PubMed Health⌕ Search

Biomedical subjects

J Altamirano

Publications and source records attributed to J Altamirano.

12 recordsLinked to original sources
PubMed1998

Regulatory volume decrease and intracellular Ca2+ in murine neuroblastoma cells studied with fluorescent probes.

The possible role of Ca2+ as a second messenger mediating regulatory volume decrease (RVD) in osmotically swollen cells was investigated in murine neural cell lines (N1E-115 and NG108-15) by means of novel microspectrofluorimetric techniques that allow simultaneous measurement of changes in cell water volume and [Ca2+]i in single cells loaded with fura-2. [Ca2+]i was measured ratiometrically, whereas the volume change was determined at the intracellular isosbestic wavelength (358 nm). Independent volume measurements were done using calcein, a fluorescent probe insensitive to intracellular ions. When challenged with approximately 40% hyposmotic solutions, the cells expanded osmometrically and then underwent RVD. Concomitant with the volume response, there was a transient increase in [Ca2+]i, whose onset preceded RVD. For hyposmotic solutions (up to approximately -40%), [Ca2+]i increased steeply with the reciprocal of the external osmotic pressure and with the cell volume. Chelation of external and internal Ca2+, with EGTA and 1,2-bis-(o -aminophenoxy) ethane-N,N,N ',N '-tetraacetic acid (BAPTA), respectively, attenuated but did not prevent RVD. This Ca2+-independent RVD proceeded even when there was a concomitant decrease in [Ca2+]i below resting levels. Similar results were obtained in cells loaded with calcein. For cells not treated with BAPTA, restoration of external Ca2+ during the relaxation of RVD elicited by Ca2+-free hyposmotic solutions produced an increase in [Ca2+]i without affecting the rate or extent of the responses. RVD and the increase in [Ca2+]i were blocked or attenuated upon the second of two approximately 40% hyposmotic challenges applied at an interval of 30-60 min. The inactivation persisted in Ca2+-free solutions. Hence, our simultaneous measurements of intracellular Ca2+ and volume in single neuroblastoma cells directly demonstrate that an increase in intracellular Ca2+ is not necessary for triggering RVD or its inactivation. The attenuation of RVD after Ca2+ chelation could occur through secondary effects or could indicate that Ca2+ is required for optimal RVD responses.

Animals↗
PubMed1997

Restoring Sinus Rhythm in Patients With Atrial Flutter and Fibrillation: Pharmacologic or Electrical Cardioversion?

Atrial fibrillation and atrial flutter, the most frequently encountered tachyarrhythmias requiring treatment, have become a major focus for clinical and basic research in recent years. Restoration and maintenance of sinus rhythmn, having been shown to improve exercise capacity, alleviate symptoms, and reduce the incidence of thromboembolic events, may be the optimal management strategy. Identification of the safest, most efficacious and cost-effective means of restoring sinus rhythm is necessary prior to the institution of optimal antiarrhythmic therapy to maintain sinus rhythm. Potential advantages of pharmacologic compared with electrical cardioversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion include lack of need for general anesthesia and likely lower cost. Pharmacologic conversion has been accomplished with drugs that prolong atrial refractorinerss, including class Ia (quinidine, procainamide, disopyramide), class Ic (flecainide, propafenone), and class II (sotalol, amiodarone) compounds. The so-called pure class III agents were created to overcome the blocker side effects of sotalol and the complex pharmacodynamic profile of amiodarone. Two such agents are dofetilide, which selectively blocks the rapid component of the delayed rectifier current (Ikr) and ibutilide, which augments the slow inward sodium current, with a smaller component of action mediated by the block of Ikr. Reported overall conversion rates for recent onset atrial fibrillation and atrial flutter were 31% and 54% for difetilide, respectively, and 29-31% and 38-63%, respectively, for ibutilide. Proarrhythmia, manifested as polymorphic ventricular tachycardia requiring cardioversion, was a significant early side effect of both agents. Data from clinical trtials with these new agents, combined with increasing nowledge of the electrophysiologic substrate for these arrhythmias, has renewed initerest in the development of safer, more efficacious class IIIdrugs for atrial fibrillation and atrial flutter conversion.

Journal Article↗
PubMed1997

Mechanical Ablation of Concealed Left Lateral Bypass Tract.

A 50-yaer-old man with hypertension had been treated for supraventricular tachycardia with several medications for nine years. In 1990, he was started on amiodarone but a year later he developed side effects causing discontinuation of amiodarone. Because of his recurrent episodes of palpitations associated with near syncope, chest pain and shortness of breath, he underwent an electrophysiology study in 1992 that showed orthodromic AVRT with the presence of a concealed left-sided accessory bypass tract. Scheduled for radiofrequency ablation the following day, after catheters were placed and during mapping of the lateralmitral annulus, his tachycardia stopped abruptly without further inducability. Isoproterenol infusion during atrial and ventricular stimulation also failed to induce his original tachycardia. A year later, the patient presented with palpitations that felt different than his previous experiences. Work-up at that point only revealed a parasystolic focus on a 24-hour ECG monitoring without any form of supraventricular tachycardia. This represents a very unusual case by which the left lateral accessory pathway was mechanically ablated with catheter manipulation. This led to the disappearance of the orthodromic tachycardia that was easily induced before due to the activity of his parasytolic focus. The latter continued for the following four years but the patient has had no recurrences of his tachycardia.

Journal Article↗
PubMed1997

Albendazole therapy for neurocysticercosis: a prospective double-blind trial comparing 7 versus 14 days of treatment. Cysticercosis Working Group in Peru.

OBJECTIVE: To compare the effectiveness of two regimens of albendazole therapy for neurocysticercosis. DESIGN: Randomized, double-blind clinical trial. SETTINGS: Patients admitted to neurologic wards in Lima, Peru. PATIENTS: Adult patients with active neurocysticercosis demonstrated by CT and Western blot (immunoblot). INTERVENTION: One week (n = 25) versus 2 weeks (n = 25) of albendazole therapy. MEASUREMENTS: Decrease in the number of cysts on CT. RESULTS: Effectiveness of albendazole was 78%, with no difference between the groups when compared 3 months after therapy. Complete cure was obtained in only 38% of patients. Patients with more than 20 cysts had poorer responses to therapy. The clinical course and EEG evolution improved in most patients. Side effects were present in 38% of patients, mainly mild, transient gastrointestinal symptoms. Therapy was also associated with exacerbation of neurologic symptoms. Two patients died in the first year after therapy, both because of aggregated infections of ventricle-peritoneal shunts. One-year follow-up CT showed lesions in three of 10 patients presumed to be cured 3 months after therapy. CONCLUSIONS: Extension of albendazole therapy for more than 7 days adds no benefits for the patients.

Adult↗
PubMed1996

The multidrug resistance P-glycoprotein modulates cell regulatory volume decrease.

Cell volume is frequently down-regulated by the activation of anion channels. The role of cell swelling-activated chloride channels in cell volume regulation has been studied using the patch-clamp technique and a non-invasive microspectrofluorimetric assay for changes in cell volume. The rate of activation of these chloride channels was shown to limit the rate of regulatory volume decrease (RVD) in response to hyposmotic solutions. Expression of the human MDR1 or mouse mdr1a genes, but not the mouse mdr1b gene, encoding the multidrug resistance P-glycoprotein (P-gp), increased the rate of channel activation and the rate of RVD. In addition, P-gp decreased the magnitude of hyposmotic shock required to activate the channels and to elicit RVD. Tamoxifen selectively inhibited both chloride channel activity and RVD. No effect on potassium channel activity was elicited by expression of P-gp. The data show that, in these cell types, swelling-activated chloride channels have a central role in RVD. Moreover, they clarify the role of P-gp in channel activation and provide direct evidence that P-gp, through its effect on chloride channel activation, enhances the ability of cells to down-regulate their volume.

3T3 Cells↗
PubMed1996

Controlling Paroxysmal Atrial Fibrillation by a Combination of Amiodarone and Flecainide: Description of a Case With 15-Year Follow-up.

A 77-year-old man with no known cardiac disease has had paroxysmal atrial fibrillation for 35 years with disabling symptoms and poor exercise tolerance when not in sinus rhythm, and he did not respond to conventional therapy. Fifteen years ago he was placed on amiodarone. His arrhythmia converted to atrial flutter with a flutter rate below 200 beats/min; DC cardioversion at 3 months led to transient sinus rhythm. At 5 months he converted spontaneously to sinus rhythm and had very few recurrences until 4 years later when he began to experience further frequent recurrences when the dose was reduced from 400 mg/day to 200 mg/day. Redosing at the higher dose led to skin discoloration; amiodarone was then replaced with sotalol, which the patient did not tolerate. After 9 months with efforts to rate control with various agents, amiodarone was reintroduced at 400 mg/day, which achieved full control, but to obviate the development of skin changes, flecainide was added at a dose of 100 mg twice a day, and the dose of amiodarone was gradually reduced to 200 mg/day. This combination regimen has produced no side effects or organ toxicity, although a degree of hypogonadism developed. It responded well to testosterone replacement. On the combination regimen, there have been no symptomatic arrhythmia recurrences over 8 years. Amiodarone and flecainide may have additive or synergistic effects in maintaining sinus rhythm in atrial fibrillation; the antiarrhythmic property of amiodarone is likely to minimize or nullify the proarryhthmic reactions of flecainide during combination therapy. This combination regimen may allow the extension of the use of flecainide in controlling refractory atrial flutter and fibrillation in patients with structural cardiac disease. The efficacy and safety of the combination regimen of the two drugs should be addressed in controlled clinical trials.

Journal Article↗
PubMed1995

Volume changes in single N1E-115 neuroblastoma cells measured with a fluorescent probe.

A non-invasive microspectrofluorimetric technique was used to investigate experimentally induced changes in cell water volume in single N1E-115 murine neuroblastoma cells, using calcein, a derivative of fluorescein, as a marker of the intracellular water compartment. The osmotic behavior of N1E-115 cells exposed to media of various osmolalities was studied. Exposure to hyperosmotic (up to +28%) or hyposmotic (up to -17%) solutions produced reversible decreases and increases in cell water volume, respectively, which agreed with near-osmometric behavior. Increases in [Ca2+]i produced by exposing the cells to the ionophore ionomycin (1 microM) in isosmotic medium, resulted in a gradual decrease in cell water volume. Cells shrank to 40 +/- 7% (n = 7) below their initial water volume at an initial rate of -1.2 +/- 0.2%/min. It is concluded that N1E-115 cells are endowed with Ca2+-sensitive mechanisms for volume control, which can produce cell shrinkage when activated under isosmotic conditions. Because the technique used for measuring cell water volume changes is new, we describe it in detail. It is based on the principle that relative cell water volume in single cells can be measured by introducing an impermeant probe into cells and measuring its changes in concentration. If the intracellular content of the probe is constant, changes in its concentration reflect changes in cell water volume. Calcein was used as the probe because its fluorescence intensity is directly proportional to its concentration and independent of changes in the concentration of native intracellular ions within the physiological range. Because calcein is two to three times more fluorescent that other fluorophores such as 2,7,-bis-[2-carboxyethyl]-5-[and 6]-carboxyfluorescein or Fura-2, and it is used at its peak excitation and emission wavelengths, it has a better signal to noise ratio and baseline stability than the other dyes. Calcein can also be esterified allowing for cell loading and because of the possibility of reducing the intensity of the excitation light, measurements can be performed producing minimal photodynamic damage. The technique allows for measurements of cell water volume changes of < 5% and it can be applied to single cells which can be grown or affixed to a rigid substratum, e.g., a coverslip.

Animals↗
PubMed1994

Transmembrane ion movements elicited by sodium pump inhibition in Helix aspersa neurons.

1. Transmembrane ion movements upon sodium-pump inhibition were studied in identified neurons of the subesophageal ganglia of Helix aspersa. A two-microelectrode, voltage-clamp technique was used to measure transmembrane currents. Changes in intracellular Na+, K+, and Ca2+ concentrations were measured, in unclamped neurons, with Na(+)-sensitive microelectrodes, K(+)-sensitive microelectrodes, and with the fluorescent probe fura-2, respectively. 2. Inhibition of the sodium pump with ouabain (1 mM) elicited an increase in intracellular Na+ concentration, [Na+]i, at an initial rate of 0.42 +/- 0.05 mM/min (mean +/- SE; n = 27), and a membrane depolarization often followed by hyperpolarization. In cells clamped at -50 or -60 mV, ouabain produced an inward shift in membrane-holding current followed by an outward current usually having two components, transient and sustained, respectively. 3. Replacing external Na+ with either N-methyl-D-glucammonium or tetraethylammonium (TEA+) abolished both the ouabain-induced inward membrane current and the rise in [Na+]i, suggesting that Na+ was the charge carrier of the inward current. 4. Cd2+ (400 microM) reduced the rate of rise of the inward current by 60% and the estimated net Na+ flux by 47%. 5. The outward current was abolished by K(+)-channel blockers (10 mM TEA+ and 5 mM 4-aminopyridine or 10 nM apamin). Cd2+ (400 microM), a Ca(2+)-entry blocker, also abolished the outward current. 6. Inhibition of the sodium pump elicited a fall in [K+]i at an initial rate of 1.4 +/- 0.2 mM/min (n = 9 cells). 7. Upon inhibition of the sodium pump in neurons loaded with fura-2, [Ca2+]i increased from an estimated resting level of 147 +/- 37 nM to a maximum of 764 +/- 248 nM (n = 12 cells). 8. The rise in [Ca2+]i in the sustained presence of ouabain was transient, lasting 19.5 +/- 2.8 min, and could be prevented by removal of external Ca2+ before ouabain application or curtailed by removal of external Ca2+ during sustained ouabain exposure. The latter effect was not a consequence of exhaustion of caffeine-sensitive intracellular Ca2+ stores. 9. It is concluded that 1) the rise in [Ca2+]i upon Na(+)-pump inhibition requires the presence of external Ca2+, 2) the outward current observed upon pump inhibition is a Ca(2+)-activated K+ current flowing through apamin-sensitive channels, 3) the resting Na+ permeability involves a Cd(2+)-sensitive component, 4) a large fraction (approximately 30-60%) of the previously described ouabain-induced cell shrinkage may result from Ca(2+)-activated K+ efflux contributing to net solute and water loss.

Adenosine Triphosphate↗
PubMedDate not supplied

Myocardial perfusion scintigraphy (SPECT) in the evaluation of patients in the emergency room with precordial pain and normal or doubtful ischemic ECG. Study 60 cases.

OBJECTIVES: To evaluate the diagnostic utility of myocardial perfusion by SPECT and Gated-SPECT in the diagnosis of acute coronary syndrome in patients with precordial pain associated with normal or doubtful ischemic ECG within the first 6 hrs of the last episode of pain. METHODS: Sixty such patients who sought attention in the Emergency room were included. Myocardial perfusion SPECT and Gated-SPECT (GSPECT) was performed in all patients using two distinct protocols. All patients underwent resting and pharmacological stress test. In 30 cases coronary angiogram were performed. RESULTS: Resting myocardial perfusion was abnormal or positive in 25 patients (42%) and normal or negative in 35 patients (58%). In the latter group perfusion became abnormal in 15 patients (43%) under stress with dipyridamole, while it remained normal in 19 (54%). The last subgroup presented no coronary events during the 12 months following their hospital discharge. In the group of 25 patients with resting perfusion abnormalities acute myocardial infarction was diagnosed in 7 patients, ischemia in 12 and reverse-reversibility in 6. Myocardial perfusion scintigraphy showed in the resting phase a low sensitivity of 61% (95% CI 39-74%), and negative predictive value of 71% (95% CI, 58-82%). During the stress phase, the utility of the test increased significantly, with a sensitivity of 97% (95% CI, 83-99%), specificity of 79% (95% CI, 57-92%), positive predictive value of 87% (95% CI, 72-95%) and, most outstanding, a negative predictive value of 95% CI, 73-99%). CONCLUSIONS: Myocardial perfusion studies have a sensitivity of 97% for identifying patients with acute coronary syndrome, with precordial pain and normal or doubtful ischemic ECG. For the intermediate or low risk patients with acute coronary syndrome the non-invasive diagnostic techniques of SPECT and GSPECT systems of evaluating myocardial perfusion achieve a high degree diagnostic accuracy, safety and reduces unnecessary admissions and costs.

Aged↗
PubMedDate not supplied

[Myocardial ischemia detection with adenosine administration and SPECT. Initial experience in Mexico].

UNLABELLED: Myocardial perfusion SPECT has a high sensitivity for the diagnosis of myocardial ischemia. Adenosine has been recently used to induce myocardial ischemia in the United States and Europe. At the present time there is not published experience using adenosine in Mexico. METHOD: We studied 22 patients with suspected myocardial ischemia. Coronary angiography was performed in 17 patients. We used a 8 mCi rest Tc-99m sestamibi followed by a 6 minute infusion of adenosine at a dose of 140 ug/kg/min; 24 mCi of Tc-99m were injected after the third minute of adenosine infusion. Patients returned 2 or 3 days later for a new stress study using physical stress or dipiridamole and the images were read using a 20 segments analysis and each segment was scored using a 5 points scale (0 = normal to 4 = absent uptake). The results were then compared with the adenosine images. RESULTS: The segmental score agreement between adenosine and physical or dipyridamole stress were good with 90% exact correlation. The side effects experienced by patients who received dipyridamole and adenosine were similar. CONCLUSION: Adenosine is a good alternative to induce myocardial ischemia. It showed a good correlation with physical or dipyridamole stress test.

Adenosine↗