Spatial anisotropy of the velocity of electrons emitted from a short-pulse laser focus.
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Biomedical subjects
Publications and source records attributed to M Saeed.
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PURPOSE: To show the effect of dysprosium diethylenetriaminepentaacetic acid bis-methylamine injection on the images of normal human myocardium. MATERIALS AND METHODS: T2-sensitive fast gradient-recalled echo (GRE) (repetition time [TR], 10.8 msec; echo time [TE], 4.2 msec) and spin-echo (SE) (TR, three RR intervals; TE, 60 msec) magnetic resonance (MR) imaging with driven equilibrium-preparation pulse was used to produce T2 contrast material enhancement. The contrast agent was injected into 12 healthy subjects at doses of 0.05, 0.1, 0.2, 0.4, and 0.6 mmol/kg. RESULTS: Driven equilibrium-prepared GRE images showed a transient decrease of myocardial signal intensity at doses of 0.2-0.6 mmol/kg. Postcontrast T2-weighted SE images showed a myocardial signal attenuation (30%-45% decrease) at a dose of 0.4 mmol/kg or higher. CONCLUSION: Dynamic MR imaging with a magnetic susceptibility contrast medium can be used to monitor the first pass of contrast media through human myocardium with a conventional MR imager and a fast GRE sequence.
BACKGROUND: The current treatment of many cases of acute myocardial infarction involves the use of thrombolytic agents. Evaluation of this therapy requires determination of the success of reperfusion and assessment of the presence and extent of infarction in the reperfused territory. The present study was designed to simulate in rat models several possible outcomes of reperfusion therapy: (1) successful reperfusion and absence of myocardial infarction, (2) successful reperfusion and presence of myocardial infarction, and (3) unsuccessful reperfusion. The usefulness of contrast-enhanced fast magnetic resonance (MR) imaging in defining the success of reperfusion was investigated. The dynamic effects were examined of low and high doses of gadolinium-BOPTA/dimeglumine (Gd-BOPTA/dimeg) on myocardial signal using MR inversion recovery echo planar imaging (IR-EPI) and gradient recalled echo planar imaging (GR-EPI), respectively. METHODS AND RESULTS: Rats were subjected to one of the following regimens: reperfused reversible myocardial injury (n = 9), reperfused irreversible myocardial injury (n = 9), and occlusive infarction (n = 9). MR echo planar images were acquired every 1 or 2 seconds before, during, and after administration of Gd-BOPTA/dimeg. In all groups, normal myocardial signal was sharply increased on IR-EPI and decreased on GR-EPI at the peak of the bolus, followed by a gradual decline to baseline. In animals subjected to reperfused reversible myocardial injury, normal and previously ischemic regions were indistinguishable during and after the passage of Gd-BOPTA/dimeg. On the other hand, enhancement of reperfused irreversibly injured myocardium was delayed but increased steadily to a higher level than normal myocardium on IR-EPI. The reperfused irreversibly injured myocardium was identified on IR-EPI as a zone of high signal (hot spot). On GR-EPI, signal loss in reperfused irreversibly injured myocardium was significantly less compared with normally perfused myocardium. In animals with occlusive infarctions, there was no change in signal intensity over the ischemic region on either IR-EPI or GR-EPI. Occlusive infarction was identified as zones of either low (cold spot) or high (hot spot) signal compared with normal myocardium, depending on MR pulse sequence and dose of the contrast medium. CONCLUSIONS: The transit of Gd-BOPTA/dimeg monitored by fast MR imaging techniques can be used to distinguish between reperfused reversibly and reperfused irreversibly injured myocardium and between occlusive and reperfused infarctions.
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Gradient recalled echo planar imaging was used to monitor changes in myocardial and left ventricular chamber blood intensity during apnea in rats. Significant signal loss in both blood (to 62 +/- 5% and 51 +/- 6% of baseline) and myocardium (to 79 +/- 2% and 76 +/- 3% of baseline) was observed at 45 and 90 s apnea while O2 saturation decreased from 98 +/- 1% to 62 +/- 7% and 36 +/- 9%, respectively. These results show that myocardial intensity is modulated by alterations in blood oxygenation.
The initial 37 consecutive patients to be treated at our institution with the Palmaz stent placed in the aortoiliac arteries were retrospectively reviewed. In these patients, 50 stenoses and six occlusions were treated with 128 stents. Nine patients with combined iliac and common femoral obstruction underwent common femoral endarterectomy and profoundaplasty with intraoperative iliac artery angioplasty and stent application. Stenoses were reduced from 57 +/- 17% to 1 +/- 5% (p < 0.01), and peak systolic pressure gradients across the lesions were reduced from 45 +/- 30 mm Hg to 1.3 +/- 3.4 mm Hg (p < 0.01). Symptoms resolved in 27 patients and improved in eight patients. One patient died and four patients were treated nonoperatively for complications. During a mean follow-up of 12 months (6 to 21 months), six patients had recurrence of symptoms (16%) and four patients died of other diseases. Routine arteriograms after 6 months in 19 patients demonstrated recurrent mild to moderate stenoses (9% to 43%) in six patients (32%), but only two were symptomatic (11%). Secondary procedures included reexpansion of aortic and iliac stents in two patients and aortofemoral bypass in two patients. Early results suggest the efficacy of the Palmaz stent in the management of aortoiliac stenoses and its use intraoperatively in conjunction with surgical correction of outflow. Close follow-up of these patients by multidisciplinary groups is warranted.
RATIONALE AND OBJECTIVES: Contrast media may have quantitatively or even qualitatively different effects in the presence of underlying pathologic states compared with normal states. This study was designed to examine and compare the hemodynamic effects of bolus administration of ionic (gadopentetate dimeglumine) and nonionic (gadodiamide) magnetic resonance (MR) contrast media in rats subjected to acute myocardial infarction. METHODS: Acute myocardial infarction was induced in two groups of rats (n = 20) by ligating the left coronary artery. Each animal received four bolus injections, iso-osmolar glucose followed by three incremental doses of either an ionic or a nonionic MR contrast agent (0.1, 0.3, and 0.5 mmol/kg). The effects of iso-osmolar glucose and each dose of MR contrast agent on the cardiovascular system were monitored for 15 minutes. RESULTS: Iso-osmolar glucose injection did not cause hemodynamic parameters to significantly differ from baseline values. Nonionic gadodiamide produced no significant hemodynamic effects at all injected doses compared with iso-osmolar glucose. However, ionic gadopentetate dimeglumine caused significant deleterious hemodynamic effects in a dose-dependent fashion. Gadopentetate dimeglumine caused depression in left ventricular (LV) systolic pressure and systemic arterial pressure at the lowest dose (0.1 mmol/kg). At the maximum dose (0.5 mmol/kg), gadopentetate dimeglumine decreased systolic arterial pressure by 48%, rate-pressure product by 55%, LV end systolic pressure by 48%, rate of rise of LV pressure (dP/dt) by 55%, and heart rate by 10%. LV end diastolic pressure increased by 46%. Arrhythmias were observed in 20% (2/10) of the animals after injection of gadopentetate dimeglumine, but not after gadodiamide. CONCLUSIONS: Compared with ionic gadopentetate dimeglumine, nonionic gadodiamide is a hemodynamically safe MR contrast agent in this experimental model when it is injected as a rapid bolus at high doses and in the presence of acute myocardial infarction.
RATIONALE AND OBJECTIVES: Gadolinium-ethoxybenzyl-DTPA (Gd-EOB-DTPA) is a recently introduced experimental magnetic resonance (MR) contrast agent for hepatic imaging. Although liver enhancement has been investigated in a number of animal models, tolerance evaluations of Gd-EOB-DTPA injection have been limited. METHODS: The authors investigated acute hepatotoxicity in an isolated perfused rat liver model, cardiovascular effects in the anesthetized rat, and potential immunogenicity of Gd-EOB-DTPA using detection of specific antibodies. RESULTS: Using perfused rat liver model, no significant deviation could be observed for functional parameters, liver enzymes, or potassium release, comparing Gd-EOB-DTPA to a control, but there was a significant choleresis (+250% bile flow). Hemodynamic effects of Gd-EOB-DTPA were observed after femoral bolus injection, but only with relatively high dosages (0.3-0.5 mmol/kg, 10-fold the likely clinical dose in humans). Experimental conditions, idealized for antibody induction, failed to cause an IgG immune response to Gd-EOB-DTPA in the intact rat. CONCLUSIONS: The results further support preliminary conclusions that Gd-EOB-DTPA is a well-tolerated MR contrast agent.
RATIONALE AND OBJECTIVES: The authors examined the relationship between myocardial infarction, high-energy phosphate compounds, and regional contractility after myocardial ischemia and reperfusion in cats. METHODS: Hemodynamic measurements, high-energy phosphate levels, and segmental shortening were measured every 30 minutes in two groups of cats subjected to 2 hours of occlusion of the left anterior descending coronary artery and 4 hours reperfusion. Group 1 (n = 10) animals were infused with a low level of lidocaine, 0.05 mg/kg/hr, while group 2 (n = 10) received a higher dose, 7.5 mg/kg/hr. The infarcted region was measured postmortem. RESULTS: Group 1 animals had larger infarcts (39 +/- 6 vs. 12 +/- 5% of jeopardy, P < .05) and less phosphocreatine recovery during reflow (52 +/- 7% vs. 73 +/- 2% of control, P < .01) than did group 2. Group 2 showed recovery of percentage systolic shortening during reflow (1.4 +/- 2% at 30 minutes vs. 7.1 +/- 2.3% at 4 hours, P < .05), whereas group 1 exhibited no improvement. A significant correlation was found between infarct size under the surface coil and phosphocreatine content during reflow, but not between contractile function and infarction size or metabolite levels during reflow. CONCLUSIONS: Lidocaine infusion enhanced recovery of myocardial contractility during reperfusion and decreased infarct size. Greater recovery of phosphocreatine during reperfusion was predictive of greater myocardial salvage during reperfusion.
RATIONALE AND OBJECTIVES: This study compared the areas demarcated by a T1-enhancing agent, Gd-DTPA-BMA, and a magnetic susceptibility agent, Dy-DTPA-BMA, with 201thallium autoradiography (indicator of perfusion) and postmortem histochemical staining with triphenyltetrazolium chloride (TTC)(indicator of infarction). METHODS: Thirteen rats were subjected to coronary artery occlusion for 3 to 4 hours before acquisition of four sets of electrocardiogram-gated spin-echo magnetic resonance (MR) images: T1-weighted images before and after 0.2 mmol/kg Gd-DTPA-BMA; and T2-weighted images before and after 0.3 mmol/kg Dy-DTPA-BMA. After MR imaging, intravenous 201thallium delineated the area of decreased myocardial perfusion. At autopsy, TTC staining delineated the area of myocardial infarction. RESULTS: A myocardial region in the distribution of the occluded artery was delinated as a hyperintense area ("hot-spot") by Dy-DTPA-BMA and as a hypointense area ("cold-spot") by Gd-DTPA-BMA. The hyperintense area demarcated by Dy-DTPA-BMA (51 +/- 3% of the area of the midequitorial slice of the left ventricle) showed a closer relationship to the area of decreased myocardial perfusion (jeopardized area) (46 +/- 3%), determined by 201thallium autoradiography, than the area of myocardial infarction (36 +/- 4%), determined by histochemical staining. However, the hypointense area demarcated by Gd-DTPA-BMA (29 +/- 2%) did not relate as closely to the area of decreased myocardial perfusion (slope = 0.54) or the area of myocardial infarction (r = 0.46). CONCLUSIONS: The abnormal myocardial area delineated by the magnetic susceptibility agent showed a closer relationship to the area of deficient myocardial perfusion (jeopardy area) after coronary occlusion than that defined by T1-enhancing contrast media.
Monensin and selenium (sodium selenite) at different toxic levels were administered orally to the broiler chickens for variable periods. A depression in haematological parameters and biochemical ones such as alanine and aspartate aminotransferase, serum total protein and cholesterol were recorded in acute and subacute toxicosis of these substances. The present experiments led to the conclusion that concurrent administration of selenium and monensin at toxic levels resulted in exasperated toxic response in broiler chickens which in turn had been produced by embellishment of toxicosis inducing properties of both examined substances.
The strategy of non-selective neuromuscular paralysis was compared with that of synchronised (fast rate) ventilation and selective paralysis in infants receiving mechanical ventilation for respiratory distress syndrome with chronic lung disease as the primary outcome measure. One hundred and ninety three infants weighing under 2000 g were randomly allocated to receive either pancuronium during mechanical ventilation in the acute phase of respiratory distress syndrome (non-selective group) or synchronised ventilation (initial ventilatory rate at or above that of the infant's) (selective group). Infants in the selective group received pancuronium if they were consistently expiring during the inspiratory phase of the ventilator cycle. There was no significant difference between the groups with respect to birth weight, gestation, and sex distribution. There was no significant difference between the group with respect to death (selective 19%, non-selective 16%), pneumothorax (selective 14%, non-selective 14%), chronic lung disease (selective 49%), non-selective 47%), and oxygen dependency at 36 weeks' postmenstrual age (selective 32%, non-selective 39%). Routine paralysis of ventilated infants has potential complications that may be avoided by using synchronised ventilation. As the latter is not associated with an increased incidence of long term respiratory complications, it is concluded that it is the optimum strategy of the two for ventilating infants with respiratory distress syndrome.
To determine whether gadodiamide injection can provide sufficient enhancement on both T1- and T2-weighted spin-echo magnetic resonance (MR) images of the heart and skeletal muscles, anesthetized rats were divided into five groups. Groups 1-3 received 0.1 (n = 9), 0.3 (n = 8), or 0.5 (n = 8) mmol/kg gadodiamide injection, respectively, and T1-weighted images were obtained. Groups 4 and 5 received 0.3 or 0.5 mmol/kg gadodiamide injection, respectively, and T2-weighted images were obtained. Gadolinium concentration was measured in myocardium by means of inductively coupled plasma-atomic emission spectroscopy. On T1-weighted images, the 0.1 and 0.3 mmol/kg doses produced a dose-dependent increase in myocardial signal intensity proportional to gadolinium concentration. A dose of 0.5 mmol/kg, which correlated with higher gadolinium concentration and did not further increase myocardial signal intensity, prolonged the imaging window. On T2-weighted images, the 0.3 mmol/kg dose caused a transient decrease in myocardial signal intensity; the 0.5 mmol/kg dose produced greater and persistent loss of signal intensity. In conclusion, the changes in signal intensity induced by gadodiamide injection depend on the dose, pulse sequence, and type of tissue.
Rapid echo-planar (EP) magnetic resonance (MR) imaging was used to monitor the first pass of a bolus of gadodiamide injection in the hearts of normal rats and rats subjected to left coronary artery occlusion. Inversion-recovery EP imaging combined with a low dose (0.05 mmol/kg) of the contrast agent caused signal enhancement of normal myocardium from 19% +/- 4 to 63% +/- 5 (mean +/- 1 standard error of the mean) of fully relaxed intensity at the peak of the bolus but only slight increase in signal intensity of the ischemic zone. Thus, ischemic myocardium was demarcated as a hypointense zone (cold spot) during passage of the bolus. A higher dose (0.20 mmol/kg) of the same agent caused signal loss of normal myocardium from 100% to 39% +/- 7 of control at the peak of the bolus on gradient-recalled echo EP images, and ischemic myocardium was visualized as a hyperintense zone (hot spot). With either method of monitoring bolus transit, myocardial signal intensity recovered slowly following the peak bolus effect, consistent with substantial extraction of the agent during the first pass through the heart. Use of gadodiamide injection can allow discrimination between ischemic and nonischemic myocardium on both T1- and susceptibility-weighted EP images during bolus transit.
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The monoclonal antibody AE-2, raised against the human erythrocyte acetylcholinesterase (AChE) dimer (acetylcholine acetylhydrolase, EC 3.1.1.7), binds to other mammalian AChEs, including the tetramer that occurs in fetal bovine serum (FBS). AE-2 partially inhibited the rate of hydrolysis of the charged substrate acetylthiocholine by FBS AChE, whereas it increased the rate of hydrolysis of the neutral substrate indophenyl acetate. Present results show that AE-2 decreases the rate of inhibition of FBS AChE by the positively charged organophosphate amiton-p-toluene sulfonate and the positively charged carbamates pyridostigmine and neostigmine but accelerates inhibition of FBS AChE by the neutral organophosphates paraoxon and diisopropylfluorophosphate. Results suggest that AE-2 may allosterically modulate an anionic site in the catalytic center of FBS AChE.
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