Functional cardiac imaging in mice using Ta-178.
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Animals↗
Biomedical subjects
C J Hartley
Publications and source records attributed to C J Hartley.
Both positive and negative portal venous and hepatic arterial glucose gradients stimulate hepatic glucose uptake after the same amount of glucose is infused into the splanchnic bed in conscious dogs.
We studied the effects of both positive and negative portal venous and hepatic arterial glucose gradients on hepatic glucose uptake after the same amount of glucose was administered into the portal vein and/or hepatic artery. Studies were performed on eight unrestrained conscious dogs with catheters in the portal vein, hepatic vein, gastroduodenal artery, superior mesenteric vein, and femoral artery and Doppler flow probes on the portal vein and hepatic artery. Glucose was infused as follows: protocol 1, 55.6 micromol/kg/min into the portal vein for the first 90 minutes; protocol 2, 27.8 micromol/kg/min into both the portal vein and hepatic artery for the next 90 minutes; and protocol 3, 55.6 micromol/kg/min into the hepatic artery for the last 90 minutes. The portal venous and hepatic arterial plasma glucose gradient was 2.1+/-0.3, -3.0+/-0.5, and -7.1+/-0.6 mmol/L, the rate of hepatic glucose uptake divided by the administered glucose load was 46%+/-11%, 42%+/-10%, and 57%+/-8%, net hepatic glucose uptake was 25.4+/-5.9, 23.5+/-5.6, and 31.6+/-4.6 micromol/kg/min; and the fractional hepatic extraction of glucose was 10.7%+/-2.2%, 11.6%+/-2.5%, and 15.0%+/-2.1%, respectively (mean+/-SEM of three points at 60, 75, and 90 minutes in each protocol). The rate of hepatic glucose uptake divided by the administered glucose load, net hepatic glucose uptake, and fractional hepatic extraction of glucose did not change significantly despite the various portal venous and hepatic arterial glucose gradients. We also studied the effect of the same amount of intraportal glucose infusion for 240 minutes on net hepatic glucose uptake. From 60 to 240 minutes, net hepatic glucose uptake did not change significantly. In conclusion, the liver took up a large amount of glucose administered into the portal vein and/or hepatic artery, regardless of positive or negative portal venous and hepatic arterial glucose gradients. Augmentation of hepatic glucose uptake is not dependent on the signal of the positive or negative portal venous and hepatic arterial glucose gradient.
Animals↗
The age-associated alterations in late diastolic function in mice are improved by caloric restriction.
Caloric restriction reduces the magnitude of many age-related changes in rodents. Cardiac function is altered with senescence in mice, rats, and healthy humans. We examined the effects of life-long caloric restriction on diastolic and systolic cardiac function in situ using Doppler techniques in ad libitum-fed 30- to 32-month-old (AL) and calorically restricted (CR) 32- to 35-month-old female B6D2-F1 hybrid mice. The heart weight to body weight ratio was similar in AL (5.74 +/- .24 mg/g) and CR (5.68 +/- .20 mg/g) mice. Two systolic functional parameters known to decrease with age in both humans and mice, peak aortic velocity and aortic acceleration, were unchanged by CR compared to AL. In contrast, diastolic function was altered by caloric restriction. Although left ventricular peak early filling velocity (E) was not different between CR and AL, peak atrial filling velocity (A) was 50% lower in CR compared to AL (p < .001). The ratio of early diastolic filling to atrial filling (E/A ratio) was 64% higher in the CR (2.74 +/- .31) than the AL (1.55 +/- .07; p = .004). The fraction of ventricular filling due to atrial systole, the atrial filling fraction, was also reduced in CR (.21 +/- .04) compared to AL (.36 +/- .02; p = .007). These changes occurred in CR without alteration in E deceleration time, which is consistent with improved diastolic function in CR. Through mechanisms that remain unknown, lifelong caloric restriction may prevent the age-related impairments in late diastolic function but does not alter the impairments in systolic or early diastolic cardiac function.
Aging↗
Noninvasive determination of pulse-wave velocity in mice.
Some transgenic mice have abnormal vascular function, but arterial geometry and dynamics are difficult to evaluate. To examine whether ultrasonic velocimetry could be used to determine arterial pulse-wave velocity (PWV) in mice, a custom-made 20-MHz pulsed Doppler instrument was used to obtain blood flow velocity signals from the aortic arch and the abdominal aorta 4 cm downstream. The upstroke (foot) of the velocity wave was timed at each site with respect to the R wave of the electrocardiogram, and PWV was calculated by dividing the separation distance by the difference in R-foot times. Doppler determinations were compared with invasive tonometry, and PWV was altered pharmacologically. It was found that the upstrokes of pressure (by tonometry) and velocity were coincident (+/-1 ms) and that PWV could be calculated by either method on exposed vessels. With the use of Doppler methods, pulse transit time was determined noninvasively with +/-1-ms resolution in 140 of 142 attempts in 82 mice. The calculated PWV in mice ranged from 220 to 850 cm/s with vasodilating anesthetics producing the low values and vasoconstricting agents producing the higher values. Thus PWV can be determined noninvasively in mice, is similar to that in other mammals, and responds as expected to vasoactive agents.
Animals↗
The effect of somatostatin analogue on glucose homeostasis in conscious dogs.
Our aim was to clarify the effect of a somatostatin analogue (octreotide) on glucose flux in conscious dogs. We monitored the effects with catheters in the portal vein, hepatic vein and femoral artery and Doppler flow probes on the portal vein and hepatic artery before and after oral glucose administration. A significant increase of portal vein plasma flow after oral glucose was completely suppressed by both 4 and 1 micrograms/kg octreotide. All doses of octreotide (4, 1 and 0.1 microgram/kg) suppressed the glucose-induced increment of arterial glucose by dose response. Only 4 micrograms/kg of octreotide slightly but significantly suppressed hepatic glucose output. Marked suppression and delayed glucose absorption by the intestine was observed after 4 micrograms/kg of octreotide. One and 0.1 microgram/kg octreotide also suppressed glucose absorption without delayed absorption. Total amounts of absorbed glucose during 3h after oral glucose were 24 +/- 11% with 4 micrograms/kg of octreotide, 37 +/- 16% with 1 microgram/kg of octreotide, and 48 +/- 8% with 0.1 microgram/ kg of octreotide, all of which were significantly less than that of the control (73 +/- 8%). Using 4 micrograms/kg of octreotide treatment, the liver took up only 5 +/- 4% of the absorbed glucose, while the liver took up 35 +/- 6% and 43 +/- 9% of the absorbed glucose with 1 and 0.1 microgram/kg of octreotide. These latter values were similar to that of the control value of 34 +/- 4%. In conclusion, we found that octreotide administered before oral glucose had a remarkable stabilizing effect on postprandial glycemic surges. Both the direct inhibitory effect of octreotide on portal vein plasma flow and impaired glucose absorption would contribute to this decreased postprandial hyperglycemia, while its suppressive effect on other hormones, such as insulin and glucagon, did not seem to influence the reduction of hyperglycemia.
Animals↗
Hemodynamic effects of different pacing ratios in chronic dynamic double cardiomyoplasty.
BACKGROUND: Dynamic cardiomyoplasty is being used clinically worldwide, and evaluated by a clinical trial (phase III) in the United States. Some centers stimulate the skeletal muscle wrap with every heart beat (1:1 [muscle:heart]), whereas others use every other heart beat (1:2). Recent concern over the possible deleterious effects of too-frequent stimulation of the muscles motivated the attempt to evaluate, in a canine model of chronic, double cardiomyoplasty, the effects of two different pacing ratios on several hemodynamic parameters of interest. METHODS: Double cardiomyoplasty was performed using both latissimus dorsi muscles in 11 dogs. Fatigue resistance was achieved using the clinical transformation protocol. At a final experiment, acute cardiac failure was induced by administration of propranolol. Hemodynamic measurements of eight physiologic variables were averaged over complete pacing cycles, including the nonpaced beat at a 1:2 pacing ratio. RESULTS: The net effects of latissimus dorsi muscle stimulation at each of two pacing ratios were compared using nonparametric statistics. With the exception of left ventricular pressure (p = 0.0262) and its first derivative, dP/dt (p = 0.0099), there was no significant difference between hemodynamic performance at the two pacing ratios. CONCLUSIONS: In this canine model, pacing every other beat produces hemodynamic results that are statistically similar to pacing every beat. Less frequent stimulation of the latissimus dorsi muscle may preserve its function and improve clinical results without compromising hemodynamic benefit.
Acute Disease↗
Noninvasive indexes of cardiac systolic and diastolic function in hyperthyroid and senescent mouse.
The mouse is a common model for transgenic manipulation, however, their small size has made hemodynamic study difficult. A noninvasive 10-MHz pulsed Doppler probe was used to measure aortic and mitral flow velocities in anesthetized, intact mice to study the effects of aging and hypethyroidism (induced by thyroxine) one systolic and diastolic cardiac function. In 10 hyperthyroid mice peak aortic velocity (PAV, an index of systolic function) was 34% higher than in 10 control mice (108 +/- 2 vs. 80 +/- 3 cm/s, P < 0.05). The ratio of early to late mitral filling velocity (E/A ratio, an index of diastolic function) was 47% higher (5.6 +/- 0.8 vs. 3.8 +/- 0.2, P < 0.05) in the hyperthyroid mice. In six old (30 mo) mice PAV was similar to eight young (4 mo) mice (73 +/- 3 vs. 75 +/- 3 cm/s), but the E/A ratio was 59% lower (1.8 +/- 0.3 vs. 4.4 +/- 0.4, P < 0.05). Despite a wide range of observed heart rates, the systolic and diastolic parameters of the groups were clearly separated. We conclude that cardiac systolic and diastolic function in mice, measured by pulsed Doppler ultrasound, are similar to larger species both in magnitude and in their response to hyperthyroidism and aging.
Aging↗
Noninvasive measurement of ascending aortic blood velocity in mice.
Mice are useful models in numerous research protocols, but monitoring cardiovascular parameters in small animals is difficult. Therefore we evaluated the use of 20-MHz pulsed Doppler ultrasound to measure ascending aortic blood velocity in intact anesthetized mice. Using a 0.5-mm-diameter 20-MHz transducer applied to the right sternal border, we recorded audio Doppler signals from the ascending aorta of 31 mice [24.4 +/- 1.5 (SD) g body wt]. The signals were played back at speed into a fast Fourier transform analyzer from which we measured heart rate (453 +/- 96 beats/min), ejection time (38 +/- 3%), peak velocity (90 +/- 11 cm/s), mean velocity (23 +/- 4 cm/s), rise time (7.3 +/- 2 ms), stroke distance (29 +/- 7 mm), and acceleration (163 +/- 63 m/s2) from the spectral envelopes. We determined aortic diameter (1.2 +/- 0.2 mm) and Doppler angle (0-20 degrees) in six mice by molding the aortic root and major systemic vessels with casting resin infused at 100 mmHg pressure. For an aortic diameter of 1.2 mm, cardiac output was estimated to be 14.8 ml/min and stroke volume to be 33 microliters. To verify the origin of the signals and to test responsiveness to known stimuli, we measured velocity signals from the aorta and other nearby vessels and varied heart rate and aortic velocity by warming or by infusion of isoproterenol in three open-chest animals. For the noninvasive applications, acoustic coupling was adequate through the moistened fur, and aortic velocity signals were obtained in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Myocardial ischemia and reperfusion: a murine model.
Myocardial ischemia followed by reperfusion promotes a complex series of inflammatory reactions as noted in a variety of large animal studies. With development of genetically altered mice, there is intense interest in developing murine models to study mechanisms operative in cardiovascular disease. We developed a mouse model to study coronary artery occlusion and reperfusion effects and the method required to perform these studies both acutely and chronically. In mice, we applied a left anterior descending coronary artery occlusion either permanently or for 30 or 60 min followed by reperfusion allowing flow through the previously occluded coronary artery bed. Reperfusion was documented visually as well as by using Doppler ultrasound and histopathological techniques. The area at risk (AAR) and infarct size (IS) were assessed by EVans blue dye and triphenyltetrazolium chloride staining with computerized planimetry using an image analysis software program. The infarct as percentage of AAR and IS as percentage of the left ventricle in 13 mice with permanent occlusion was 68.6 +/- 4.4 and 28.0 +/- 2.8%, respectively. Reperfusion after occlusions of 60 and 30 min resulted in a significant decrease in IS as a percentage of the AAR compared with permanent occlusion. Histological examination of the ischemic and reperfused myocardium shows infiltration of leukocytes into the ischemic region as well as contraction bands classically associated with reperfusion. This new model allows assessment of AAR, IS, cardiac function, and pathophysiology in the mouse. With the current technology to develop genetically altered mice for overexpression or targeted mutations of various genes, this model is used to understand the complex pathophysiology of ischemia and reperfusion injury.
Animals↗
Inhibitory effect of a hydrophilic alpha-tocopherol analogue, MDL 74,405, on generation of free radicals in stunned myocardium in dogs.
A previous study has demonstrated that the hydrophilic (alpha-tocopherol analogue, MDL 74,405, attenuates postischemic myocardial dysfunction ("stunning") in dogs. The present study was undertaken to determine directly whether the salutary effect of this drug on myocardial stunning results from inhibition of the generation of oxygen-derived free radicals. Open-chest dogs undergoing a 15-min coronary artery occlusion and 3 h of reperfusion received an intravenous infusion of either saline (controls, n = 7) or MDL 74,405 (n = 6) starting 30 min before coronary occlusion and ending 60 min after reflow at a dose of 0.3 mg/kg/h. To measure free radical production, all dogs received an intravenous infusion of the spin trap alpha-phenyl N-tert-butyl nitrone (PBN) and local coronary venous plasma was analyzed by electron paramagnetic resonance (EPR). In control dogs, the myocardial production of PBN adducts exhibited an initial burst immediately after the onset of reflow and remained elevated until 10 min after reperfusion. Dogs treated with MDL 74,405 demonstrated a marked decrease in PBN adduct production. This effect of MDL 74,405 could not be attributed to nonspecific factors such as differences in ischemic zone size, collateral flow, arterial pressure, heart rate, coronary flow or other hemodynamic variables. These results demonstrate that the hydrophilic vitamin E analogue, MDL 74,405, inhibits free radical generation after myocardial ischemia-reperfusion in vivo. This finding provides direct evidence that the salutary effects of MDL 74,405 on myocardial stunning are due to attenuation of oxidative stress.
Animals↗
Myocardial reperfusion injury: role of oxygen radicals and potential therapy with antioxidants.
Experimental studies have demonstrated that reperfusion is associated with a host of distinctive pathophysiologic derangements, the most important of which are reperfusion arrhythmias, transient mechanical dysfunction or "myocardial stunning," and cell death. Reperfusion arrhythmias and myocardial stunning occur in experimental animals after transient ischemia followed by reperfusion, and there is considerable evidence that these derangements also develop in humans, although the existence of malignant reperfusion arrhythmias in humans remains uncertain. Reperfusion arrhythmias and myocardial stunning can be considered manifestations of sublethal, reversible cellular injury. The pathogenesis of reperfusion arrhythmias and stunning has not been conclusively established; however, there is considerable evidence that generation of oxygen radicals and perturbations of calcium homeostasis play an important role. Antioxidants and calcium antagonists have been shown to mitigate these manifestations of reperfusion injury. In contrast, the likelihood of lethal reperfusion-induced injury remains highly controversial. Although many studies have reported reduction of infarct size with antioxidants, numerous others have failed to reproduce these results. Consequently, intense controversy persists regarding whether oxygen radicals contribute to extending cell death following reperfusion and whether reperfusion itself causes cell death. Neither the resolution of this controversy nor the availability of clinical therapies to reduce reperfusion-induced cell death is likely in the near future.
Animals↗
Acute impairment of coronary blood flow by dynamic cardiomyoplasty.
The aim of this study was to quantify the effects of three different configurations of cardiomyoplasty on coronary blood flow in an acute dog model. Thirteen dogs had both latissimus dorsi muscles harvested and transposed to the chest. Coronary blood flow was measured using Doppler cuff probes on the left anterior descending and circumflex coronary arteries during each of three cardiomyoplasty configurations: left posterior, right anterior, and double. Multiple beat measures were made of systolic and diastolic flow during a control protocol and a subsequent protocol with the muscle(s) paced. Significant flow reductions during pacing were observed in the left anterior descending coronary artery during left posterior (17%, p = 0.003), right anterior (29%, p < 0.0001), and double (35%, p = 0.0001) myoplasty. Similar reductions occurred in the circumflex artery (14%, p = 0.0009; 20%, p = 0.001; 27%, p = 0.0053). The net flow over an entire pacing cycle also was reduced significantly: left anterior descending artery (11%, p = 0.0035; 23%, p = 0.0001; 23%, p = 0.0047) and circumflex artery (10%, p = 0.0025; 17%, p = 0.0018; 21%, p = 0.0091). Thus, in the acute setting cardiomyoplasty depresses coronary blood flow. A chronic setting will be needed to determine the ultimate significance of these results.
Animals↗
Ultrasonic Doppler detection of laser-tissue interaction.
Laser therapy for the safe and effective coagulation and ablation of tissues requires precise control of the amount of energy delivered to and absorbed by the volume of tissue of interest. We propose that an ultrasonic transducer pointing in the same direction as the laser fiber could be used to monitor the changes in ultrasonic properties caused by the absorption of light by the tissue. A modified 20 MHz pulsed Doppler was used to evaluate the ultrasonic effects of 35 exposures of beef liver and muscle to a high power diode laser in vitro in real time. We found two distinct levels of acoustic activity in the tissue. Type 1 activity consisted of slow variations in the phase and small changes in the amplitude of the echoes, while type 2 activity consisted of large and rapid fluctuations in amplitude and phase. We found that the residual increase in echogenicity of the tissue and the delay to the onset of type 2 activity were functions of laser power and tissue type and were correlated to lesion severity. We hypothesize that type 1 activity corresponds to motion (thermal expansion and contraction) of the tissue, and that type 2 activity corresponds to the creation of gas bubbles (vaporization) in the tissue. We conclude that the absorption of energy changes the acoustic properties of tissue during and after exposure and that Doppler signal processing can be used to differentiate various levels of laser-tissue interaction in real time.
Animals↗
Doppler quantification of echo-contrast injections in vivo.
It is difficult to quantify myocardial perfusion using contrast echocardiography because the echogenicity of injected contrast is unknown. We propose that a measurement of Doppler amplitude from blood in a systemic artery during the passage of contrast could define the needed input function. Time-amplitude curves from pulsed Doppler cuffs on coronary and carotid arteries of 7 dogs were analyzed during aortic root and left atrial injections of Albunex. We found in individual animals that the areas under the Doppler time-amplitude curves were correlated to the amount of Albunex injected (R = 0.87-0.99), inversely correlated to cardiac output (R = 0.83), and uncorrelated to coronary flow (R = 0.18). Due to better mixing, the coronary and carotid response areas correlated better for left atrial injections (R = 0.96) than for aortic root injections (R = 0.56). We conclude that Doppler amplitude detection can be used to quantify the passage of echo-contrast agents, that the measurements comply with indicator-dilution principles, and that systemic measurements in the carotid artery could be used to predict the coronary input function for injection sites with good systemic mixing.
Albumins↗
New configuration of double cardiomyoplasty based on studies of the length-tension properties of the latissimus dorsi muscle.
A new configuration of double cardiomyoplasty was designed according to studies of the length-tension properties of the linear latissimus dorsi muscle. Four dogs had both their right and left latissimus dorsi muscles dissected from the chest wall and attached to a tensiometer to measure force of contraction. The maximum active tension obtained with stimulation of the linear latissimus dorsi muscle was observed when the muscle was at its resting anatomic length and up to 5% above this length. Eight dogs had a double cardiomyoplasty in which the resting anatomic length of both muscles was maintained. Control hemodynamic parameters obtained with the muscles at rest were compared with stimulated muscle protocols. In a normal heart state, stimulation of the double cardiomyoplasty increased the cardiac output 32% (p < 0.05), the stroke volume 39% (p < 0.05), and the left ventricular pressure 42% (p < 0.05). When acute heart failure was induced with high-dose intravenous propranolol (5 mg/kg), stimulation of the double cardiomyoplasty increased the cardiac output 32% (p = 0.01), the stroke volume 32% (p < 0.05), rate of pressure rise 39% (p < 0.01), and myocardial thickening 39% (p < 0.01). The study demonstrated that this configuration of double cardiomyoplasty provides significant hemodynamic assistance in the normal and acutely failing canine heart.
Acute Disease↗
Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.
To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.
Anesthetics↗
Clinical relevance of myocardial "stunning".
Experimental studies have demonstrated that myocardium reperfused after reversible ischemia exhibits prolonged depression of contractile function ("stunning"). Despite the multiplicity of clinical situations in which myocardial stunning would be expected to occur, investigation of this phenomenon in humans has been hindered by several major problems, including the limited accuracy of the methods available to measure regional left ventricular function, the inability to quantify regional myocardial blood flow during acute ischemia, the difficulty in establishing with certainty, the beginning and end of an ischemic episode, and the uncontrolled influence of variables (such as preload, afterload, adrenergic tone, and inotropic therapy) that have a major impact on postischemic dysfunction. The main problem is to discern whether a reversible defect of contractility is caused by stunning, silent ischemia, or hibernation (i.e., chronic ischemia). This differential diagnosis requires the simultaneous measurement of regional myocardial function and flow, which thus far has not been generally possible. Despite these limitations, however, numerous clinical observations suggest that stunning does occur in various settings in which the myocardium is exposed to transient ischemia, including coronary angioplasty, exercise-induced angina, angina at rest (unstable or variant), acute myocardial infarction with early reperfusion, open-heart surgery, and cardiac transplantation. Recognition of this entity is important, amongst other reasons, because it is likely to cause significant morbidity and because it is potentially correctable with inotropic therapy or even preventable with antioxidant therapy. In addition, the appreciation of the phenomenon of myocardial stunning should allow the clinician to assess the efficacy of reperfusion therapy with greater accuracy and to recognize that patients should not be denied mechanical revascularization solely because of an abnormal left ventricular wall motion. Perhaps the most intriguing clinical implication of the concept of myocardial stunning is the possibility that in patients who exhibit frequent episodes of ischemia in the same territory, the myocardium may not be able to fully recover between episodes and thus may remain reversibly depressed for prolonged periods of time, or even chronically, which could account for some cases of "ischemic cardiomyopathy." Our understanding of myocardial stunning in humans is still relatively crude and will not significantly improve until studies are performed that measure simultaneously regional myocardial perfusion and function (so that stunning can be differentiated from silent ischemia and hibernation). Future important areas of research should also include the elucidation of whether stunning can become chronic and the evaluation of therapies (such as antioxidant treatments) designed to prevent this contractile abnormality.(ABSTRACT TRUNCATED AT 400 WORDS)
Angina, Unstable↗
Effects of enflurane and isoflurane on hepatic and renal circulations in chronically instrumented dogs.
Seven dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic, portal, and renal blood flows. Each animal was studied on two separate occasions, awake and during 1.2, 1.4, 1.75, and 2.0 MAC isoflurane and enflurane. Both anesthetics induced tachycardia; to a greater degree than isoflurane, enflurane lowered mean aortic blood pressure in a dose-dependent manner (-37, -45, -48, and -62% vs. -19, -25, -41, and -44%, respectively) and cardiac output (-20, -26, -41, and -48% vs. -3, -5, -11, and -15%, respectively). With isoflurane, cardiac output decreased only at 1.75 and 2.0 MAC, and portal blood flow did not change significantly, whereas hepatic arterial blood flow increased at 1.75 and 2 MAC (by 28 and 33%, respectively). With enflurane, no significant changes were recorded in hepatic arterial blood flow, whereas portal blood flow decreased in a dose-dependent manner. Except at 2 MAC, hepatic circulation did not differ between anesthetics. Likewise, neither anesthetic significantly changed renal blood flow, except for enflurane at 2.0 MAC, which was associated with a 35% reduction. Both anesthetics led to similar systemic, hepatic, and renal vasodilations. Our data suggest that high concentrations of enflurane are associated with decreases in portal, total hepatic, and renal blood flows, most likely as a result of an anesthetic-induced cardiac depression.
Animals↗