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Biomedical subjects

A Sidi

Publications and source records attributed to A Sidi.

At least 19 recordsLinked to original sources

False low pulse oximetry reading associated with the concomitant use of a peripheral nerve stimulator and an evoked-potential stimulator.

One of the sources of error in pulse oximetry readings is associated with an abnormal signal-to-noise ratio. The pulse oximeter distinguishes the light absorbance of arterial blood from that of other absorbers by differentiating between a constant component and a pulsating component. The pulsating component is almost exclusively the result of arteriolar bed pulsations. Because pulse oximetry is based on the assumption that arterial blood is the only pulsatile absorber, any other fluctuating phenomenon could constitute a source of error. We report a case in which a low pulse oximetry reading was associated with concomitant use of a pulse oximeter and a peripheral nerve stimulator on the same arm. Further tests conducted using a nerve stimulator and a sensory evoked potential stimulator with different amplitudes and frequencies confirmed the association and delineated the relationship between frequency and amplitude of stimulation and the degree of artificial desaturation. A theoretical explanation for this phenomenon is presented.

Electric Stimulation

An alternative to radioactive microspheres for measuring regional myocardial blood flow, Part 1: Colored microspheres.

OBJECTIVE: To compare measurements of regional myocardial blood flow between color and radioactive microspheres. DESIGN: Prospective, randomized, controlled. SETTING: University research laboratory. PARTICIPANTS: Pigs. INTERVENTIONS: Pigs underwent constriction of the left anterior descending artery, either incremental and then 0 constriction with epinephrine, 0.5 to 3 mu/kg/min (n = 5; "variable") or only 0% and 100% constriction without epinephrine (n = 4, "single"). Radioactive and color microspheres were injected simultaneously. For variable constriction, 5 colors (3 x 10(6)/mL) were tested in random order and, for single, red and yellow (6 x 10(6)/2 mL). MEASUREMENTS AND MAIN RESULTS: Measurements of regional endocardial, epicardial, and transmural myocardial blood flow were compared by regression analysis (linear and nonlinear). With radioactive measurements as the point of reference, when regional flow was 50 to 150 mL/min/100 g, correlation was high (r = 0.85), although regression slope was low. With endocardial and epicardial flow between 30 and 100 mL/min/100 g, correlation was close (r = 0.84). Overall nonlinear correlation was higher with single than variable constriction (r = 0.72). When regional flow was less than 100 mL/min/100 g, linear correlation was r = 0.72. When transmural flow measured by color microspheres was less than 25 mL/min/100 g, correlation was high (r = 0.86) but, with endocardial or epicardial flow, low (r = 0.67). When transmural flow was greater than 100 mL/min/100 g, correlation was extremely low (r = 0.1; n = 26 data points). The overall correlations for regional endocardial and epicardial flows were also low, except in the ischemic zone. CONCLUSIONS: Color and radioactive measurements correlate well during moderate and ischemic regional myocardial blood flow, ischemic blood flow requiring a higher concentration of color microspheres. A major limitation of using color microspheres is imprecision when flow is greater than 150 mL/min 100 g.

Animals

An alternative to radioactive microsphere for measuring regional myocardial blood flow, Part 2: Laser-Doppler perfusion monitor.

OBJECTIVE: To compare measurements of regional myocardial blood flow volume between microsphere measurement of regional flow (0.5- to 2- g tissue sampling) and a potential alternative measure, local flow (1 mm3) in the microcirculation measured by laser-Doppler perfusion monitor. DESIGN: Prospective, randomized, controlled. SETTING: University research laboratory. PARTICIPANTS: Pigs. INTERVENTIONS: After anesthetization, in 5 pigs (25 to 30 kg), the left anterior descending coronary artery was isolated and its resting flow measured by a perivascular-Doppler flowmeter. Left ventricular pressure and first time derivative of left ventricular pressure were measured. The laser-Doppler probe needle (type N) (Model ALF-21, Transonic Systems, Inc, Ithaca, NY) was inserted 2 to 3 mm into the wall of the left ventricle, parallel to the coronary artery. All 5 pigs were subjected to 0 (control), 50% , 75%, and 100% constriction of the left anterior coronary artery. MEASUREMENTS AND MAIN RESULTS: Measurements by radio-active microspheres correlated poorly with those by laser-Doppler and extremely poorly with those by perivascular Doppler flowmeter. For percent change from baseline in the constricted arterial zone, radioactive measurements correlated well with those by laser-Doppler but not those by Doppler flowmeter. Also, radioactive measurements of percent change in flow in the circumflex (nonconstricted) zone and laser-Doppler measurements in the constricted arterial zone did not correlate well. CONCLUSIONS: Laser-Doppler can be recommended for experimental research to monitor local flow. These measurements may relate to change in regional flow during normal perfusion and hypoperfusion. Before the laser-Doppler perfusion monitor can be used clinically, tissue trauma from the 0.55-mm needle needs to be evaluated.

Animals

Left-sided stellate ganglion ablation or "rate-controlled" vagal nerve stimulation decreases regional myocardial metabolic impairment during acute ischemia in dogs.

This study was designed to see whether during ischemia a metabolic advantage results with left-sided ablation of the stellate ganglion (SGA), an available clinical technique. Its effects on hemodynamics and regional metabolism during myocardial ischemia were compared with those of electrical stimulation of the left vagus nerve (VS), a nonclinical technique, and those of a control condition (ischemia without intervention). The left anterior descending coronary artery (LADa) of 30 dogs was constricted to reduce blood flow by 50% and then 75% from that before constriction and after autonomic intervention (baseline). Electrocardiogram, left-ventricular (LV) first-time derivative (dP/dt), and systemic, LADa, and LV end-diastolic pressures were continuously recorded. Before and during each constriction, cardiac output and regional myocardial blood flow (by microspheres), blood gas tensions, pH, hemoglobin O2 saturation, lactate, glucose, sodium, and potassium concentrations were measured. During ischemia, SGA and VS each decreased heart rate, myocardial contractility (dP/dt), and filling pressures, the decrease in each variable being greater with VS. Also during ischemia, myocardial O2 delivery and consumption decreased to the same extent in the ischemic zone with VS, but the O2 delivery/consumption ratio was higher only with SGA. In addition, ischemic lactate production was lower with SGA and VS than with no autonomic intervention. It is concluded that left-sided SGA or VS to a heart rate of 80 to 90 beats per minute similarly mitigated metabolic impairment during myocardial ischemia. Although the study was only designed to compare modification of ischemia by two different techniques, the results suggest that ischemic zone O2 delivery/consumption ratio and hemodynamic stability were better with SGA.

Animals

Midazolam's effects on myocardial load and coronary perfusion: reduced regional O2 consumption and lactate production during ischemia in dogs.

It is hypothesized that because of its potential to increase coronary flow and simultaneously decrease myocardial performance and O2 consumption, midazolam would minimize regional metabolic impairment during myocardial ischemia. Therefore, the hemodynamic and regional metabolic effects of systemic midazolam administration were compared during moderate and severe constrictions of the left anterior descending artery (LADa) to nontreated but ischemic animals in a canine model of acute coronary occlusion. In 16 anesthetized, ventilated, surgically prepared, and catheterized dogs, resting flow in the LADa was decreased by 50% and 75% for 15 minutes with 1 hour of normal flow in between. By arbitrary assignment, 7 dogs received midazolam (0.3 mg/kg and then 0.05 mg/kg/min) before thoracotomy. In all dogs, heart rate, electrocardiogram, LADa flow, left ventricular (LV) first time-derivative, and aortic, pulmonary artery, LADa, and LV pressures were measured continuously. Before and during constrictions, cardiac output by thermodilution and regional myocardial blood flow by microspheres were measured and blood was sampled for analysis. Data (mean +/- SEM) were compared within and between groups using ANOVA. Before placement of the LADa ligature, midazolam decreased heart rate and mean aortic pressure. Before ischemia, heart rate and LADa pressure were lower with midazolam than without it, but baseline metabolic variables were similar between the two groups (except for O2 consumption in the ischemic zone, which was lower with midazolam than without it). During 75% constriction with midazolam, LV end-diastolic pressure, coronary resistance, and ischemic zone O2 consumption were lower than without midazolam. Ischemic zone O2 delivery/consumption ratio was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Cardiovascular effects of a non-xanthine-selective antagonist of the A1 adenosine receptor in the anaesthetised pig: pharmacological and therapeutic implications.

OBJECTIVE: To study antagonism of A1 adenosine receptors in an anaesthetised open chest swine model, the selective A1 receptor antagonist, N6-endonorbornan-2-yl-9-methyladenine (N-0861), was examined to see if it attenuates bradycardia, augments reflex tachycardia associated with adenosine infusion, or both. Its effects were compared with those of the non-selective antagonist of adenosine A1 and A2 receptors, 8-(p-sulphophenyl)-theophylline (8-pST). METHODS: Twenty nine pigs were studied. The prolongation of P-R interval mediated by A1 receptors, the increase in left anterior descending coronary artery blood flow mediated by A2 receptors, and decreases in systemic and left ventricular pressures and first derivative of left ventricular pressure (dP/dt) were monitored in each animal assigned to one of three protocols. (1) Adenosine, 40 to 180 micrograms.kg-1.min-1, was infused for more than 6 min before and immediately after rapid infusion of 8-pST, 5 mg.kg-1 intravenously, or a solvent that did or did not contain N-0861, 0.2 mg.kg-1 intravenously (n = 14). (2) In the same animal, we compared N-0861 and 8-pST in reversing responses mediated by A1 and A2 receptors during two 10 min infusions of adenosine separated by a 1 h washout period (n = 7). (3) N-0861 with adenosine (mean dose, 0.4 mg.kg-1) was infused with or without complete autonomic blockade with atropine (2.5 mg.kg-1) and propranolol (2 mg.kg-1) (n = 8). RESULTS: Adenosine prolonged P-R interval (and cycle length in non-paced hearts), increased coronary flow, and decreased calculated coronary resistance. N-0861 alone did not affect any variable, but N-0861 with adenosine prevented or reversed A1 receptor mediated prolongation of P-R interval in paced hearts and cycle length in non-paced hearts and enhanced A2 receptor mediated coronary vasodilatation. Left ventricular dP/dt and rate-pressure product were maintained with N-0861 and adenosine, and N-0861 unmasked a postadenosine reflex tachycardia. Prolonged PR interval, decreased heart rate, and increased coronary flow were prevented or reversed by the non-selective antagonist 8-pST. CONCLUSIONS: Selectivity of N-0861 for the adenosine A1 receptor may, without reducing coronary blood flow, ameliorate bradyarrhythmia and maintain the positive inotropic response when exogenous adenosine is given or when interstitial myocardial adenosine is increased.

Adenine

Early administration of amrinone does not impair regional metabolism of O2 or lactate and, by improving myocardial performance, preserves myocardial blood flow in the ischemic canine heart.

The inotropic and vasodilating effects of amrinone can upset the balance of O2 supply and demand by changing those components in opposite directions simultaneously. We used a canine model of acute coronary artery occlusion to test our hypothesis that early administration of amrinone (before failure of the heart) would have beneficial effects on hemodynamic status and regional metabolism during ischemia, even before heart failure. Twenty dogs anesthetized with thiamylal were subjected to 50%, 75%, and 100% occlusion of the left anterior descending coronary artery. Half of the dogs were given a bolus injection of amrinone (0.75 mg/kg) 1-2 min before each occlusion, immediately followed by continuous infusion (10 micrograms.kg-1 x min-1) during occlusion; the other half did not receive amrinone (control). Hemodynamic and metabolic variables were measured in the ischemic area (the left anterior descending coronary artery) and in a nonischemic area (the circumflex vein). Amrinone not only decreased heart rate, left ventricular systolic and end-diastolic pressures, and mean pulmonary arterial pressure during constrictions but also maintained contractility, stroke volume index, and stroke volume index/left ventricular end-diastolic pressure before and during constrictions. Regional myocardial blood flow in ischemic areas decreased with amrinone during constrictions but was still higher than in untreated animals. Regional ischemic and nonischemic metabolic variables (metabolism of intracoronary potassium, CO2, O2, glucose, and lactate) were similar for both groups and changed to the same extent. Amrinone appears to improve left ventricular performance and increase blood flow to ischemic myocardium while not worsening regional metabolic effects during various grades of ischemia in the dog.

Amrinone

Adenosine for controlled hypotension: systemic compared with intracoronary infusion in dogs.

We hypothesized that either through local myocardial or systemic effects, adenosine could be used to control hypotension during ischemia. Therefore, we compared the effects of systemic with intracoronary infusion of adenosine on myocardial hemodynamics and metabolism during ischemia in 27 dogs. Left anterior descending artery (LADa) flow was measured and the LADa constricted by a micrometer to restrict resting flow by 50%, 75%, and 100%. Adenosine was infused either systemically (n = 9), to maintain mean aortic pressure at 50-60 mm Hg, or directly into the LADa (n = 9), to create maximal coronary hyperperfusion; no adenosine was infused in the control group (n = 9). With systemic adenosine, during each constriction aortic pressure, left ventricular first derivative (LV dP/dt), and heart rate (HR) decreased: aortic pressure by 56.1% +/- 2.9% (mean +/- SEM), LV dP/dt by 36.2% +/- 2.2%, systemic resistance by 42.7% +/- 5%, and HR by 38.7% +/- 3% during 50% constriction (P less than 0.05 for each variable). Intracoronary adenosine decreased only aortic pressure, LV dP/dt, and HR, all to a lesser extent: aortic pressure by 5% +/- 2.8%, LV dP/dt by 15% +/- 1.2%, and HR by 4.6% +/- 1.7% (P less than 0.05, compared with systemic adenosine for each variable). With systemic adenosine only in the nonischemic area, regional myocardial blood flow increased and remained high, from 224.6 +/- 65.2 to 342 +/- 46.2 mL.min-1.100 g-1 during 50% constriction (P less than 0.05); with intracoronary adenosine, ischemic zone regional myocardial blood flow increased, but not consistently. In the ischemic area, O2 consumption was less with than without systemic adenosine; also, lactate flux production was less positive (-60.2 +/- 37.6 compared with 80.3 +/- 20.2 mmol.min-1.100 g-1 x 10(-3) during 50% constriction; P less than 0.05). Systemic infusion of adenosine during coronary hypoperfusion improves regional metabolism during ischemia and, thus, may mitigate myocardial ischemia. The mechanism by which systemic infusion improves metabolic status may be by decreases in both systemic pressure and systemic vascular resistance.

Adenosine

Decreased regional lactate production and output due to intracoronary continuous infusion of esmolol during acute coronary occlusion in dogs.

This study was designed to test the hypothesis that intracoronary administration of esmolol can confer metabolic protection during coronary constriction or occlusion, without affecting hemodynamic parameters, in a canine model. Seventeen anesthetized open-chest dogs underwent direct cannulation of the left anterior descending coronary artery (LADa), its companion vein (LADv), and the distal circumflex vein (CFXv). LADa flow was measured with an electromagnetic flowmeter. Using a micrometer-driven snare around the LADa, flow was reduced by 50%, 75%, and 100% for 15 minutes, with 1 hour of normal flow before each constriction. In 7 dogs (group 1) chosen randomly, esmolol, 15 to 20 micrograms/kg/min, was infused continuously into the LADa; the rate was adjusted to maintain baseline hemodynamic values. The second group (10 dogs) was not treated with esmolol. Heart rate (HR), electrocardiogram (ECG), LADa flow, LV dP/dt, and aorta (Ao), pulmonary artery (PA), LADa, and left ventricular (LV) pressures were recorded continuously. Cardiac output (CO) (thermodilution) was measured and blood was sampled from all catheters before and after constrictions for analysis of glucose, lactate, sodium, potassium, and blood gases. Flow and pressure in the LADa in both groups decreased similarly during each corresponding constriction. Systolic LV pressure, LV dP/dt, and LV stroke work index were affected in both groups only during 100% constriction. HR, Ao, and PA pressures, and total and peripheral pulmonary resistances were affected similarly in both groups during each constriction. Myocardial lactate extraction and consumption were less negative (negative = net production and output) in the LAD perfusion bed during corresponding constrictions with esmolol than without it.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists

Prolonged neuromuscular blockade and ventilatory failure after renal transplantation and cyclosporine.

In a retrospective one-year study, we documented respiratory failure or prolonged neuromuscular blockade in eight of 65 patients with chronic renal failure who had received either vecuronium (four of 29 patients) or atracurium (four of 36 patients) during anaesthesia for kidney transplantation. We reviewed the charts of the patients and recorded all aspects of medication and anaesthesia to try to determine whether there might be a single factor associated with this high incidence (12 per cent) of respiratory failure. Anaesthesia for all patients was induced with thiopentone, isoflurane, and N2O/O2. Tracheal intubation was facilitated with muscle relaxants in a single bolus of vecuronium, 0.07 to 0.1 mg.kg-1, or atracurium, 0.3 to 0.5 mg.kg-1. Additional doses were given according to neuromuscular activity, which was monitored visually by response to train-of-four and tetanic stimulation. Anaesthesia was maintained with fentanyl/isoflurane and N2O/O2. After induction of anaesthesia, each patient received methylprednisolone, cefazolin, mannitol infusion for 24 hr beginning at the start of renal artery anatomosis, and either azathioprine (n = 57) or cyclosporine (n = 8). Relaxation was evaluated toward the end of the operation by train-of-four stimulation. Neuromuscular blockade was reversed with edrophonium (0.75-1 mg.kg-1) or neostigmine (0.06-0.08 mg.kg-1). The eight patients with prolonged neuromuscular blockade received ventilatory support for one to three hours after operation. Respiratory failure was significantly more frequent in patients who received cyclosporine (P less than 0.05).

Adult

Direct cannulation of myocardial blood vessels without interfering with regional blood flow distribution, resting blood flow, or reactive hyperemia.

An in vivo technique of directly cannulating coronary arteries and veins for sampling blood and measuring hemodynamic parameters is described. The cannulation procedure was evaluated for its effects on regional myocardial blood flow (RMBF), transmural RMBF distribution, and reactive hyperemia. In a group of ten dogs, RMBF was measured by using radionuclide microspheres. Values for left anterior descending (LAD) perfusion zone (with catheter) and circumflex (CX) zone (no catheter) did not differ significantly (119 +/- 14 mL/min/100 g v 123 +/- 14 mL/min/100 g, respectively). Likewise, endocardial-to-epicardial RMBF ratio was similar for the two areas (0.99 +/- 0.06 and 1.04 +/- 0.06, respectively). In five dogs, aortic and left ventricular pressures agreed closely with the LAD coronary artery pressure measured with the described catheter system. Arterial flow during rest and reactive hyperemia was measured in five additional dogs by using electromagnetic flow probes placed around the LAD and CX coronary arteries. During both rest and reactive hyperemia, flow was greater in the CX than in the LAD (65.46 +/- 4.12 and 169.62 +/- 9.04 in the CX v 30.24 +/- 0.78 and 102.28 +/- 5.38 in the LAD; P less than 0.05 for both); however, the percentage change from rest to reactive hyperemia was similar for both vessels. In each perfusion zone, flow during rest and reactive hyperemia and the percentage change were not affected by cannulation. The effects of an infusion of adenosine (20 to 40 micrograms/min) into the pulmonary artery with and without the LAD coronary catheters (artery and vein) were tested in six other dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine

Lactate extraction fails to accurately reflect regional lactate production in ischemic myocardium.

Lactate extraction (defined as arteriovenous lactate concentration difference divided by arterial concentration and expressed as a percent) is often reported as the indicator of anaerobic cardiac metabolism in studies dealing with myocardial ischemia. However, lactate extraction ignores the effect of regional blood flow and, therefore, fails to consider the total mass of lactate consumed or produced (lactate flux). This study examined the relationship between lactate flux and calculated lactate extraction. Fourteen anesthetized dogs were instrumented to allow sampling of blood from the left anterior descending coronary artery (LADa) and vein (LADv) and a circumflex coronary vein (CFXv), as well as measurement of regional myocardial blood flow (RMBF) using microspheres, and measurement of systemic hemodynamic variables. Complete data sets (before LADa occlusion, after 15 minutes of LAD occlusion, and after 1 hour of reperfusion) were obtained in nine dogs. Only minor systemic hemodynamic changes occurred during LADa occlusion when compared with "before" and "after" values. Likewise, LADa occlusion produced only minor alterations in blood gas tensions, pH, concentrations of glucose, lactate, and RMBF in samples from the CFX perfusion zone. In contrast, LAD occlusion decreased RMBF in the LADa perfusion zone and produced significant hypercarbia and acidemia, as well as an increased LADv lactate concentration. In the LAD zone, lactate extraction decreased significantly from 15.9% +/- 7.0% before LAD occlusion to -77.4% +/- 21.8% during LAD occlusion (P less than 0.05). However, lactate flux (arteriovenous concentration difference x RMBF) in the LAD zone before and during LAD occlusion was not statistically significantly different (1.3 +/- 0.8 mg/min/100 g and -1.5 +/- 0.8 mg/min/100 g, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Effect of isoflurane on the extent of myocardial necrosis and on systemic hemodynamics, regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion.

Anesthetized dogs were studied in two protocols to determine the effect of isoflurane on the extent of myocardial injury resulting from left anterior descending coronary artery (LAD) occlusion. In 22 dogs (11 treated with isoflurane 1% inspired, beginning 1 hr after LAD occlusion, and 11 control) myocardial infarct size measured postmortem after 6 hr of LAD occlusion was significantly less with isoflurane than without it, 23.4 +/- 3.8% vs 36.2 +/- 2.4% of left ventricle; regional myocardial blood flow (RMBF) did not differ between groups and hemodynamic differences were slight. Fifty-two other dogs underwent two 15-min periods of LAD occlusion separated by 1 hr of reperfusion. Without isoflurane (n = 12), hemodynamic, RMBF, and regional metabolic data did not differ between the two occlusion periods. When isoflurane 1.3% inspired was administered during one of the two occlusion periods by random assignment, coronary perfusion pressure, left ventricular stroke work index, and systolic left ventricular pressure decreased more than when isoflurane was not administered. Both oxygen (O2) consumption and supply in ischemic myocardium decreased proportionately during LAD occlusion, but more so with isoflurane. Neither lactate production, potassium release, glucose extraction, nor coronary venous carbon dioxide (CO2) or O2 content differed between LAD occlusion periods with and without isoflurane. Thus, isoflurane decreased the extent of myocardial necrosis produced by LAD occlusion but neither RMBF nor metabolic indications were improved during transitory ischemia.

Animals

Experimental closed head injury in rats: mechanical, pathophysiologic, and neurologic properties.

A model of closed head injury in rats was developed using a calibrated weight-drop device. The development of edema was studied in various brain regions (cerebral hemispheres, brain stem, cerebellum) using a linear specific gravity gradient column. Regional brain tissue density was measured within 1 min, at 15 and 60 min, 18 h, 4 and 10 days after injury to the left cerebral hemisphere, and was compared with values in sham-operated and control rats. Significant edema (i.e., reduced specific gravity) occurred only in the traumatized hemisphere and was maximal at 18 h. A neurologic severity score (NSS) was developed to evaluate the status of the rat after injury. Specific gravity was significantly correlated with NSS at 18 h after injury. The affected hemisphere displayed hemorrhagic lesions as early as one hour post head trauma (HT), which evolved into hemorrhagic necrosis at 18 h. A pathologic score, evaluated 18 h post HT based on size and severity of the lesion, was correlated with the NSS and evaluated for each rat at one hour and 18 h postimpact. This correlation was found to be highly significant. This model of brain injury may be useful in future studies on the effects of therapeutic agents.

Animals

Esmolol decreases the adverse effects of acute coronary artery occlusion on myocardial metabolism and regional myocardial blood flow in dogs.

This study was designed to test the hypothesis that beta-adrenergic receptor blockade with esmolol would decrease the hemodynamic and myocardial metabolic impairment produced by left anterior descending coronary artery (LADa) occlusion. Twenty-three anesthetized open-chest dogs underwent direct cannulation of the LADa, its companion vein (LADv), and a distal circumflex vein (CFXv) for blood sampling. All dogs were subjected to two consecutive 15-minute periods of total LADa occlusion; group 1 (n = 11) received an infusion of esmolol (150 micrograms.kg-1.min-1) during either occlusion period (randomly assigned) and group 2 (n = 12) received no intervention during either occlusion period. One hour of reperfusion was interposed between the two periods of LADa occlusion. Hemodynamic measurements were made and blood was sampled from the aorta, CFXv, LADa, and LADv before and during both periods of LADa occlusion. Without esmolol infusion, LADa occlusion was associated with decreases in stroke index, coronary perfusion pressure, and left ventricular stroke work index; with esmolol infusion these hemodynamic decrements did not occur. During both LADa occlusion periods in both groups, lactate extraction became negative, i.e., there was net lactate production. Despite this, the magnitude of lactate production was less with esmolol than without it. Finally, average endocardial-to-epicardial blood flow ratio in the LAD perfusion area was decreased during each LAD occlusion period except when esmolol was infused, during which the baseline value was maintained. Thus, infusion of esmolol during temporary LADa occlusion preserved certain hemodynamic variables, preserved the ratio of endocardial-to-epicardial blood flow, and decreased the apparent magnitude of lactate production.

Analysis of Variance

Methylene blue and indocyanine green artifactually lower pulse oximetry readings of oxygen saturation. Studies in dogs.

The effects of fluorescein, methylene blue, and indocyanine green on hemodynamic variables and on pulse oximetry and co-oximetry measurements of arterial hemoglobin oxygen saturation (SaO2) and oxyhemoglobin percentage (% HbO2) were evaluated in 16 anesthetized dogs in vitro by co-oximetry (% HbO2) and in vivo by pulse oximetry (SaO2). The light absorbance (optical density) in plasma (range 500 to 800 nm) was measured by a spectrophotometer. Fluorescein did not affect oximetry measurements, plasma light absorbance in the range measured, or hemodynamic variables. Methylene blue caused dose-dependent decreases in measurements made with both forms of oximetry for up to 30 minutes, the decrease being greater and longer lasting with pulse oximetry (P less than 0.05). Hemodynamic measurements in 5 dogs showed that methylene blue (1 to 5 mg/kg) increased arterial pressure transiently, after which cardiac output, stroke index, and left ventricular stroke work index decreased and left ventricular end-diastolic pressure and systemic and pulmonary vascular resistances increased (P less than 0.05 with 5 mg/kg). Methemoglobin concentration measured by co-oximetry increased significantly (to 19.9 +/- 1.4%, P less than 0.05) 1 minute after 5 mg/kg of methylene blue was injected. Methylene blue had a dose- and time-dependent effect on plasma light absorbance, and this effect peaked in the 660- to 670-nm range. The data do not distinguish the relative contributions of physiology (hemodynamic change), chemistry (methemoglobin production), and physics (optical properties) to the decrease in pulse oximetry and co-oximetry measurements that follows injection of methylene blue. Indocyanine green affected neither hemodynamic variables nor co-oximetry readings but decreased pulse oximetry readings for up to 10 minutes dose dependently.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals