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V Alfaro

Publications and source records attributed to V Alfaro.

33 records · Page 2Linked to original sources
PubMed1997

Long-term domiciliary treatment with nasal intermittent positive-pressure ventilation plus supplemental oxygen in COPD with severe hypercapnia.

An effective treatment of advanced states of chronic obstructive pulmonary disease (COPD) has yet to be established. We report the case of a COPD patient with severe hypoxemia (pO2 = 32.0 mm Hg) and hypercapnia (pCO2 = 90.0 mm Hg) who was successfully treated for 8 months with nasal intermittent positive-pressure ventilation (NIPPV) plus supplemental O2 in a domiciliary treatment. The reduction of hypoxemia parallel to the alleviation of hypercapnia reversed the patient's continuously declining condition.

Blood Gas Analysis↗
PubMed1996

Factors influencing the acid-base changes in the air-pouch exudate following carrageenan induced inflammation in rats.

The interactions between the acid-base variables that contribute to exudate acidosis were studied in the subcutaneous air-pouch after carrageenan injection in rats. We studied the concurrent changes of exudate gases (PCO2 and PO2), main ions ([Na+], [K+], [Ca2+], [Mg2+], [Cl-] and [Lac-]), inorganic phosphate (P(i)) and albumin in acutely inflamed rats (4, 8, 12, 24 and 48 h of inflammation). A notable hypercapnia was found in the exudate after only 8 h (exudate PCO2 = 64.3 +/- 2.9 mm Hg) but this hypercapnia decreased after 48 h (32.9 +/- 12.7 mm Hg), coincident with the greatest increase in exudate cells. With respect to the metabolic acid-base variables, the most important changes found were a parallel decrease in the strong ion difference ([SID]) and exudate pH, as well as increases in the exudate weak acid buffers ([ATOT]) due to albumin and inorganic phosphate (P(i)) increases. However, after 12 h, the exudate acidosis was stable at around pH 7. A similar acid pH was obtained after 24 h of inflammation when the carrageenan solution injected was previously adjusted to a physiological pH (7.4). This pH, analogous to that of the exudate, was the result of compensation by the acid-base independent variables, a fact which suggests that acid pH may be a beneficial condition for cells taking part in inflammatory processes.

Acid-Base Equilibrium↗
PubMed1996

Acute mild hypothermia in awake unrestrained rats induces a mixed acid-base disorder.

The interactions between components that contribute to acid-base homeostasis were studied in the first steps of acute hypothermia [body temperature (Tb) 37-31 degrees C] in awake unrestrained rats as an experimental model of accidental hypothermia in mammals. The concurrent changes in blood gases, plasma ions, and plasma protein concentrations in arterial blood were analyzed. Acute decreases in Tb decreased PCO2 and increased pH. The ratio of Na+ concentration to Cl- concentration increased at 35-33 degrees C Tb, leading to an increase in the plasma strong ion difference ([SID]). These increases were transient, and levels returned to baseline at lower Tb (31 degrees C). Lack of change in hematocrit, hemoglobin, plasma osmolality, or plasma protein concentration indicated stability in plasma volume. Therefore, [SID] changes were related to ionic shifts with respect to the extravascular space and not to ionic depletion. A feasible role in this ionic exchange for contracting skeletal muscle during shivering thermogenesis is given. Significant decrease in HCO3- concentration at lower Tb (31 degrees C) was related to an apparent increase in relative ventilation (lung ventilation per unit of CO2 removed). It is concluded that, during the first stages of body cooling, the blood acid-base status of conscious hypothermic rats is affected by PCO2 changes, apparently because of uncoupled changes between ventilation and metabolism, but it is also affected by a transitory metabolic disorder due to ion imbalance.

Acid-Base Imbalance↗
PubMed1996

Blood sampled in rats from right ventricle may not always be truly representative of a mixed venous sample.

Blood samples from the right ventricle (RV) in rats are usually assumed to be representative of mixed venous blood. However, results presented here suggest that this assumption may not be true in all experimental circumstances. Nineteen male Wistar rats were anaesthetized with urethane and mechanically ventilated. The six gases used in the multiple inert gas elimination technique (MIGET) were administered continuously and samples of mixed expired air and blood from the left carotid artery and RV were simultaneously withdrawn. While inert gas concentrations in arterial blood and mixed expired air were almost homogeneous, those obtained from RV blood showed a high variability, specially evident for the less soluble gases in blood. As inert gases are cleared in the lungs according to their solubility in blood and they are only replaced through the lower systemic circulation, higher or lower concentrations found in RV samples than those expected suggests a preferential collection of blood from the lower or upper systemic circulation, respectively.

Animals↗
PubMed1996

Blood acid-base changes during acute experimental inflammation in rats.

Acidosis has often been reported in inflamed tissues, and changes in strong relevant ions at the site of inflammation may provoke alterations in blood acid-base status. We measured changes in blood acid-base variables during carrageenan-induced inflammation in rats. We found a mixed acid-base disorder in rat blood during acute inflammation (12, 24, and 48 h). A metabolic acid contribution was found during the first 12 h and maintained further, as revealed by a decrease in plasma strong ion concentration difference ([SID]) and an increase in plasma weak acid concentration due to a rise in inorganic phosphate ([ATOT]P(i)). Plasma [SID] and [ATOT]P(i) changes were probably due to exchange of Na+ and P(i) between the inflammatory exudate and rat blood. A secondary respiratory compensation for the metabolic acid changes occurred in the blood of inflamed rats, resulting in significant hypocapnia. Furthermore, a progressive decrease in the total weak acid buffer concentration due to a decrease in plasma albumin ([ATOT]Alb) also counteracted the impact of changes in [SID] and P(i) to increase blood acidity. Therefore, despite the metabolic acid-base disorders induced by inflammatory processes, hydrogen ion (H+) homeostasis was maintained, and blood pH remained essentially unchanged in the inflamed rats.

Acid-Base Imbalance↗
PubMed1996

Improvement in exercise tolerance and spirometric values in stable chronic obstructive pulmonary disease patients after an individualized outpatient rehabilitation programme.

OBJECTIVE: We sought to determine whether patients with stable chronic obstructive pulmonary disease (COPD) whose exercise performance is mainly limited by dyspnoea are able to improve their exercise tolerance after rehabilitation with an individualized programme based on aerobic training at the ventilatory threshold (VT) level. PATIENTS AND EXPERIMENTAL DESIGN: Thirteen stable and moderate to severe COPD patients took part in an outpatient rehabilitation programme lasting 4 months. This individualized programme consisted of exercise training (general training on cycle and upper-limb training by rowing at the heart rate corresponding to VT) together with provision of adequate calorie and protein support. RESULTS: Lung function test after rehabilitation revealed significant increases in FVC (82.9 vs 69.2 % pred) and FEV1 (47.2 vs 39.7 % pred), although FEV1/FVC were unchanged (44.8 vs 46.8%). Incremental exercise test performed on cycle revealed significant increases in time, work rate (82.0 vs 63.2 W), peak VO2 (14.6 vs 10.7 ml.kg-1.min-1), peak VO2 (840 vs 701 ml.min-1), peak VT (1309 vs 980 ml), and O2-pulse (8.3 vs 6.7). However, exercise tests were always symptom-limited by dyspnoea. CONCLUSIONS: We conclude that this individualized outpatient rehabilitation programme is able to improve exercise tolerance in stab le COPD patients affected by dyspnoea during exercise, through an apparent reconditioning of both skeletal and respiratory muscles and improved gas exchange during exercise, thus reducing the ratio of dead space to tidal volume. In consequence, patients whose exercise capacity is so reduced that they cannot develop significant lactic acidosis may reduce the ventilatory cost for exercise through this individualized therapy.

Aged↗
PubMed1996

A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease.

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.

Acid-Base Equilibrium↗
PubMed1995

Factors influencing acid-base status during acute severe hypothermia in unanesthetized rats.

Blood acid-base changes were studied during acute hypothermia (4-6 h) induced by cold exposure in the unanesthetized rat. Stewart's quantitative analysis was applied as a complementary approach to determine the relative contributions of several non-respiratory components to the arterial acid-base response. Acute decrease in body temperature (TB) lowered PaCO2 (32.5 to 14.5 mmHg) and [HCO3-]a(24.20 mEq/L to 17.56 mEq/L), increased pHa (7.481 to 7.608) and diminished the [OH-]/[H+] ratio, but had no significant effect on [SID] or [Atot], although both total phosphorus [PT] and inorganic phosphate [Pi] increased. The acid-base changes found were intermediate between those predicted by alpha-stat and pH-stat hypotheses. Deviation from the regulative alpha-imidazole strategy was more apparent in the plasma than in the intraerythrocyte compartment. We conclude that blood pH changes observed were mainly caused by increased relative ventilation (lung ventilation per unit of CO2 removed) and by resulting changes in PCO2, with a minor metabolic component but without significant contribution from ionic shifts or changes in plasma protein concentration.

Acid-Base Imbalance↗
PubMed1995

Human autologous serum for the treatment of full-thickness macular holes. A preliminary study.

BACKGROUND: Recent studies have shown the usefulness of pars plana vitrectomy with/or without the use of transforming growth factor-beta in treating macular holes. The purpose of the present study is to test the efficacy of autologous serum in conjunction with current surgical techniques in the repair of stage 3 or 4 macular holes. METHODS: A total of 11 eyes in nine patients with stage 3 or 4 full-thickness macular holes were treated. The patients ranged in age from 53 to 80 years (mean, 68 years). These patients were followed for 4 to 11 months (mean, 8.4 months). Preoperative best-corrected visual acuity ranged from 2/200 to 20/80 (mean, 20/200). A standardized pars plana vitrectomy was performed with removal of the posterior hyaloid and/or removal of epiretinal membranes, fluid-gas exchange. Autologous serum (0.1 ml) was instilled over the macular hole followed by perfluorocarbon gas tamponade and head positioning for 2 weeks. RESULTS: All 11 (100%) of the eyes in 9 patients had resolution of the surrounding subretinal fluid and flattening of the macular hole. All of the eyes showed an improvement of at least two lines or more (mean, 4.7 lines) in visual acuity. Three eyes (27%) had visual acuities of 20/40 or better, and seven (64%) had visual acuities of 20/60 or better. No exuberant fibrosis proliferation was noted in any eye. CONCLUSION: The results of this preliminary study indicate the possible benefit of autologous serum when used in conjunction with current surgical techniques in treating stage 3 or 4 macular holes.

Aged↗
PubMed1993

Comparison of acid/base status in conscious and anaesthetized rats during acute hypothermia.

Acute hypothermia was surface-induced in unrestrained conscious rats at two different levels, moderate (30 degrees C TB) and severe (20 degrees C TB). Data reflecting the acid/base status were determined. The values obtained for moderate hypothermia were compared with the acid/base pattern observed during hypothermia induced by two different anaesthetics, sodium pentobarbital and urethane, at room temperature. Conscious, hypothermic animals developed an apparent respiratory alkalosis, with an increase in pHa (from 7.476 to 7.546 in moderate hypothermia and from 7.484 to 7.563 in severe hypothermia) correlated with a decrease in arterial bicarbonate levels (from 22.9 to 16.8 mmol l-1 and from 20.7 to 14.9 mmol l-1 respectively). Lactate increased slightly in conscious, severely hypothermic rats (1.02 mmol l-1). This acid/base pattern was clearly different from that seen in sodium pentobarbital (mild respiratory acidosis) and urethane-induced hypothermia (metabolic acidosis). These results suggest that conscious rats follow a pattern closer to that underlying the relative alkalinity shown by many poikilotherms than to that underlying the constant pH shown in hibernating mammals. This latter pattern, nevertheless, approaches that observed during moderate pentobarbital hypothermia and the acid/base pattern during shallow hypothermia in birds. Anaesthesia may interfere with the development of the processes that lead to the acid/base pattern observed in conscious animals.

Acid-Base Equilibrium↗
PubMed1993

Erythrocyte osmotic resistance during acute hypothermia in awake unrestrained rats.

Erythrocyte osmotic fragility and plasma ionic composition were studied in rats subjected to acute hypothermia. A decrease in osmotic fragility and a significant increase in plasma magnesium and total phosphorus were observed in blood from hypothermic rats in relation to control. A decrease in erythrocyte osmotic fragility from hypothermic animals was observed when the test was performed at 37 degrees C, whereas osmotic fragility was unaltered if the test was carried out at body temperature. This could be interpreted as an adaptative response to counteract the opposite effect on erythrocyte osmotic fragility observed at low temperature 'in vitro'.

Animals↗
PubMed1992

Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats.

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.

Acid-Base Equilibrium↗
PubMedDate not supplied

Multiple inert gas elimination technique for determining ventilation/perfusion distributions in rat during normoxia, hypoxia and hyperoxia.

1. The use of the multiple inert gas elimination technique (MIGET) in quantifying ventilation/perfusion distributions (V*A/Q*) in small animals, such as the rat, may cause results to be biased due to haemodilution produced by the large volume of liquid infused intravenously. 2. We tested two methods of administering inert gases in rats using the MIGET: (i) standard continuous intravenous administration of inert gases (method A); and (ii) a new method based on the physicochemical properties of each inert gas (method B). This method included acute simultaneous inert gas administration using three pathways: inhalation, intravenous infusion and rectal infusion. Both MIGET methods were applied to obtain data while breathing three different inspiratory fractions of oxygen (FIO2): normoxia, hypoxia and hyperoxia. 3. Inert gas levels obtained from blood or expired air samples were sufficient for chromatographic measurement, at least during a 2 h period. The V*A/Q* distributions reported using both methods were acceptable for all the physiological conditions studied; therefore, the alternative method used here may be useful in further MIGET studies in rats because haemodilution resulting from continuous intravenous infusion of less-soluble gases can be avoided. 4. Normoxic rats showed lower mean values of the V*A/Q* ratio of ventilation distribution and higher mean values of the V*A/Q* ratio of perfusion distribution with the usual method of inert gas administration (method A). These non-significant differences were observed under almost all physiological conditions studied and they could be caused by haemodilution. Nevertheless, the effect of interindividual differences cannot be discarded. An additional effect of the low haematocrit on cardiovascular changes due to low FIO2, such as pulmonary vasoconstriction or increased cardiac output, may explain the lower dispersion of perfusion distributions found in group A during hypoxia.

Animals↗
PubMedDate not supplied

[Glutamate-related excitotoxicity neuroprotection with memantine, an uncompetitive antagonist of NMDA-glutamate receptor, in Alzheimer's disease and vascular dementia].

AIM: To review the therapeutic efficacy of memantine, an uncompetitive antagonist of N-methyl-D-aspartate (NMDA)-glutamate receptor. DEVELOPMENT: Alzheimer's disease (AD) is the most common neurodegenerative disorder and cause of dementia with ageing worldwide. The main AD symptoms are a gradual loss of cognitive function and a functional impairment. Glutamatergic excitatory neurotransmission, an important process in learning and memory, is severely disrupted in AD, probably due to the oxidative stress associated with the beta-amyloid peptide (1-42) increase. The glutamate-related excitotoxicity, mainly mediated by NMDA subtype of the glutamate receptors, is a common clue of pathogenesis for neurodegenerative disorders. CONCLUSIONS: Memantine, a moderate-affinity, voltage-dependent, uncompetitive antagonist of NMDA receptor, shows neuroprotective effects in patients with moderate-to-severe AD. Memantine is a drug with neuroprotective and cognition-enhanced properties, which can be combined with other treatments for AD. Thus, memantine does not stop or reverse AD, but its moderating effect in protecting the brain from the toxic levels of calcium, allows normal signaling among brain neurons. The efficacy and safety profile of memantine have been reported in several clinical trials for treatment of AD and vascular dementia.

Alzheimer Disease↗