A comparison of the cardiovascular effects of enflurane, halothane, methoxyflurane and fluroxene during open cardiac surgery.

During open heart surgery hemodynamic changes due to 1.5% enflurane, 0.75% halothane, 0.18% methoxyflurane and 3.4% fluroxene have been compared. The following parameters have been measured: arterial pressure, heart rate, cardiac output, right and left atrial pressure, left ventricular pressure and dp/dt. The strongest effects were found with enflurane and halothane. Marked reduction in cardiac index, stroke index, left ventricular dp/dt as well as reduction of peripheral resistance caused severe systemic hypotension. Because of its slow uptake methoxyflurane was followed by small hemodynamic changes in this study. The rapid acting fluroxene had caused only minor reductions of cardiac output, stroke volume and dp/dt. There was no decrease in peripheral resistance.     

Effects of acute hypoxia on cardiovascular dynamics, myocardial metabolism and ECG in dogs

In pentobarbital-pancuronium anesthetized open chest dogs, left ventricular pressure (LVP), first derivative of LVP (dp/dt) and left ventricular end-diastolic pressure (LVEDP) were measured by a micromanometer tipped catheter, stroke volume and cardiac output (CO) by an electromagnetic flow meter and coronary sinus blood flow (CSBF), by a thermal dilution catheter, respectively. Mean arterial pressure (mAP), mean pulmonary arterial pressure (mPAP), lead II of ECG and esophageal temperature were monitored. Blood gas, catecholamines and lactate of arterial blood and coronary sinus blood were measured and myocardial lactate extraction ratio (MCL) was calculated. As an index of contraction, maximum positive dp/dt (+dp/dt max), and as an index of relaxation, the time constant (T) of isovolumic left ventricular pressure fall were employed, respectively. Acute hypoxia was induced by the inhalation of a 5% O2-95% N2 gas mixture and arterial blood oxygen pressure was maintained between 15 and 20 mmHg. Along with the advancement of hypoxia, +dp/dt max, CO and mAP gradually increased and peaked in 5 minutes. Thereafter, these parameters began to decrease and CO fell to zero in 20 minutes. mPAP and HR slowly increased and peaked in 9 and in 12 minutes, respectively. T was progressively prolonged throughout the hypoxia. CSBF/CO ratio was increased and stayed at a high level even after CO began to decrease. MCL decreased and changed from positive values to negative ones in 5 minutes. Epinephrine and norephinephrine concentrations slowly increased and peaked in 16 minutes. A gradual decrease in the R wave, shortening of the R-R interval and lengthening of the QTc interval were observed in ECG. This study indicated that the left ventricular relaxing function was impaired earlier than contracting function by acute hypoxia and that conversion of the augmented left ventricular contractile state to the depressed one coincided with conversion of myocardial lactate extraction to its production.     

Maximal rate of fall of left ventricular pressure in cardiomyopathy and constrictive pericarditis.

The maximal rate of fall of left ventricular pressure (peak negative dp/dt) was measured in 4 patients with congestive cardiomyopathy (primary myocardial disease), in 5 patients with constrictive pericarditis and in 3 controls. Measurements were made at rest, with leg raising, after a bolus of 6 mug intravenous isoprenaline, and in patients with constrictive pericarditis during pulsus paradoxus. Peak negative dp/dt was 1810 +/- 234 mmHg/sec in controls; it was reduced in patients with constrictive pericarditis (1337 +/- 514 mmHg/sec) and greatly decreased in patients with congestive cardiomyopathy (812 +/- 190 mmHg/sec). There was close linear correlation between resting peak positive and peak negative dp/dt and there was little change with leg raising. Isoprenaline caused an increase in peak positive dp/dt, but there was only a small change in peak negative dp/dt. In patients with constrictive pericarditis, peak negative dp/dt varied during pulsus paradoxus: the linear relationship to peak positive dp/dt was maintained throughout the respiratory cycle. Peak negative dp/dt may be a useful index of myocardial function.     

Mechanism Responsible for the Cardiovascular Depressant Effect of Protamine Sulfate

The mechanism of protamine-induced hypotension and bradycardia was investigated in anesthetized, heparinized dogs. Several groups of animals with intact circulation were studied for their responses to protamine under control conditions and following the administration of various pharmacological agents. The parameters observed include femoral arterial pressure (FAP), central venous pressure (CVP), left ventricular pressure (LVP) and its rate of rise (dp/dt), left ventricular contractile element velocity of shortening (Vce), maximal Vce (V max) and cardiac output (CO). Various groups were studied under the following pharmacological conditions: autonomic cholinergic blockade by atropine; alpha and beta adrenergic receptor blockade using phenoxybenzamine and propranolol respectively; ganglionic and adrenal medullary block using hexamethonium, and depletion of endogenous histamine by means of compound 48/80. Another group was placed on total cardiopulmonary bypass thus isolating the heart from the peripheral circulation. The effect of protamine on the vascular tree alone was then observed by monitoring FAP before and after protamine administration. The findings indicate that the cardiovascular effects of protamine are produced by a direct effect on the myocardium and vascular tree.     

Left ventricular diastolic function of the reperfused postischemic donor heart

This study examined the pathophysiological relationship between left ventricular diastolic function and myocardial biochemical changes during reperfusion following hypothermic cardioplegic preservation of the donor heart. Isolated canine hearts (n=47) were preserved for 6 h at 5°C, followed by normothermic reperfusion for 2 h. Regression analysis demonstrated a highly significant correlation between: Left ventricular maximum –dp/dt and the left ventricular end-diastolic pressure (r=–0.56, P=0.001); myocardial concentrations of adenosine triphosphate (ATP) and Ca²⁺ (r=–0.59, P=0.0001); maximum –dp/dt and myocardial concentrations of: (1) ATP, (2) Ca²⁺, and (3) total adenine nucleotide with left ventricular volume loading (r=–0.53, P=0.003, r=0.51, P=0.002; and r=0.52, P=0.002, respectively); and left ventricular end-diastolic pressure and myocardial Ca²⁺ (r=0.66, P=0.0001). These results suggest that left ventricular relaxation, as assessed by maximum –dp/dt, has a negative correlation with left ventricular stiffness, as determined by the end-diastolic pressure in preserved donor hearts. Furthermore, increased myocardial Ca²⁺ concentrations reflect exhaustion of myocardial ATP. Thus, the myocardial Ca²⁺ concentration correlates directly with wall stiffness and inversely with ventricular relaxation, while ATP concentration correlates directly with ventricular relaxation.     

Experiences with parenteral administration of diltiazem in coronary surgery patients

Diltiazem is a calcium channel blocker whose effects lie between those of the two other important calcium antagonists nifedipine and verapamil. In addition to vasodilation, it has a negative dromotropic effect with prolongation of the A-V interval. In animal experiments and human investigations, diltiazem improves the function of ischemic myocardium due to a direct dilating effect on coronary vessels. The purpose of the present study was to investigate the hemodynamic effects of diltiazem in patients before and during coronary revascularization. METHODS. The study included 60 consenting male patients with coronary heart disease. Twenty premedicated patients randomly received 0.3 mg/kg diltiazem or placebo within 3 min before induction of anesthesia. Hemodynamic measurements (arterial pressure, heart rate, mean pulmonary arterial pressure, pulmonary capillary pressure, right atrial pressure and cardiac output) were taken during the following 21 min. Before cannulation of the great vessels for institution of extracorporeal circulation (ECC), 20 other patients received 0.014 mg diltiazem or placebo/kg per min over 20 min. In addition to the above mentioned hemodynamic measurements, left ventricular parameters (LVP, LVEDP, dp/dt) were directly registered, and 5 min after the end of ECC the measurements were repeated with the same preload as before the ECC. Twenty additional patients received 0.014 mg diltiazem or placebo/kg per min within 21 min during ECC observing arterial perfusion pressure and oxygenator volume. RESULTS. Pre- and intraoperatively diltiazem caused a decrease in mean arterial pressure; cardiac index increased only during the preoperative investigation period (Tables 1, 2), whereas stroke volume index increased pre- and intraoperatively; heart rate decreased in all patients as well as dp/dt (Fig. 1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of transmyocardial punctures on left ventricular performance after coronary occlusion in the acute experiment

The results of multiple transmyocardial punctures were studied in 12 dogs in which ligation of the left descending coronary artery had been performed. Instead of improvement, deterioration in the electrocardiogram, paradoxical movement, left ventricular pressure, left ventricular dp/dt max, and mean aortic flow were observed. These results are in contrast to the acute effects observed by Sen et al. (1965, 1968) but do not exclude the possibility of beneficial long-term effects.     

Thoracic epidural anaesthesia in conscious and anaesthetized rats. Effects on central haemodynamics compared to cardiac beta adrenoceptor and ganglionic blockade

A simple technique for cannulation of the thoracic epidural space in rats was described. 40-50 microliter of epidural bupivacaine 5 mg/ml induced a distribution of sensory analgesia from lower cervical to lower thoracic segments. With this model, effects of thoracic epidural anaesthesia (TEA) on mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), stroke volume (SV), heart rate (HR), central venous pressure (CVP), left ventricular end-diastolic pressure (LVEDP) and maximal increase of pressure in the left ventricle (max dp/dt) were studied in six groups of animals: 1) In conscious animals (n = 10) MAP, CO, SV and HR decreased significantly by 12%, 25%, 10% and 16%, respectively, while SVR increased significantly by 20% during TEA; 2) In chloralose-anaesthetized animals (n = 7) the reduction in CO during TEA was less pronounced and there were no significant changes in SV or SVR; 3) In conscious animals (n = 6) LVEDP, CVP and max dp/dt decreased significantly during TEA; 4) Hexamethonium, when administered to pharmacologically vagotomized conscious animals during TEA (n = 8), induced a significant decrease in SVR (23%) but no change in HR; 5) Changes in haemodynamics after cardiac adrenoceptor blockade with metoprolol, in conscious animals (n = 12), did not differ significantly from those seen during TEA, except for an unchanged SV after metoprolol; 6) 50 microliters of bupivacaine (5 mg/ml) when given i.v. to conscious animals (n = 8) did not affect CO, SV, HR or TPR significantly, while MAP increased slightly but significantly. Thus, in this conscious animal model, TEA almost completely and rather selectively blocked probably mediated by a reflex activation of unblocked sympathetic efferents.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of glucagon in animals on chronic propranolol therapy

Eleven adult mongrel dogs were divided into two groups. Group 1 animals served as controls and Group 2 received propranolol (6 mg/kg/day) orally in divided doses for 15 to 21 days. Prior to cardiopulmonary bypass, cardiac output, first derivative of left ventricular pressure (dp/dt), peak systolic pressure, heart rate, and central venous pressure were recorded. The animals were then placed on cardiopulmonary bypass and subjected to 30 minutes of global ischemia at the myocardial temperature of 32 degrees C. Following cessation of cardiopulmonary bypass the baseline studies were repeated. In Group 2 animals following the repeat studies, glucagon was administered at a rate of 0.13 microgram/kg/min. The cardiac index and dp/dt were decreased by 43.3% (p less than 0.001) and 40.5% (p less than 0.001) in comparison to Group 1 animals. In Group 2 dogs, after bypass and glucagon infusion, cardiac index increased by 38% (p less than 0.02), dp/dt rose by 78% (p less than 0.05), and peak systolic pressure increased by 24.8% (p less than 0.05). These studies show the benefit of glucagon in the treatment of low cardiac output in the presence of beta-adrenergic blockade.     

Hemodynamic effects of endothelin in anesthetized dogs

The purpose of the present study was to investigate and compare the hemodynamic responses that can be elicited in anesthetized dogs by intravenous administration of endothelin at rates of 300 (group E-I, n = 9) and 600 pmol.kg-1 (group E-II, n = 9) for 15 minutes. In group E-I, no significant pressure response was observed after administration of endothelin and cardiac index remained unchanged throughout the experiment. However, right and left ventricular work indices increased significantly but left ventricular maximum dp/dt and pulmonary vascular resistance decreased significantly. In group E-II, mean arterial pressure increased significantly by elevating systemic vascular resistance with marked decrease in cardiac index. However, right and left ventricular work indices remained unchanged throughout the experiment. On the other hand, each dose of endothelin significantly increased pulmonary capillary wedge pressure and left ventricular end-diastolic pressure but decreased heart rate. The present data revealed that the hemodynamic effects were different according to the doses of endothelin infused. In conclusion, our results show that endothelin (600 pmol.kg-1 BW) produces a long lasting increase in arterial pressure and endothelin-induced pressure responses are caused by an elevation in systemic vascular resistance.     

The effects of arterial blood halothane or enflurane concentration on the circulatory system]

The effects of halothane (H) or enflurane (E) concentration on the circulatory system were studied in dogs. Two hours of halothane or enflurane anesthesia resulted in a linear dose-dependent decrease in circulatory indices including mean arterial pressure (mAP), cardiac index (CI) and left ventricular peak dp/dt/IP (peak dp/dt/IP). Systemic vascular resistance (SVR) was unchanged during either anesthesia. The correlations between the percent change of circulatory indices and the logarithm of the blood anesthetic concentrations were expressed by correlation coefficients (r): mAP, r = -0.718 (H), and -0.650 (E): HR, r = -0. 329 (H), and -0.352 (E): CI, r = -0.597 (H), and - 0.596 (E): SI, r = -0.389 (H), and -0.449 (E): SVR, r = -0.161 (H), and -0.030 (E): peak dp/dt/IP, r = -0.708 (H), and -0.871 (E). Using several indices of anesthetic depth including MAC, MAC-EI and MAC-BAR, the percent changes of mAP, CI and peak dp/dt/IP were calculated at the same anesthetic depth using halothane or enflurane. These results indicate that enflurane depresses these circulatory indices more than halothane. The differences were: mAP, 14.51 +/- 1.46%: CI, 8.14 +/- 1.86%: peak dp/dt/IP, 7.38 +/- 3.95% (mean +/- SD).     

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.     

Functional reductions in left ventricular volume. Minimum chamber size consonant with effective hemodynamic performance.

A heart model in dogs was developed to evaluate quantitatively the extent to which left ventricular chamber size could be reduced and yet retain residual mechanical function to perform adequately as a pump. In 9 animals placed on right heart bypass perfusion to control systemic flows; left ventricular performance was estimated from high-fidelity left ventricular pressure and aortic flowmeter recordings and from lateral plane left ventricular angiograms. Studies were made during unrestricted left ventricular filling at varying cardiac outputs and with inflation of a balloon in the left ventricular cavity at a physiological cardiac output. As compared with control data (cardiac output 1.4 L. per minute), balloon inflation to 18.7 ml. caused an increase in total left ventricular end-diastolic volume (from 35.4 to 44.3 ml., p less than 0.001) and left atrial pressure (from 7.8 to 21.2 mm. Hg; p less than 0.001); it also caused a reduction in left ventricular stroke work (from 12.5 to 8.1 Gm.-M., P LESS THAN 0.005) ANd max. dp/dt (from 2,487 to 1,320 mm. Hg per second, p less than 0.05). Importantly, left ventricular stroke volume was unchanged. When compared with preload augmentation (with the balloon deflated), the magnitude of depression of cardiac performance caused by balloon inflation was more fully appreciated (left ventricular stroke work, max. dp/dt, and ejection fraction reduced 69, 61, and 45 per cent, respectively). Even so, with appropriate compensations, principally by the Frank-Starling mechanism, up to 42 per cent of the left ventricular cavity volume could be functionally eliminated with retention of adequate mechanical performance. Such data may have implications regarding the extent of resections possible in patients undergoing surgery for left ventricular aneurysm.     

Quantitative analysis of myocardial revascularization on left ventricular diastolic function

To evaluate the effects of myocardial revascularization on left ventricular diastolic function, we studied three groups of subjects. Group I consisted of 10 patients without any previous myocardial infarction. Group II consisted of 10 patients with previous myocardial infarction. The control group consisted of 8 normal subjects, all with no evidence of cardiac disease as determined by cardiac catheterization. Left ventricular diastolic function was assessed by maximum negative dp/dt, constant T, diastolic compliance and 1/3 fractional filling before and after surgical revascularization. (1) Constant T, maximum negative dp/dt and diastolic compliance: There was no significant difference among groups I, II and the control group preoperatively, and the variables were not improved postoperatively. (2) 1/3 fractional filling: 1/3 fractional fillings in groups I and II were significantly lower (p less than 0.05, p less than 0.01) than the control group preoperatively, and it was significantly improved in group I, but unchanged in group II postoperatively. In conclusion, myocardial revascularization improves left ventricular diastolic function in the patients without previous myocardial infarction. The effects of myocardial revascularization, however, in the patients with prior myocardial infarction do not bring about an enhancement of left ventricular diastolic function.     

Are the cardiovascular actions of dopamine altered by isoflurane?

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 ug · kg^-1 · min^-1. At the dose 20 μf · kg^-1 · min^-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 μg · kg^-1 · min^-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 μg · kg^-1 · min^-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+ 132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone. However, the increase in SVR (at the dose 20 μg · kg^-1 · min^-1) and MAP (at the 10 and 20 μg · kg^-1 · min^-1 doses) by DA was significantly more pronounced with ISO than without ISO. In conclusion, the pressor effects of DA seem to be potentiated by ISO. DA restores systemic arterial pressure during ISO anesthesia by attenuating the cardiac depressant effects of ISO and by increasing SVR above pre-ISO control levels.     

The influence of infused calcium on the postischemic myocardium

Despite evidence for calcium-induced damage in the postischemic myocardium, calcium remains a frequently used inotropic agent following cardiopulmonary bypass surgery with cardioplegic arrest. The purpose of this study was (1) to challenge the postischemic myocardium with incremental doses of ionized calcium, and (2) to relate postischemic calcium reperfusion concentration to final recovery of left ventricular contractile function. Rabbit hearts (N = 38) were perfused and equipped with a ventricular balloon to monitor developed pressure (DP) ±dp/dt, and left ventricular end diastolic pressure (LVEDP). Hearts underwent 40 min of global ischemia. Hearts were then assigned to one of four groups to receive a variable calcium concentration (0.6, 1.2, 2.5, 5.0 mM) for the initial 5 min of reperfusion followed by 55 min of reperfusion (Ca⁺² = 1.25 mM). No differences were found between groups for final recovery of DP ±dp/dt, or final LVEDP. It was concluded that: (1) within the physiologic range, variable calcium infusions during the first 5 min of postischemic reperfusion do not impair final recovery of LV contractile function, (2) irreversible partial recovery of left ventricular function appears due to mechanisms other than mitochondrial or myofibrillar calcium loading during reperfusion, and (3) infused calcium is a safe inotropic agent even in the postischemic myocardium.     

Acute orthotopic transplantation of hearts stored for 72 hours

Using a storage method based on hypothermic (4° C) perfusion with a water-based asanguinous solution the dog heart has been preserved for up to 72 hours in a viable condition. The ultimate functional test of the viability of such hearts is orthotopic transplantation. Seven of eight dog hearts stored for 72 hours were able to support the recipient circulation in a stable manner after acute orthotopic transplantation. The donor hearts maintained a mean arterial pressure of 70-100 mmHg, left atrial pressure 5-12 cm H₂O, and maximum dp/dt of the left ventricular pressure was 1,200-2,400 mmHg/second. No myocardial stimulants were used. The results of 72 hours' hypothermic perfusion storage were superior to those of previously reported six hours' non-perfusion storage. A comment is made on the empirical nature of this field.     

ACTIONS OF 4-AMINOPYRIDINE ON THE CARDIOVASCULAR SYSTEMS OF ANAESTHETIZED CATS AND DOGS

The effects of the anti-curare agent 4-aminopyridine on thecardiovascular systems of cats and greyhounds under barbiturate-chloraloseanaesthesia have been studied. In both species, 4-aminopyridineproduced a transient atropine-sensitive decrease in arterialpressure followed by a prolonged adrenergically-mediated increase.In the cat, the cardiac responses to vagal stimulation and thenictitating membrane responses to sympathetic stimulation wereaugmented after injection of 4-aminopyridine, and the evidenceindicated that these effects were the results of increased releaseof neurotransmitters. In the greyhound, 4-aminopyridine producedincreases in left ventricular systolic pressure and dP/dt max,right atrial pressure, stroke volume, myocardial blood flow,myocardial oxygen consumption, external cardiac work, arterialoxygen content and blood haemoglobin. These effects were attributableto facilitation of sympathetic transmission to the blood vessels,heart and spleen. Heart rate was not much affected because facilitationof vagal transmission to the S-A node counteracted the increasedsympathetic effect. In the greyhound, 4-aminopyridine also producedtemporary cardiac arrhythmia which was only partly attributableto facilitated sympathetic transmission. In addition there wasevidence of a central stimulant action of 4-aminopyridine andof a stimulant action on visceral activity. It is concludedthat, while 4-aminopyridine may be useful in certain relativelyrare conditions of neuromuscular transmission failure, its actionsare too widespread for routine use as an antagonist to non-depolarizingneuromuscular blocking drugs.     

Effects of fluid resuscitation on cardiac dysfunction following thermal injury

To test the hypothesis that low cardiac output in burns is secondary to hypovolemia, the effects of resuscitation on isovolumic contracting rat heart following a full-thickness burn were studied. Sprague-Dawley rats were randomly assigned into three groups: (1) Sham burn, (2) 30% body surface area burn nonresuscitated, (3) 30% body surface area burn with 15 cc Ringer's lactate/180 g body wt ip at the time of burn resuscitated. Twenty hours postburn, the hearts were mounted on a Lagendorff perfusion apparatus. A balloon-tipped catheter placed in the left ventricle measured pressure and dp/dt. Coronary flow was determined. Myocardial samples for ATP and water were obtained. Left ventricular function was evaluated by recording peak systolic pressure, end diastolic pressure, and maximum +/- dp/dt while balloon volume was increased to 0.3 cc. Results are with end diastolic volume constant at 0.15 cc. Compared to sham burn, burn nonresuscitated generated lower peak systolic pressure +/- dp/dt and higher end diastolic pressure while hearts from burn resuscitated generated the same as sham burn. Coronary flow and tissue water content was similar in all. ATP content was lower in burn nonresuscitated. Our data support that impaired systolic and diastolic function in burn nonresuscitated hearts is associated with lower ATP levels not seen in burn resuscitated and reperfusion of burn nonresuscitated hearts does not reverse the myocardial depressant effect.     

Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog

The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. Systemic and coronary hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.25 and 1.75 MAC desflurane, isoflurane, halothane, and enflurane. Desflurane (+79 +/- 12% change from control) produced greater increases in heart rate than did halothane (+44 +/- 12% change from control) or enflurane (+44 +/- 9% change from control) at 1.75 MAC. Desflurane preserved mean arterial pressure to a greater degree than did equianesthetic concentrations of isoflurane. This result was attributed to a smaller effect on peripheral vascular resistance as compared to isoflurane and greater preservation of myocardial contractility as evaluated by peak positive left ventricular dP/dt and the rate of increase of ventricular pressure at 50 mmHg (dP/dt50) compared to other volatile anesthetics. Increases in diastolic coronary blood flow velocity (+19 +/- 6 and +35 +/- 12% change from control at 1.75 MAC, respectively) and concomitant decreases in diastolic coronary vascular resistance (-41 +/- 12 and -58 +/- 6% change from control at 1.75 MAC, respectively) were produced by desflurane and isoflurane. In the presence of autonomic nervous system blockade, the actions of desflurane and isoflurane were nearly identical with the exception of coronary vasodilation. After autonomic nervous system blockade, isoflurane increased coronary blood flow velocity, but desflurane did not. Furthermore, both desflurane and isoflurane continued to produce less depression of myocardial contractility than did halothane and enflurane. In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.