 ± 7 to 16 ± 8, P < 0.05), mean normalized shortening rate (from 0.87 ± 0.34 to 0.71 ± 0.37 segment lengths/sec, P < 0.05), and peak positive left ventricular dP dt (by 10 ± 11%, P < 0.07), although left ventricular systolic pressure was only modestly decreased (126 ± 20 and 113 ± 17 mm Hg before and after doxorubicin, respectively, P < 0.01). Intracoronary doxorubicin also slowed the rate of left ventricular relaxation, as evidenced by an increase in the time constant for isovolumic pressure fall from 32.0 ± 9.0 to 36.9 ± 7.5 msec, and significantly altered the relationship between left ventricular pressure and dimension at end-diastole. We conclude that a single dose of doxorubicin can acutely alter both systolic and diastolic left ventricular function in dogs. These effects are nearly immediate in onset, and are independent of potential functional alterations due to drug-induced systemic hypotension.

Effects of Oral Amiodarone on Left Ventricular Function in Dogs: Clinical Implications for Patients with Life-Threatening Ventricular Tachycardia

Twenty-four mongrel dogs were divided into two equal groups to determine the effects of orally administered amiodarone on left ventricular function. Measurements of left ventricular function included left ventricular contractility as denoted by maximum rate of rise of left ventricular pressure (dP/dt max), cardiac index (CI), left ventricular stroke work index (LVSWI), and peripheral vascular resistance (PVR). Left ventricular function was measured in 6 of the 12 animals in Group 1 before and after 14 days of amiodarone administered orally; the remaining animals served as controls. The dP/dt max was reduced from 2,855 to 1,291 mm Hg/sec ( p < 0.01), and LVSWI fell from 1.6 to 0.74 gm-m/beat/kg ( p < 0.05) in the 6 animals given amiodarone. The 12 animals in Group 2 underwent 30 minutes of ischemic arrest. Six animals in Group 2 underwent 30 minutes of ischemic arrest. Six animals were given amiodarone orally for 14 days prior to cardiopulmonary bypass and ischemic arrest; the other 6 served as controls. Before cardiopulmonary bypass, the dogs administered amiodarone had significantly greater depression of dP/dt max ( p < 0.01) and LVSWI ( p < 0.05). Thirty minutes of ischemia produced significant depression of left ventricular function in all animals in Group 2. However, a significantly greater reduction in dP/dt max and LVSWI occurred in those animals receiving amiodarone. Furthermore, 4 of the 6 dogs receiving amiodarone were unable to sustain sufficient cardiac output following cardiopulmonary bypass to permit long-term survival ( p < 0.05). These data demonstrate that the oral administration of amiodarone results in a significant depression of left ventricular function and suggest that amiodarone should be used with caution in patients with impaired left ventricular function.

Effects of direct-current electrical shocks on systolic and diastolic left ventricular function in dogs

Although direct-current (DC) electrical shocks do not significantly alter left ventricular systolic performance, their effects on ventricular diastolic properties and the role of sympathetic stimulation in maintaining postshock contractility are unknown. Accordingly, we studied both diastolic and systolic left ventricular performance in seven open-chest dogs before and after three consecutive 50 joule DC shocks applied directly to the heart. High-fidelity left ventricular pressure and segmental dimensions were recorded as pressure was varied systematically under conditions of beta-adrenergic blockade. The exponential left ventricular end-diastolic pressure-segment length relationship was not significantly altered by electrical shocks. Likewise, pre- and postshock beats matched for loading conditions did not differ in peak positive dP dt , end-systolic segment length, or percentage of segment shortening, although mean normalized shortening rate decreased by approximately 11% ( p < 0.05). However, the time constant (T) for isovolumic pressure fall, an index of the rate of left ventricular relaxation, increased after shocks in all animals (T = 42.2 ± 5.3 and 51.1 ± 7.0 msec before and after shock, respectively; ( p < 0.01). We conclude that high-energy electrical shocks applied directly to the heart cause modest slowing of left ventricular relaxation but do not have important effects on left ventricular compliance or on systolic myocardial performance. These data suggest that DC shocks have only minor functional consequences when applied to normal hearts, even when sympathetic compensation is prevented.

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.

Effect of sodium nitroprusside on cardiovascular function and pulmonary shunt in canine oleic acid pulmonary edema.

The authors investigated the acute effects of nitroprusside on intrapulmonary shunt (Qs/Qt), cardiac output, and left ventricular function in dogs with normal lungs, and again after they developed oleic acid pulmonary edema. Before oleic acid, nitroprusside reduced pulmonary capillary wedge pressure (PCWP) and stroke volume, and there were no changes in Qs/Qt. Ninety minutes after oleic acid, PCWP, Qs/Qt, and systemic vascular resistance increased and stroke volume decreased. Then nitroprusside increased cardiac output by 35 per cent and increased Qs/Qt from 12 to 18 per cent. After oleic acid, stroke volume increased on nitroprusside from 18 to 23 ml (P less than 0.05) despite reduced preload, as PCWP decreased from 10.4 to 4.4 torr on nitroprusside (P less than 0.05). Increased stroke volume may be explained by the reduction in resistive afterload, as nitroprusside reduced systemic vascular resistance from 60 to 34 torr . l-1 . min. To the extent that canine oleic acid pulmonary edema represents low pressure edema in patients, nitroprusside is a potential treatment to reduce PCWP, pulmonary microvascular pressure, and pulmonary edema while maintaining cardiac output.

Quantitative effects of sodium nitroprusside on coronary hemodynamics and left ventricular function in dogs.

HomeCirculation ResearchVol. 45, No. 3Quantitative effects of sodium nitroprusside on coronary hemodynamics and left ventricular function in dogs. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBQuantitative effects of sodium nitroprusside on coronary hemodynamics and left ventricular function in dogs. D G Pennington, M P Vezeridis, G Geffin, D D O'Keefe, D G Lappas and W M Daggett D G PenningtonD G Pennington Search for more papers by this author , M P VezeridisM P Vezeridis Search for more papers by this author , G GeffinG Geffin Search for more papers by this author , D D O'KeefeD D O'Keefe Search for more papers by this author , D G LappasD G Lappas Search for more papers by this author and W M DaggettW M Daggett Search for more papers by this author Originally published1 Sep 1979https://doi.org/10.1161/01.RES.45.3.351Circulation Research. 1979;45:351–359 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Jugdutt B Nitric Oxide and Cardioprotection During Ischemia-Reperfusion The Role of Nitric Oxide in Heart Failure, 10.1007/1-4020-7960-5_20, (231-245) Lefer A and Scalia R (2001) Nitric Oxide in Inflammation Physiology of Inflammation, 10.1007/978-1-4614-7512-5_22, (447-472), . Zhao G, Zhang X, Xu X, Wolin M and Hintze T (2000) Depressed modulation of oxygen consumption by endogenous nitric oxide in cardiac muscle from diabetic dogs, American Journal of Physiology-Heart and Circulatory Physiology, 10.1152/ajpheart.2000.279.2.H520, 279:2, (H520-H527), Online publication date: 1-Aug-2000. Dorszewski A, Müller-Beckmann B, Kling L and Sponer G (2012) Haemodynamic profile of an inhibitor of phosphodiesterase III, adibendan (BM 14.478): comparison with nitroprusside and dobutamine in conscious dogs, British Journal of Pharmacology, 10.1111/j.1476-5381.1990.tb14141.x, 101:3, (686-690), Online publication date: 1-Nov-1990. Katsamouris A, Mastrokostopoulos G, Hatzinikolaou N, Lappas D and Buckley M (2016) Control of Left Ventricular and Proximal Aortic Dimensional Decompensation During Clamping of Descending Thoracic Aorta, Vascular Surgery, 10.1177/153857448802200505, 22:5, (316-327), Online publication date: 1-Sep-1988. Imai N, Liang C, Stone C, Sakamoto S and Hood W (1988) Comparative effects of nitroprusside and pinacidil on myocardial blood flow and infarct size in awake dogs with acute myocardial infarction., Circulation, 77:3, (705-711), Online publication date: 1-Mar-1988. Gott J, Cox S and Mavroudis C (1987) Nitroprusside abolishes the deleterious effects of surface cooling–induced hypothermia on immature pigs with ventricular septal defects, The Journal of Thoracic and Cardiovascular Surgery, 10.1016/S0022-5223(19)36343-3, 93:5, (647-657), Online publication date: 1-May-1987. Juggi J (1985) Role of Cardioplegia in Cardiac Stress during Surgery Stress and Heart Disease, 10.1007/978-1-4613-2587-1_29, (364-386), . Kawashima S, Liang C, Richeson J and Hood W (1984) Nitroprusside infusion in experimental acute myocardial infarction with systemic hypertension: Effects on systemic hemodynamics and regional myocardial blood flows, The American Journal of Cardiology, 10.1016/0002-9149(84)90093-6, 53:9, (1354-1359), Online publication date: 1-May-1984. Isoyama S, Maruyama Y, Ashikawa K, Sato S, Suzuki H, Watanabe J, Shimizu Y, Ino-Oka E and Takishima T (1983) Effects of afterload reduction on global left ventricular and regional myocardial functions in the isolated canine heart with stenosis of a coronary arterial branch., Circulation, 67:1, (139-147), Online publication date: 1-Jan-1983. Feldman R, Day R, Hill J, Conti C and Pepine C (1983) Comparison of the effects of nitroprusside and nitroglycerin on coronary size, Catheterization and Cardiovascular Diagnosis, 10.1002/ccd.1810090410, 9:4, (391-399), . Sparks H, Scott J and Gorman M (1983) Microcirculation of the Heart The Physiology and Pharmacology of the Microcirculation, 10.1016/B978-0-12-508301-0.50016-8, (361-395), . Yin F, Guzman P, Brin K, Maughan W, Brinker J, Traill T, Weiss J and Weisfeldt M (1983) Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure., Circulation, 67:6, (1330-1339), Online publication date: 1-Jun-1983. Utsunomiya T, Krausz M, Shepro D and Hechtman H (1981) Induction of myocardial damage with nitroprusside, Journal of Surgical Research, 10.1016/0022-4804(81)90221-3, 31:3, (195-200), Online publication date: 1-Sep-1981. Drop L, Geffin G, O'Keefe D, Newell J, Jacobs M, Fowler B, Daggett W and Titus J (1981) Relation between ionized calcium concentration and ventricular pump performance in the dog under hemodynamically controlled conditions, The American Journal of Cardiology, 10.1016/0002-9149(81)90210-1, 47:5, (1041-1051), Online publication date: 1-May-1981. September 1, 1979Vol 45, Issue 3 Advertisement Article InformationMetrics Copyright © 1979 by American Heart Associationhttps://doi.org/10.1161/01.RES.45.3.351 Originally publishedSeptember 1, 1979 PDF download Advertisement

Effect of positive end-expiratory pressure on ventricular function in dogs

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.

Effects of intravenous anesthetic agents on left ventricular function in dogs.

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

Drip retrograde coronary sinus perfusion for myocardial protection during aortic cross-clamping

Moderate hypothermia is one of the methods utilized for myocardial protection when the aortic root is cross-clamped but not opened. A combination of low-pressure, low-flow retrograde coronary sinus perfusion (RCSP) with oxygenated blood at moderate hypothermia (29 degrees C.) was demonstrated to yield significantly better protection to left ventricular function in dogs than does moderate hypothermia alone. Ventricular function was recorded before and after 1 hour of aortic cross-clamping at identical preloads and heart rates. Aortic pressure was returned to a level as close to base line as possible by constriction of the descending aorta. The average mean aortic pressure of the animals perfused retrograde at 29 degrees C. was returned to within 4 per cent of base line. By contrast, in the animals protected with moderate hypothermia alone, the pressure could be returned only to a level which was 37 per cent lower than base line. In animals protected with moderate hypothermia alone, cardiac output dropped 62 per cent, left ventricular stroke work (LVSW) 75 per cent, and peak dp/dt 44 per cent. In the animals protected with RCSP and moderate hypothermia, the cardiac output dropped 6 per cent, LVSW 9 per cent, and peak dp/dt 5 per cent. The differences in the changes noted between these two groups were significant for LVSW and dp/dt at a level of p less than 0.01 and for cardiac output and aortic pressure at a level of p less than 0.05. These results suggest that RCSP may be indicated when moderate hypothermia is otherwise chosen to be the sole source of myocardial protection.

Influence of efferent vagal stimulation of left ventricular function in dogs.

Influence of efferent vagal stimulation of left ventricular function in dogs.

Effect of free fatty acid on the oxygen consumption of perfused rat heart.

Effect of free fatty acid on the oxygen consumption of perfused rat heart.