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Biomedical subjects

C Izquierdo

Publications and source records attributed to C Izquierdo.

34 records · Page 2Linked to original sources
PubMed1984

Measurement of infarct size in acute canine myocardial infarction by single-photon emission computed tomography with technetium-99m pyrophosphate.

The location and extent of myocardial infarction (MI) are important predictors of patient course. The current study tests the hypothesis that MI size could be measured accurately using rotating gamma camera single-photon emission computed tomography ( SPECT ) and technetium-99m pyrophosphate (PPi) and that the accuracy of these measurements was independent of MI location and transmural or nontransmural distribution. SPECT was performed in 38 dogs 48 hours after ligation of the left anterior descending coronary artery (14 dogs) or left circumflex coronary artery (LC) (24 dogs) at the mid-level or below. Projection images were corrected for center-of-rotation and field nonuniformity and processed with a 1-dimensional low-pass filter to diminish rib activity. Sixteen 0.5-cm-thick transverse sections, including the entire left ventricle, were reconstructed by filtered backprojection , low-pass filtered, contrast enhanced and processed with a 3-dimensional boundary enhancement operator. The boundary of PPi uptake in each slice was marked automatically using an algorithm that combined a directional derivative and a threshold, and required continuity of the boundary in 3 dimensions. The total number of volume elements that showed abnormal tracer uptake were summed, corrected to absolute volume, and multiplied by the specific weight of cardiac muscle. Scintigraphic MI weight was compared with pathologic MI weight. There was an excellent correlation between scintigraphic and pathologic MI weight. The poorer correlation for nontransmural compared with transmural MIs is most likely a function of size alone, since MIs that weighed less than 10 g (n = 12, range 1.3 to 9.5 g), both transmural and nontransmural, showed a similar correlation: S = 1.07 X P + 0.56 (r = 0.81, standard error of the slope = 0.245).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. III. Influence of basal heart rate.

The influence of basal heart rate (HR) on the effects of inotropic (dobutamine infusion) and chronotropic (atrial pacing) stimuli during acute myocardial ischemia was assessed by measurement of intramural carbon dioxide partial pressure (PCO2) in open-chest dogs undergoing transient 10-minute left anterior descending coronary artery occlusions. In protocol I, in 5 dogs anesthetized with pentobarbital alone, HR increased from 153 +/- 10 to 182 +/- 7 beats/min between experimental coronary occlusions, but the increase in ischemic zone intramural carbon dioxide tension (delta PmCO2) was not altered by this significant increase in HR. In protocols II to V, dogs were anesthetized with combinations of morphine, thiamylal and pentobarbital and had a basal average HR of 81 beats/min. Atrial pacing in protocol II (13 dogs) increased HR from 76 +/- 21 to 134 +/- 19 beats/min (p less than 0.001); left ventricular (LV) myocardial oxygen consumption (MVO2) rose from 3.9 +/- 1.6 to 4.9 +/- 1.4 ml/min/100 g (p less than 0.05), and delta PmCO2 rose from 42 +/- 14 to 50 +/- 15 mm Hg (p less than 0.01), indicating more severe ischemic injury during the second experimental coronary occlusion. In protocol III, 11 dogs received 20 micrograms/kg/min of dobutamine before the second experimental occlusion, which significantly (p less than 0.02) increased HR, LV dP/dt and MVO2; delta PmCO2 increased from 46 +/- 13 to 63 +/- 18 mm Hg (p less than 0.01). The 7 dogs in protocol IV received 3.9 +/- 1.9 micrograms/kg/min of dobutamine, titrated such that HR was unchanged (84 +/- 10 vs 81 +/- 15 beats/min), but LV dP/dt increased by 92% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A mechanism for fibrin monomer aggregation based on a kinetic study.

A kinetic study was carried out of the aggregation of fibrin monomers under different reaction conditions. At either acid or base pH values, second-order kinetic processes were observed throughout the concentration range studied. At neutral pH (6.8 less than or equal to pH less than or equal to 7.3) the kinetics were of second order at fibrin monomer concentrations of less than 0.3-0.4 mg/ml, while at higher concentrations they changed to first order. Both the second order rate constants and the opacity of the fibrin gels are highly dependent on pH, ionic strength, the concentration of calcium ions and on temperature. A three-step reaction mechanism is proposed for the aggregation of fibrin monomers to explain the kinetic behaviour observed in the different reaction media.

Blood Coagulation↗
PubMed1983

A comparison of infarct identification with technetium-99m pyrophosphate and staining with triphenyl tetrazolium chloride.

The topographic relationship between the uptake of technetium-99m pyrophosphate (PPi) and myocardial infarction delineated by 2,3,5-triphenyl tetrazolium chloride (TTC) was studied in a canine model of permanent coronary occlusion (24-48 hr). Photographs of TTC staining and scintigraphic images of PPi uptake were planimetered for infarct area. In addition, narrow tissue samples (3 X 10 mm) were taken on both sides of the TTC border and counted for PPi uptake. A significant correlation (p less than 0.001) was found between area of PPi uptake and area of myocardium unstained by TTC (r = 0.84 in epicardium and r = 0.91 in endocardium). The slope relating PPi to TTC for all infarcts was 1.01 +/- 0.11, indicating that variations in infarct size were followed equally by the two techniques. Tissue counting showed the ratio of PPi activity just inside the infarct to activity just outside the infarct to be 9.2 +/- 0.6 (mean +/- s.e.m.). Thus, PPi is distributed topographically in a manner identical to the distribution of irreversibly injured myocardium as delineated by TTC.

Animals↗
PubMed1982

Kinetic studies of the transphosphorylation reactions catalyzed by alkaline phosphatase from E. coli: hydrolysis of p-nitrophenyl phosphate and o-carboxyphenyl phosphate in presence of Tris.

1. Transphosphorylation of p-nitrophenyl phosphate and o-carboxyphenyl phosphate to Tris, has been studied at alkaline and acid pH. 2. The rate of release for all reactions products was Tris-dependent for both substrates, with a slight maximum for phenol at alkaline pH. These dependences have been analyzed from a mechanistic standpoint. 3. Individual constants of rate of a simple transphosphorylation mechanism have been determined. 4. At high Tris concentration (greater than 1.0 M) a slight competitive inhibition has been observed. 5. Inhibition in NH4+-NH3Cl buffer has been found at alkaline pH but not at acid pH. It would therefore seem that the non-protonated NH2 group of Tris is responsible for inhibition. 6. The results suggest the formation of complexes between Tris and the enzyme. Other possible alternatives are also analyzed.

Alkaline Phosphatase↗
PubMed1982

Negative cooperativity in alkaline phosphatase from E. col: new kinetic evidence from a steady-state study.

1. A study has been carried out on the steady-state kinetics followed by the alkaline phosphatase from Escherichia coli at different pH, temperatures, ionic strengths, phosphate concentrations and in the presence of the effectors such as Tris, NH4+--NH3 and CH3OH; p-nitrophenyl phosphate was used as substrate. 2. Contrary to what has generally been accepted, in most cases the enzyme follows non-Michaelian kinetics for a wide substrate concentration range, giving concave-down Lineweaver-Burk plots. Only at high phosphate concentrations (5 . 10(-3) M) and at high ionic strengths (2.0 M) is a linear Lineweaver-Burk plot obtained (Michaelian kinetics). 3. In order to analyse the kind of kinetics obtained, a non-linear regression fitting method was used to obtain rate vs substrate concentration equations as polynomial quotients of minimum degree with positive coefficients. 4. Most of the data obtained follows 2:2 degree type equations. 5. These results tend to suggest an idea of cooperativity rather than one of independence between the sites of the dimeric enzyme. A model is discussed for cooperativity between the sites with a wide concentration range giving concave-down Lineweaver-Burk plots.

Alkaline Phosphatase↗
PubMed1982

Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion.

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.

Animals↗
PubMed1982

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. I. Studies with dobutamine in the anesthetized dog.

The effect of i.v. dobutamine on acute myocardial ischemic injury was assessed in 22 anesthetized dogs subjected to serial 10-minute occlusions of the left anterior descending coronary artery. The severity of ischemic injury was determined by mass spectrometric measurement of the increase in intramural carbon dioxide tension (delta PmCO2) in the ischemic zone. In the time protocol 1 dogs, dobutamine, 20 micrograms/kg/min, infused between the control and final occlusion, significantly increased both heart rate (HR) and left ventricular (LV) dP/dt; delta PmCO2 was significantly higher during the dobutamine infusion that during control occlusion (76 +/- 21 vs 56 +/- 13 mm Hg, p less than 0.01). The nine protocol 2 dogs were atrially paced at a HR of 20--30 beats/min above baseline values during the control occlusion and received dobutamine (12.6 +/- 7.8 micrograms/kg/min) at doses necessary to attain an equal HR (mean 149--154 beats/min) during the last occlusion. Although LV dP/dt was higher after dobutamine, delta PmCO2 was similar during the two occlusions. Protocol 3 dogs (n = 4) received lower doses of dobutamine (5.6 +/- 3.2 micrograms/kg/min) to produce an increase in LV dP/dt, but not in HR compared with baseline values; delta PmCO2 was similar during control and dobutamine occlusions. There were no major change in arterial or left atrial pressures. Rate-pressure product, an indirect measurement of myocardial oxygen consumption, was increased only by the higher doses of dobutamine in protocol 1. Thus, inotropic stimulation with dobutamine during coronary occlusion does not cause important augmentation of acute myocardial ischemic injury in the nonfailing heart unless HR is increased simultaneously.

Animals↗
PubMed1982

Radionuclide techniques for valvular regurgitant index: comparison in patients with normal and depressed ventricular function.

We compared contrast angiography with three techniques of quantitating valvular regurgitation from radionuclide ventriculograms in 70 patients: 45 with documented regurgitation graded 1-4+, and 25 without regurgitation. The radionuclide "regurgitant index" (ratio of L to R ventricular stroke counts) was measured from fixed end-diastolic regions of interest (method A), from separate end-diastolic and end-systolic regions of interest (method B), and from a "stroke-volume image" (method C). Sensitivities for detecting 1+ or more regurgitation were: method A = 57.8%, method B = 37.8% and method C = 62.2%. Sensitivities for detecting 2+ or more regurgitation were: method A = 74.2%, method B = 54.8%, and method C = 77.4%. All methods are greater than 97% specific. Interobserver coefficients of variability were: method A = 9.1%, method B = 19.2%, and method C = 5.4%. The sensitivity of each method was improved when left-ventricular ejection fractions were greater than 0.35. No method consistently differentiated between 2+, 3+, and 4+ valvular regurgitation.

Angiography↗
PubMed1981

Effect of various degrees of systemic arterial hypertension on acute canine myocrdial ischemia.

There is continuing uncertainty about the effects of various degrees of systemic arterial hypertension on myocardial ischemia. In 46 open-chest anesthetized dogs, intramural carbon dioxide tension (PmCO2) was measured directly with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow. During each occlusion, transmural regional myocardial blood flow (RMBF) in the ischemic area was quantitated with the injection of radioactive microspheres (7-10 micrometers diam). In all dogs the increase in PmCO2 from before to 10 min after the first occlusion (delta PmCO2) exceeded that during subsequent occlusions. In those dogs in which systemic arterial hypertension was not produced (controls), delta PmCO2 during the third occlusion was similar to that during the second occlusion. When phenylephrine was administered during the third occlusion to increase systemic arterial pressure mildly (diastolic pressure 95-115 mmHg), RMBF to the ischemic myocardium was unchanged, and the severity of myocardial ischemia was reduced, as reflected by a fall in delta PmCO2. When diastolic pressure was elevated moderately (116-140 mmHg), RMBF was augmented, but the extent of myocardial ischemia was neither diminished nor worsened. In contrast, when diastolic pressure was increased markedly (greater than 140 mmHg), myocardial ischemic injury was intensified (as reflected by an increase in delta PmCO2) even though RMBF rose significantly. Thus, in the dog with acute coronary artery occlusion, an increase of systemic arterial pressure exerts an influence on the severity of myocardial ischemic injury that is related directly to the magnitude of systemic arterial hypertension: a mild increase of pressure reduces ischemic injury, a moderate increase exerts no consistent effect on ischemia, and a marked increase worsens ischemic injury.

Acute Disease↗
PubMed1981

Interrelationships between regional left ventricular function, coronary blood flow, and myocellular necrosis during the initial 24 hours and 1 week after experimental coronary occlusion in awake, unsedated dogs.

This study examined the relationships between the left ventricular (LV) regional function, regional myocardial blood flow (RMBF), and myocellular necrosis after sudden proximal occlusion of the left anterior descending coronary artery (LAD) in 36 awake, unsedated dogs. Net wall thickening during systole (NET) was used to assess regional LV function, was expressed as percent control, and was measured with chronically implanted ultrasonic crystals. RMBF was measured with 8- to 10-micrometer radioactive microspheres. In regions with a moderate degree of functional loss, NET fell to 35.3 +/- 2.2% of control at 5 minutes when RMBF fell from 1.9 +/- 0.08 to .086 +/- 0.09 ml/g per min (P less than 0.05). No significant change occurred in midwall or epicardial RMBF. The relationship between endocardial flow and NET was non-linear (r = 0.69, P less than 0.0001). In these segments, subsequent changes in RMBF were unrelated to corresponding functional alterations through 24 hours. In segments with paradoxic systolic wall thinning RMBF fell in endocardial, midwall, and epicardial layers; endocardial ischemia was most severe (0.30 +/- 0.05 ml/g per min). Segmental myocellular necrosis was most severe in the endocardial layer and correlated significantly with both RMBF and segmental function. Myocellular necrosis increased in severity as flow was reduced below 70-75% of normal. Thus, in this model of LV ischemia, (1) regional LV functional loss is most sensitive to reductions in endocardial RMBF; (2) subsequent increases in RMBF are largely unassociated with functional recovery; (3) transmural ischemia results in paradoxical systolic wall thinning.

Animals↗
PubMedDate not supplied

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. II. Studies with dopamine and ouabain in the barbiturate-anesthetized dog.

To test the hypothesis that selective increases in inotropic state without concomitant acceleration of heart rate would not augment acute ischemic injury in the non-failing heart of the anesthetized dog, we carried out studies in 16 dogs subjected to serial 10-min occlusions of the left anterior descending coronary artery. The severity of ischemic injury was determined by mass spectrometric measurement of the rise in intramural carbon dioxide tension (delta PmCO2) in the ischemic zone, and inotropic stimulation was provided by either dopamine or ouabain. In Group I dogs (n = 9), dopamine [4 +/- 1 (SD) micrograms/kg/min] was infused before the final occlusion to increase left ventricular (LV) dP/dt without changing heart rate; delta PmCO2 was not significantly different between control (64 +/- 21 mm Hg) and postdopamine (67 +/- 22 mm Hg) occlusions. In Group II dogs (n = 7), ouabain (0.03 mg/kg) was administered 15 min before the final occlusion, resulting in a significant increase in LV dP/dt and a slight decrease in heart rate (average 13 beats/min); delta PmCO2 was slightly decreased in the occlusion after ouabain (60 +/- 12 mm Hg) compared with the preceding occlusion without inotropic stimulation (67 +/- 13 mm Hg), p less than 0.05. Throughout the studies in both groups, there were no significant changes in collateral blood flow to the central ischemic zone, or in heart rate-systolic arterial pressure product, an estimate of myocardial oxygen consumption. Analyses of individual responses revealed that when LV dP/dt increased by 50% or more after dopamine or ouabain, ischemia was more likely to intensify.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMedDate not supplied

[Etiology of enteritis in a university general hospital in Barcelona (1992-1995)].

BACKGROUND: The aim of the study was to describe the etiology of enteropathogenic agents over a four-year period (1992-1995) in a University Hospital in Barcelona. METHODS: We studied 12,793 stool samples, 4519 were obtained from patients under 15 years and 8274 were obtained from patients over 14 years. The specimens were examined for bacteriological, parasitological and virological enteropathogens. RESULTS: In 3380 specimens of 12,793 stool samples studied were identified an enteropathogen (26.4%). Polymicrobial associations were observed in the 6.8% of the cases. Pathogens were identified in 45% of children samples and 16.3% of adults samples. The etiological enteritis agents more frequently detected in the paediatric patients were Campylobacter (13.5%), rotavirus (11.3%) and Salmonella (10.2%); and Salmonella (4.9%), Campylobacter (3.1%) and Giardia intestinalis (2.1%) in adults. Cryptosporidium (13.5%) was the most frequent cause of gastrointestinal tract infections in HIV-infected subjects. In the children with stools positives, the presence of red and white blood cells were more frequent than the adults with stools positives (73% versus 26.6%). CONCLUSIONS: The enteropathogenic agents such as Campylobacter, Salmonella, and Giardia were the most frequent cause of gastroenteritis in our environment. In the children, rotavirus infections predominated during the cold months. The most frequent cause of gastroenteritis in HIV-infected patients was Cryptosporidium followed by Campylobacter.

Adolescent↗