Aortic Output Research Articles

Temperature-dependency of nifedipine as a protective agent during cardioplegia in the rat.

An isolated working rat heart preparation was used to characterise the temperature-dependency of the anti-ischaemic properties of nifedipine. In this study hearts were subjected to pre-ischaemic infusion with the St Thomas' cardioplegic solution with or without added nifedipine (0.075 mumol X litre-1). Hearts were then rendered globally ischaemic for various periods, (35, 42, 48, 56, 55, 65, 80, 105 or 130 min) at various temperatures (37.0, 35.5, 34.0, 32.5, 31.0, 29.0, 27.0, 24.0 or 20.0 degrees C, respectively). The duration of ischaemia at each temperature was selected to produce a post-ischaemic (37 degrees C) recovery of aortic flow that was approximately 50% of its pre-ischaemic (37 degrees C) control. In addition to functional indices (aortic flow, cardiac output, coronary flow, aortic pressure and heart rate) creatine kinase leakage during reperfusion was measured. At all temperatures at or above 31 degrees C the addition of nifedipine enhanced significantly (maximal value = 43%) the post-ischaemic recovery of aortic flow and other indices of pump function, while at the same time reducing significantly (by up to 56%) enzyme leakage. At ischaemic temperatures below 31 degrees C nifedipine failed to afford any significant additional protection when assessed functionally or enzymatically. It would therefore appear that hypothermia either blocks the action of nifedipine or, by acting on some common mechanism, renders the actions of the drug redundant.

Use of gated perfusion to study early effects of anoxia on cardiac energy metabolism: a new 31P NMR method.

A novel 31P NMR method is described that is capable of determining rapid changes in the intracellular levels of various phosphorus-containing compounds in an isolated, perfused working rat heart. This technique involves the gating of 31P NMR measurements to a heart that is alternately perfused with a modified Krebs-Henseleit medium containing 10 mM pyruvate and equilibrated with either 95% O2/5% CO2 or 95% N2/5% CO2. The experimental design allows up to three NMR measurements to be made during a single O2/N2 perfusion cycle. When these measurements are repeated at different intervals during the cycle, rapid changes in metabolite levels can be determined. Preliminary studies have shown that hearts remain hemodynamically stable to the aerobic/anoxic perfusion cycle as judged by heart rate, peak systolic pressure, aortic output, and coronary flow for at least 80 min in the magnet when subjected to cycle times of 4.5-s O2 and 1.5-s N2 perfusions. NMR measurements made under these conditions showed that a transition from full aerobic perfusion to this cycle revealed a new steady state, with an increased inorganic phosphate level from 6% total observable phosphorus to 10% and a possibly significant decreased measurement of creatine phosphate level (from 35 to 31%). Comparison of individual NMR measurements made during this perfusion cycle shows apparent rapid cyclical variations in intracellular pH and the levels of Pi, ATP, and NAD(H). These changes, expressed as variations above and below mean values measured during the cycle, showed that (a) intracellular pH, as measured by the chemical shift of Pi, reversibly decreases by more than 0.1 pH unit within 0.5-1 s following maximal anoxic perfusion and (b) coincident with a decrease in intracellular pH, Pi levels increased by a maximum of 30-40% whereas ATP levels decreased by a maximum of 15-20%. The amount of total observable phosphorous detected during the cycle is essentially constant. Unexpectedly, creatine phosphate levels are most stable, indicating that their levels are being maintained at the expense of ATP. Also unexpected is the finding that NAD(H) levels varied from maximal to undetectable levels during the perfusion cycle. The current method of aerobic/anoxic perfusion is capable of resolving metabolic events much faster than previous NMR methods and yielding information that is unobtainable by any other technique.

Hyperosmolarity and cardiac function in chronic diabetic rat heart.

Serum hyperosmolarity is commonly associated with the poorly controlled diabetic state. The current investigation revealed that increased perfusate osmolarity using either glucose or mannitol caused a gradual decline in the aortic output of hearts from both normal and diabetic rats. However, aortic output decreased less rapidly in hearts from diabetic rats. Decreasing the extracellular calcium concentration to a level resulting in one-third of the maximal aortic output elicited a greater and more prolonged increase in aortic output from the diabetic compared with the normal heart when perfusate osmolarity was progressively increased. The coronary conductance of diabetic rat hearts improved when hyperosmolar solutions of either mannitol or glucose were utilized, irrespective of the external calcium ion concentration. In normal hearts, the coronary conductance tended to decline at higher perfusate osmolarities. The increased coronary conductance may play a role in the enhanced performance of diabetic hearts at higher levels of osmolarity. Hyperosmolar solutions influence the performance of hearts from chronic diabetic rats in a positive inotropic manner at low extracellular calcium concentrations (1 mM). These lower calcium levels are close to the normal physiological range of the freely ionized serum calcium. This effect is greater in hearts from diabetic animals than from normal animals and is similar to that obtained when perfusate calcium is increased. The results suggest that hyperosmolar solutions enhance calcium availability in the hearts of diabetic animals.

Response of the bronchial circulation to acute hypoxemia and hypercarbia in the dog.

We have examined the effect of acute hypoxemia and hypercarbia on bronchial blood flow (Qbr) in 10 anesthetized, ventilated, open-chest dogs using a modification of the radioactive microsphere technique. After surgery, dogs were divided into two groups of five. Group 1 was ventilated for 30 min with each of the following gas mixtures: 1) room air; 2) 15% O2-85% N2; 3) 10% O2-90% N2, and group 2 with 1) room air; 2) 5% CO2-30% O2-65% N2; 3) 10% CO2-30% O2-60% N2. Measurements of pulmonary arterial, left atrial and aortic pressures, cardiac output, and blood gases were made before injection of 46Sc-, 153Gd-, and 103Ru-labeled microspheres into the left atrium as a marker of Qbr. After the final measurements, dogs were killed and the lungs removed and the parenchyma stripped off the large and small airways of the left lung. Knowing the radioactivity in the trachea, bronchi, parenchyma, and in the blood from the reference-flow sample and also the aortic and left atrial pressures, total and regional Qbr, and bronchovascular resistance (BVR) were calculated. Results showed that acute hypoxemia (10% O2) caused a significant (P less than 0.05) decrease in Qbr and increase in BVR and acute hypercarbia (10% CO2) caused a significant (P less than 0.05) increase in Qbr and decrease in BVR.

Large V waves in the pulmonary capillary wedge pressure tracing without mitral regurgitation: the influence of the pressure/volume relationship on the V wave size.

We have previously demonstrated that a large V wave in the pulmonary capillary wedge tracing may occur in the absence of mitral regurgitation. This study evaluates the role of left atrial and pulmonary vein compliance on such a finding. We studied 11 patients with coronary disease, without clinical or angiographic mitral regurgitation. Heart rate, pulmonary capillary wedge mean, A and V waves, V-wave slope, left ventricular and aortic pressures, cardiac output, and left atrial echo and apical phonocardiogram were recorded simultaneously. Preload was modified acutely by volume overload and by the administration of i.v. nitroglycerine. Volume administration induced a marked increase in V-wave pressure (13.0 +/- 9.6 vs. 27.0 +/- 9.6 mmHg, p less than 0.05), without producing mitral regurgitation, and without appreciable change in left atrial dimension by echo (33.0 +/- 4.9 vs. 35.5 +/- 5.2 mm, NS), or stroke volume (101.7 +/- 26.2 vs. 97.8 +/- 34.3 ml, NS). An increase was also seen in the A wave (13.6 +/- 8.9 vs. 23.3 +/- 8.5 mmHg, p less than 0.05), pulmonary capillary wedge mean pressure (9.8 +/- 7.2 vs. 20.6 +/- 7.8 mmHg, p less than 0.05), and left ventricular diastolic pressure (7.4 +/- 5.5 vs. 14.6 +/- 6.3 mmHg, p less than 0.05). All values returned to baseline after nitroglycerine. The compliance of the left atrium/pulmonary veins decreased with increasing pulmonary capillary wedge pressures. With large filling volumes, a small stroke volume brings on a large pressure change, thus explaining the finding of large V waves in patients with elevated pulmonary capillary wedge pressure and without mitral regurgitation.

Pharmacological effects of pyrethroids on the cardiovascular system of the rat

The cardiovascular actions of two pyrethroids, deltamethrin and cismethrin, were assessed using the pithed rat, the isolated working heart, and perfused mesentery preparations. Deltamethrin but not cismethrin, increased mean arterial pressure and differential pressure in the pithed rat, and the aortic output and mean systolic aortic pressure in the working heart. Reserpine pretreatment reduced, but did not abolish, the pressor response to deltamethrin in the pithed rat and working heart, but did not reduce the increase in aortic output following deltamethrin in the working heart. In the perfused mesentry, deltamethrin did not modify the action of exogenous noradrenaline, but increased the response to 10 Hz stimulation. It is concluded that the cardiovascular effects of deltamethrin are due to both increased catecholamine release in peripheral vascular beds, and to a direct positive inotropic effect on the heart. The results also provide a distinction between the action of the two pyrethroids in terms of their cardiovascular activity.

Effects of acute vagally-mediated bradycardia on systemic hemodynamics and coronary blood flow before and after coronary stenosis.

The effects of short episodes (1 min) of vagally-mediated bradycardia were studied in 9 anesthetized dogs utilizing vagal stimulation and slow atrial pacing (120 and 80 beats/min) before and after graded coronary constriction of the left anterior descending (LAD) and the left circumflex (CCA). In the presence of 90% LAD stenosis, bradycardia tended to restore both the elevated total LAD coronary vascular resistance (CVR-LAD) and the reduced, total CVR-CCA towards control levels obtained at corresponding slow rates in the absence of coronary stenosis; as a result, LAD coronary flow (F-LAD) was relatively less reduced and the accessory rise of F-CCA disappeared. In the presence of combination of 90% LAD plus 70% CCA stenosis, the effects of bradycardia on total CVR-LAD and F-LAD were similar to those obtained with single 90% LAD stenosis, but the accessory flow through the CCA was abolished resulting in no significant difference of the rate-dependent alterations of total CVR-CCA and F-CCA as compared with those observed in the absence of coronary stenosis. In the presence of single or combined coronary stenosis, bradycardia restored the depressed aortic pressure and cardiac output towards control values obtained at comparable slow rates before coronary stenosis. The results support the concept that in the presence of 90% LAD stenosis vagally-mediated bradycardia 1) decreases the tension-time index (myocardial nutritional demand) shifting cardiac performance to less expensive "flow work" and 2) facilitates antegrade flow through the highly stenotic LAD thereby inhibiting accessory flow through the nonstenotic CCA.

Measurement of regional bronchial arterial blood flow and bronchovascular resistance in dogs.

Little is known about normal variations and control of bronchial blood flow and bronchovascular resistance. We have used the reference-flow technique and 15-microns-diameter microspheres to measure bronchial blood flow under physiological conditions. Dogs (n = 13) were anesthetized and ventilated, and their chests were opened. A ligature was placed loosely around the left main pulmonary artery, and the left atrium was cannulated. In six dogs three sets of microspheres were injected simultaneously into the left atrium, and in another seven dogs the three sets of microspheres were injected sequentially at 0.5-h intervals. Prior to each injection measurements of pulmonary arterial, left atrial, and aortic pressures, cardiac output, and blood gases were made. Five seconds after injection the left main pulmonary artery was transiently occluded to prevent recirculation. After the final injection, dogs were killed, the lungs were removed, and the parenchyma was stripped off the large and small airways of the left lung. Knowing the radioactivity in the trachea, bronchi, parenchyma, and in the reference flow blood and also the aortic and left atrial pressures, we calculated bronchial blood flow (ml X min-1 X g dry lung-1) and bronchovascular resistance (cmH2O X ml-1 X min X 100 g dry lung). Results showed that there were no significant differences between the three measurements of bronchial blood flow when microspheres were injected simultaneously or sequentially. Bronchial blood flow to the left lung was 0.4% of cardiac output; 55% of the total flow went to lung parenchyma and 45% to trachea and bronchi. Expressed as flow/g dry lung the greatest flow was to the airways.

Influence of vascular parameters on the effectiveness of intra-aortic balloon pumping: a model study.

The intra-aortic balloon pump has been widely used as a temporary heart-assist device. In this investigation, a nonlinear mathematical model of the arterial system and intra-aortic balloon pump was studied analytically. Thus, the influences of a number of vascular parameters on the effectiveness of intra-aortic balloon pumping (IABP) were determined. The effects of changes in vascular parameters of the model on a number of performance indexes were investigated. These performance indexes (aortic mean diastolic pressure, aortic end diastolic pressure, cardiac output, coronary flow and phase differences between the fundamental Fourier components of aortic root pressure and flow) were used as the criterion for an evaluation of the effectiveness of the assist pump. The following vascular parameters were perturbed by four steps (±10%, ±20%) from the values in the standard model: heart rate, peripheral resistance, left ventricular pressure, aortic elastance, aortic radius, arterial wall thickness, and aortic length. This model was evaluated for a wide range of balloon-pump phase-control settings (assisted case) and for the unassisted case (when the pump is disabled). It is concluded that changes in heart rate, peripheral resistance and left ventricular pressure cause the most significant changes in pump performance.

Improved functional recovery of ischemic myocardium by suppression of adenosine catabolism

Isolated working rat heart preparations were used to ascertain whether the addition of adenosine and prevention of its catabolism could aid in the functional recovery of hearts following global ischemia. Hearts were infused with either 80 micro M EHNA (an adenosine deaminase inhibitor) or 20 micro M adenosine and EHNA in either normal (2.4 mM) or low (0.05 mM) calcium-containing buffer prior to clamping of the aorta for 30 minutes. In one series of hearts, postischemic concentrations (mumoles/gram wet weight) of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP), adenosine, inosine, and hypoxanthine were measured; in another series, the recovery of aortic flow rate was used as a measure of functional recovery of ventricular muscle. With normal electrolyte balance, EHNA was unable to protect hearts against ATP loss and ventricular failure. Hearts with EHNA + adenosine recovered 14% of preischemic aortic output and ATP levels were slightly elevated at 0.93 mumole/gm. Those treated with either EHNA or EHNA + adenosine in low-calcium buffer recoverd 100% of their original aortic output. However, EHNA + adenosine maintained considerably higher ATP levels (1.57 mumoles/gm) than did EHNA alone (1.14 mumoles/gm) and was associated with faster initial recovery of aortic output. Thus the prevention of adenosine catabolism was insufficient for adequate ventricular recovery unless the tissue ATP was maintained above about 1.0 mumole/gm. EHNA + adenosine in a 0.05 mM Ca++ infusion solution conserved ATP, markedly improved the functional recovery of hearts, and thus may have a role to play in myocardial preservation during elective cardiac arrest.

Baroreceptor output during normal and obstructed breathing and Mueller maneuvers.

Cardiovascular control during asthma and other forms of obstructed breathing has not been extensively investigated. Previous studies in dogs have shown that obstructed breathing or an inspiratory effort against a blocked airway (Mueller maneuver) provoke large oscillations in blood pressure. During the inspiratory phase transmural systolic pressure relative to atmosphere drops initially, but transmural systolic pressure relative to intrathoracic pressure can remain unchanged or even increase. Because the carotid baroreceptors are located in the extrathoracic circulation, whereas the aortic baroreceptors are located in the intrathoracic circulation, and each responds to local transmural arterial pressure, simultaneous baroreceptor output from these two areas was measured in the anesthetized cat during normal and obstructed breathing and during Mueller maneuvers. Both whole-nerve and single-fiber preparations showed a significantly decreased output from the carotid baroreceptors during obstructed inspiratory efforts, whereas aortic baroreceptor output decreased significantly less or not at all. Transmural systolic pressure decreased significantly less in the aorta than in the carotid regions. Further, the aortic baroreceptors were more sensitive to changes in pulse pressure than were the carotid baroreceptors. These results suggest a mechanism for stabilizing the cardiac responses to precipitous falls in blood pressure that occur in obstructed breathing.

Reflex cardiovascular response during injection of capsaicin into skeletal muscle.

In an anesthetized dog, injections of capsaicin, a potent stimulator of small myelinated and unmyelinated fibers that originate as free nerve endings, into a neurally intact donor-perfused hindlimb produced a significant (P less than 0.05) increase in mean aortic pressure (20%), heart rate (12%), cardiac output (28%), and respiratory minute volume (97%). Organ blood flows were measured with 25-micrometers radioactive microspheres. During the injection of capsaicin, there was a decrease in renal blood flow (-25%), but liver, spleen, brain, heart, and skeletal muscle flows remained near control values. After section of the afferent neural connection from the donor perfused hindlimb, the responses to the injection of capsaicin were abolished. These reflex cardiovascular and respiratory responses and changes in organ flow caused by stimulation of capsaicin-sensitive receptors in skeletal muscle are similar to those that occur during induced isometric exercise in the hindlimb.

Inhibition by (aminooxy)acetate of the malate-aspartate cycle in the isolated working guinea pig heart.

The quantitative importance of the malate-aspartate cycle and the sn-glycerol 3-phosphate cycle, with respect to the flux of cytosolic reducing equivalents across the mitochondrial membrane, was studied in isolated perfused guinea pig hearts. The heart preparations performed pressure-volume work and metabolized glucose, lactate, pyruvate or 3-hydroxybutyrate. With glucose or lactate as the substrate, (aminooxy)acetate, an inhibitor of the malate-aspartate cycle, caused left ventricular failure, manifested by reduced aortic pressure and cardiac output, in association with a decrease in myocardial oxygen consumption and a depletion of high energy phosphate stores; lactate and particularly sn glycerol 3-phosphate accumulated in the myocardium. Moreover, lactate release rates increased more than 10-fold in presence of glucose and (aminooxy)acetate. Pretreatment of the animals with high doses of triiodothyronine did not prevent the hemodynamic and metabolic alterations caused by (aminooxy)acetate. In contrast, (aminooxy)acetate did not affect performance and energy-yielding metabolism when hearts metabolized pyruvate or 3-hydroxybutyrate as the substrate. From the findings it is concluded that the malate-aspartate cycle preponderates over the sn-glycerol 3-phosphate cycle in the working guinea pig heart, even when sn-glycerol 3-phosphate accumulates.

Inhibition of fatty acid oxidation in normal and hypoxic perfused rat hearts by 2-tetradecylglycidic acid

Studies with a new fatty acid oxidation inhibitor, 2-tetradecylglycidic acid, showed that half-maximal inhibition of oleate oxidation occurred at concentrations of 3 × 10 −6 m. 2-Tetradecylglycidic acid also inhibited endogenous fatty acid oxidation, but had little effect on octanoate oxidation. The inhibition of long chain fatty acid oxidation produced by 2-tetradecylglycidic acid depended on its time exposure to the hearts. At low work loads it had no effect on left ventricular pressure development or aortic output, but was inhibitory at high work loads when the capacity for glucose oxidation was exceeded. The relationship of oleate concentration (with 2% albumin present) to pyridine nucleotide fluorescence and to the stimulation of oxygen consumption was examined using hearts perfused with glucose. Pyridine nucleotide fluorescence and oxygen consumption were both increased, with half-maximal effects occurring at 0.08 m m and 0.2 m m oleate, respectively. Oleate addition, both in the absence and presence of insulin, increased oxygen consumption to a greater degree than expected from the theoretical decrease of the P O ratio associated with fatty acid oxidation. At fatty acid/albumin molar ratios of 2.5 or greater, contractility was impaired and oxygen consumption increased even further. Pyridine nucleotides remained reduced indicating the absence of an uncoupling effect on oxidative phosphorylation. The oxygen wasting effect of fatty acids is interpreted as caused by long chain fatty acyl-CoA formation and hydrolysis. In working heart preparations made hypoxic by lowering the perfusate oxygen content to about 35%, addition of 1 m m oleate to the perfusate resulted in a reversible decrease in left ventricular pressure development and aortic output. Perfusion with 5 × 10 −5 m 2-tetradecylglycidic acid for 40 min before oleate addition prevented this deleterious effect of oleate during hypoxia. Photographs of the surface pyridine nucleotide fluorescence showed that addition of oleate to the hypoxic heart resulted in an increase in the size and number of anoxic areas. Subsequent addition of 10 −5 m 2-tetradecylglycidic acid caused the anoxic areas to disappear. These results indicate that the deleterious effects of fatty acids on the hypoxic myocardium are due to an increased oxygen demand resulting from accelerated fatty acid oxidation.

Cardiac performance of isolated perfused hearts from alloxan diabetic rats

Acute alloxan diabetes (3 days) in the rat resulted in a decreased ability of the isolated perfused working heart to respond to increased atrial filling pressure with normal systolic (aortic) pressure development, using a physiologic concentration of glucose (5 mM) as substrate. The diabetic heart also exhibited impaired cardiac output, which could be attributed entirely to decreased aortic output without any apparent effect on coronary flow. This decrease in ventricular performance was accompanied by a 40% reduction in glucose uptake and a 20% reduction in tissue ATP concentrations even though perfusate glucose levels remained at or near physiologic levels. Perfusion of hearts with 5 mM glucose plus 10(-8) M insulin, with 10 or 30 mM glucose, or 1 mM octanoate reversed the diabetes-related decrease in systolic pressure development, cardiac output, and tissue ATP content. These data demonstrate that the defect in cardiac performance with increased work loads associated with acute insulin deficiency is due to the relative inability of the heart to utilize physiologic concentrations of glucose as substrate for energy production.

Use of a model for simulating individual aortic dynamics in man

A simulation model is suggested for the analysis of aortic dynamics in man. The aortic model consists of six segments and is part of a larger model of the closed-loop human circulation. The model is simulated on a special-purpose analogue computer. Three parameters are employed to characterise the arterial system; peripheral resistance, aortic compliance and peripheral damping. Using a method for adapting the model to the individual patient, measurements of aortic pressure, cardiac output and pulse transmission time from 29 patients were used to test the validity of this approach. The model is able to simulate the pressure course along the aorta satisfactorily. The compliance calculated from the transmission properties of the aorta was compared with the complicance calculated from the stroke volume and pressure pulse. An adequate correlation (r=0.98) was found between these two independent methods. The mean compliance of the total aorta was 0.6 ml/mm Hg at a mean pressure of 104 mm Hg. The compliance showed large individual variations and decreasing values with increasing age of the patient. It is concluded that the model enables simulation of the individual aorta.

Reversal of myocardial dysfunction in endotoxin shock with insulin

Recent data reported from this laboratory have documented myocardial functional depression in endotoxin shock. The purpose of the present study was to determine the effects of insulin on the dysfunctioning canine myocardium subjected to lethal endotoxin shock. Experiments were conducted on isolated working left ventricular preparations in which LD90-100 endotoxin was administered prior to, or following, isolation of the heart. Determinations of myocardial performance were conducted under the conditions of controlled mean aortic pressure and cardiac output. Myocardial dysfunction occurred between 2 and 6 h postendotoxin, as evidenced by significantly increased left ventricular end-diastolic pressure, decreased power, and depressed negative dP/dt, although blood glucose concentrations were maintained at control values. Intraatrial infusions of insulin at rates of 6 U/min reversed all signs of myocardial dysfunction. During insulin infusion, heart rates decreased (p less than 0.02) and myocardial lactate uptake increased (p less than 0.02), while oxygen uptake and coronary blood flow were insignificantly altered.

Evaluation of a nonhemolytic left ventricular assist pump

Cardiogenic shock following acute myocardial infarction is associated with a mortality rate as high as 95%. The treatment of cardiogenic shock with inotropic agents increases heart work and myocardial oxygen consumption. The increase in oxygen consumption is, in general, not met by a proportionate increase in coronary blood flow because of existing coronary artery disease and an inadequate coronary filling pressure. One technique to assist the heart, counterpulsation, employed a suction withdrawal pump connected to a cannula in the abdominal aorta [3, 6, 201. The pump was synchronized with the cardiac cycle to withdraw blood from the aorta during systole and reinfuse it during diastole, reducing aortic pressure and myocardial oxygen consumption while increasing coronary flow. Unfortunately, the excellent hemodynamic result was overshadowed by significant levels of hemolysis as a result of the pumping process [6]. The catheter technique of counterpulsation has been abandoned for the balloon assist technique [ 141. A sausage shaped balloon tipped catheter placed in the descending thoracic aorta is inflated in diastole and deflated in systole. This technique augments aortic diastolic pressure and cardiac output and reduces tension time

Production of Controlled Reversible Left Ventricular Failure in Calves Using Intracoronary Lidocaine Hydrochloride: A Useful Method of Evaluating Left Ventricular Assist Devices

The experimental production of stable, controlled, short-term left ventricular failure is valuable in the evaluation of implantable circulatory support systems. Acute or chronic left ventricular failure produced by occlusion or embolization of coronary arteries results in muscle dysfunction and degrees of failure that may be difficult to control. The effects of varying amounts of intracoronary lidocaine were studied during short- and long-term evaluations of intracorporeal left ventricular assist pumping. In 8 Hereford calves the left main coronary artery was cannulated with an intracoronary catheter in open and closed chest preparations. Dose-related negative inotropic effects were noted when lidocaine was injected at individual doses of 50, 75, and 100 mg. Following 100 mg doses, mean aortic pressure, cardiac output, and maximum rate of rise of left ventricular pressure decreased; left ventricular end-diastolic pressure increased fourfold. Similar effects were noted with short continuous infusions of lidocaine. The initial responses to injection or continuous infusions, if effective, were noted within 40 to 60 seconds. Several episodes of failure could be produced with either method following recovery periods of 10 to 15 minutes. In all instances, actuation of a left ventricular assist device immediately reversed the hemodynamic effects of the pharmacologically induced failure.

Hemodynamic evaluation of the Lillehei-Kaster pivoting disc valve in patients

Forty-five patients with Lillehei-Kaster pivoting disc valves had intraoperative assessment of valve hemodynamic function by simultaneous recording of aortic, left ventricular, and left atrial pressures and cardiac output. Mean transvalve gradients and prosthetic valve areas were calculated and recorded. Comparison of the results with data previously reported on the caged-ball valves indicates that the Lillehei-Kaster pivoting disc valve has superior hemodynamic characteristics.