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Biomedical subjects

J Sandoval

Publications and source records attributed to J Sandoval.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

[Effect of chronic altitude hypoxia on the behavior of the respiratory center. Study on normal subjects living at the altitude of Mexico City (2,240 meters)].

Respiratory center (RC) output has been shown to be increased in hypoxemic Chronic Obstructive patients at sea level. In order to asses the separate role of chronic hypoxia on the RC output we studied 30 normal subjects all of them native and residents of Mexico City (altitude: 2,240 m, PaO2: 65-70 torr.). The parameters studied were: occlussion pressure (P0.1), mean inspiratory flow (Vi), and the ratio inspiratory time to total duration of the respiratory cycle (Ti/Ttot). The inspiratory impedance of the respiratory system as well as the minute ventilation (VE) and lastly to ensure isocapnic conditions, the end-tidal CO2 (PECO2), were also measured. These parameters were determined: 1) While breathing room air (RA), 2) after 30 min of breathing an inspired oxygen fraction (FiO2) of 30% and again 3) after 30 min of breathing and FiO2 of 100%. Fifteen of the subjects were studied on supine and the other 15 in the seated position. In most of the subjects the baseline (RA) values of P0.1 were found to be higher than those reported for normals at sea level. In every case, independent of body position, the P0.1 decreased (less than 0.01) to normal sea level values after 30 min of breathing O2 30%. Likewise, Vi and mechanical impedance also decreased (p less than 0.01) and no changes in Ti/Ttot were noted at this FiO2. No further changes occurred after breathing 100%. The above results show that: 1) The RC output in normal people at altitude (i.e. without mechanical abnormalities but with chronic hypoxia) is increased as compared to sea level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Effects of nifedipine in patients with unstable chronic obstructive pulmonary disease].

The hemodynamic and gas exchange effects of 20 mg of nifedipine (NFD), at rest and exercise were evaluated in seven patients with unstable COPD and pulmonary hypertension. The cause of instability was pulmonary infection (n = 6) and pulmonary emboli (n = 1). At rest, pulmonary hypertension (Pp = 40 +/- 3 mmHg), severe hypoxemia (PaO2 +/- 2 mmHg) and elevated pulmonary vascular resistance (Rp) = 9 +/- .6 u.sq.m, were found. At exercise, Pp raised to 52 +/- 5 mmHg with no change in cardiac index (CI), Rp or gas exchange. After NFD at rest, significant (p less than 0.05) increases in CI, oxygen transport and venous admixture occurred. Also, Rp and systemic arterial pressure and resistance decreased significantly. Pp and blood gas exchange did not vary. Rp and systemic resistance were lower at exercise after NFD than without the drug with no change in blood gas exchange. The pulmonary flow pressure relationship showed a right shift after NFD in both, rest and exercise conditions. We conclude that NFD can be of value for the management of pulmonary hypertension that aggravates COPD.

Adult↗
PubMedDate not supplied

[Effects of hydralazine in hypoxic vasoconstriction. Its study in a canine model of lobar atelectasis].

To determine whether hydralazine (H) a systemic vasodilator, inhibits hypoxic pulmonary vasoconstriction (HPV) we studied in a canine model of lobar atelectasis (LA) the circulatory changes during the following interventions: a) control 1 (LA = HPV), b) during the acute effect produced by opening bilateral arteriovenous fistulas (OF), c) after the closure of the fistulas (CF) (control 2), d) after infusing H (0.33 mg/kg) and e) bleeding the animal at the end of the experiment (control 3). Once HPV was stabilized (control 1), both opening the fistulas and infusing H produced a similar and significant increase in cardiac output and a decrease in resistance (p less than 0.05). Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output (Qt). Intrapulmonary shunt (Qs/Qt) significantly increased (p less than 0.05) with the fistulas open and with H infusion. CF and bleeding the animal at the end of the experiment reversed the changes in Qt and Qs/Qt. The similar increases in Qt and Qs/Qt by OF or infusing H seems to be related to the levels of pVO2. Our data suggest that hydralazine inhibits pulmonary vasoconstriction probably by raising the level of pVO2 although a direct pulmonary vasodilatory effect of the drug could not be ruled out.

Animals↗
PubMedDate not supplied

[Hydralazine and oxygen transport in interstitial and chronic obstructive pneumopathies].

We studied the effect of hydralazine (HDL) on peripheral oxygen transport (TO2) in 8 patients with chronic obstructive lung disease (EPOC, group I) and 11 patients with chronic interstitial lung disease (NI, group II) and pulmonary arterial hypertension (HAP). Mean pulmonary artery pressure (Pp) at basal conditions were 31 +/- 3 mmHg for the EPOC group and 26 +/- 9 mmHg for NI patients. After HDL, pulmonary vascular resistance (Rp) decreased significantly only in NI patients (Rp basal = 7.1 +/- 4, Rp post HDL = 5.9 +/- 3u m2). In EPOC patients Pp increased after HDL (Pp basal = 31 +/- 3, Pp post HDL = 36 +/- 4 mmHg, p less than 0.05). This was not the case for NI patients in whom Pp did not change. Both groups showed reduction in systemic vascular resistance after HDL. PaO2, PvO2, SaO2, CvO2 and TO2 were significantly increased in both groups after HDL. TO2 change was correlated with the increasing cardiac index in both diseases and with arterial oxygen content in group II only. Our study suggest that TO2 improves in EPOC and NI patients after HDL, however only in NI was associated with a reduction in pulmonary vascular resistance.

Adult↗
PubMedDate not supplied

[Hypercapnia induced by acetazolamide and its effect on pulmonary circulation. Experimental study].

In order to evaluate the isolated hemodynamic effects of acute hypercapnea on pulmonary circulation, we designed a canine model in which vascular pressures. PaO2, and arterial pH were maintained within normal limits. Six mongrel dogs were studied. Hypercapnea was achieved by a single intravenous doses of acetazolamide (120 mg/Kg) while maintaining mechanical ventilation constant. Both arterial and mixed venous PCO2 increased from 27 to 41 mm Hg and from 31 to 46 mm Hg respectively, and remained constant through the rest of the experiment (up to 3 Hs). With hypercapnea, total pulmonary vascular resistance increased from 312 +/- 156 to 435 +/- 173 d.s.cm-5 (p less than 0.05) and the stroke index decreased from 20.7 +/- 8.3 to 13.2 +/- 4.8 ml/beat (p less than 0.05). There were no changes either in pulmonary capillary wedge pressure or in the right ventricular end diastolic pressure. The above changes suggest a pulmonary vasoconstrictor effect of hypercapnea in the absence of other known vasoactive factors.

Acetazolamide↗
PubMedDate not supplied

[Natural history of experimental pulmonary atelectasis in dogs with closed chest].

In order to establish an animal model of pulmonary vasoconstriction we followed the time course of intrapulmonary shunt (Qs/Qt) in a canine model of lobar atelectasis with closed chest. Ten mongrel dogs were studied. Bronchial occlusion of the right lower lobe (RLL) was performed by inflating the balloon of a Foley catheter placed through a rigid bronchoscopy. Analysis of variance was used for statistical analysis. (15 minutes) After occlusion Qs/Qt reached its maximum increasing from 8.2 +/- 3.6 to 29.7 +/- 11.7% (p less than 0.05) and PaO2 decreased from 357 +/- 49 to 100 +/- 43 mm Hg (p less than 0.05). Afterwards, there was a progressive decline of Qs/QT accompanied by an also progressive increase in PaO2. At the end of the experiment (3 hrs post atelectasis) Qs/Qt was 11.2 +/- 4.9 and PaO2 251 +/- 124 mm Hg (p less than 0.05). Pulmonary vascular resistance increased post atelectasis from 439 +/- 168 to 598 +/- 256 d.s.cm-5 (p less than 0.05). Complete atelectasis of the RLL was confirmed postmortem. As the changes in Qs/Qt and PaO2 did not parallel the change in cardiac output we conclude that the mechanism of decrease in Qs/Qt was hypoxic vasoconstriction.

Analysis of Variance↗
PubMedDate not supplied

[Pulmonary blood volume in patients with interstitial pneumopathy and pulmonary heart disease. Its study at rest and during exercise].

Pulmonary blood volume (PBV) measurements have been reported in chronic lung disease that do not include diffuse interstitial lung disease (ILD) and cor pulmonale (CP). In this study, PBV was measured using the double injection single sampling method, at rest and at exercise in ten patients with ILD due to extrinsic allergic alveolitis (n = 6) or usual interstitial pneumonia (n = 4). Lung biopsies were obtained in 8 patients, and in none of them the stage of fibrosis was predominant over inflammation. The degree of vascular lesions was in four patients grade I and in four grade II (Heath-Edwards classification). At rest, most of the patients had elevated mean pulmonary artery pressure (PAP) and vascular resistance (PVR), (mean PAP 30 +/- 4 mmHg and 336 +/- 171 d.s. cm.-5, respectively), hypoxemia (paO2 = 48 +/- 2 mmHg) and a severely reduced PBV (53.6 +/- 11 ml.s.qm.). At exercise, pulmonary arterial hypertension worsened and, although PBV value increased significantly (rest = 53.6 +/- 11.6 ml.m2, s.qm. exercise 132 +/- 28 ml.s.qm.p less than 0.01) it remained abnormally low with respect to normal value. Comparison of the mean intravascular pressure-PBV measurements relationship in different lung diseases showed that ILD patients with CP have the greatest abnormality. Possible explanations for the severe reduction in PBV include restriction of extra-alveolar vessels as a consequence of lung volume loss, restriction of intra-alveolar vessels due to structural and functional changes imposed by the inflammation-fibrosis process and vascular restriction due to vasoactive factors (alveolar hipoxia).

Adult↗
PubMedDate not supplied

[Vascular conductance and critical closing pressure in the isolated canine lung in situ. Its natural history].

The vascular pressure-flow relationship (P-QL) in West's zone II condition were studied in isolated, in situ, canine, left lower lobe (ISLL) in order to characterize the total resistance in the pulmonary vascular bed (Rp), the normal values for pulmonary vascular conductance (Cv) and for critical closing pressure (PLc). After the basal parameters were obtained, measurements of Cv and PLc were done every 30' in order to know the natural history (NH) of this canine ISLL preparation. The P-QL relationship of the pulmonary vasculature of the ISLL preparation, perfused under classical zone II conditions, can be characterized by a rectilinear segment at high flow, a curvilinear segment at low flow and a pulmonary arterial pressure that exceeds alveolar (PA) pressure at zero flow. This demonstrates the existence of critical closing pressure (PLc) in the pulmonary vascular bed. The mean control Cv and PLc were 38.5 +/- 14 (ml. min)/mmHg and 7.9 +/- 2.2 mmHg respectively; those parameters did not change through the observation of the experiment. PLc was found to be independent of bronchial flow and it was not related to PA when the values for this pressure were less than 5 cm H20. On the contrary, higher levels of PA pressure were significantly related to PLc (r = 0.94, p less than 0.05). We conclude that in this model of ISLL in West's zone II condition it is possible to study the two components of Rp, one given by vessels that determine changes in flow resistance and for the other vessels disclosing critical closure. The values of these components remained stable over 180' of observation.

Animals↗
PubMedDate not supplied

[Pneumonitis caused by hypersensitivity to the antigen(s) of pigeons. I. Clinical study].

We studied twenty six patients with hypersensitivity pneumonitis due to pigeon antigens (pigeon breeder's disease). This insidious illness, causes an interstitial lung disease, with restrictive pattern and also pulmonary hypertension. Most of the cases showed circulating antibodies against pigeon serum proteins, polyclonal hypergammaglobulinemia and rheumatoid factor. Treatment based on avoidance of pigeon droppings and glucocorticoids gave good results.

Adolescent↗
PubMedDate not supplied

[Active and passive factors in the genesis of pulmonary arterial hypertension in various cardiopathies and pneumopathies].

The role of active and passive factors involved in the genesis of Pulmonary Arterial Hypertension (PAH) is analyzed in a group of eighty patients with several cardiopathies and pneumopathies. The group include: 20 patients with Chronic Obstructive Lung Disease (NODC), 20 with Diffuse intersticial pneumopathy (NI), 12 with Cardiorespiratory Syndrome of the grossly obese (OB), 6 with Pulmonary Embolism (TEP), 6 with Mitral Stenosis (CRI), 5 with Hypertensive Ventricular Septal Defect (CIV + HAP) and 11 patients with Pulmonary Arterial Hypertension of Unknown etiology (HAP-ED). For the analysis, the Harvey and Enson's formulas were used. The conclusions of the study are: 1) The compliance of the elastic arteries of the lung in the groups of NOC, NI and OB is normal but in the other groups seems to be modified. 2) In the groups of NI and OB the interrelationship of factors such as alveolar hypoxia and pulmonary wedge pressure (PWP) play the major role in the genesis of PAH, although the role of the PaCO2 in the OB group remains to be established. 3) In the groups of NOC, CRI and TEP the PWP is not determinant. The absence of a significant correlation between arterial oxygen unsaturation and pulmonary diastolic pressure in the NOC group suggests other factors. 4) The vascular structural damage seems to be the most important factor in the genesis of PAH in the HAP-ED and CIV + HAP groups.

Carbon Dioxide↗
PubMedDate not supplied

[Pulmonary alveolar microlithiasis. Study of pulmonary circulation].

Pulmonary alveolar microlithiasis is a rare disease of unknown etiology which consists of alveolar deposit of calcium microspheres. We report the procedures for the diagnosis of this disease, as well as the hemodynamic features of the pulmonary circulation. Pulmonary arterial hypertension (PAH), and cor pulmonale were documented. The active and passive factors involved in PAH are analyzed. We conclude that alveolar hypoxia and estructural vascular changes play a major role in the genesis of PAH.

Calculi↗
PubMedDate not supplied

[Respiratory function in extrinsic allergic alveolitis caused by pigeons. Clinical, pathological and functional correlation].

Lung function tests (LFT) were performed in 71 patients with proven extrinsic allergic alveolitis due to pigeons (EAA-P), and they were correlated with lung biopsy (LB) findings. Lung function studies were analyzed to evaluate the clinical course of these patients treated with corticosteroids. Restrictive pulmonary function impairment was found in all cases (vital capacity 38 +/- 4%), residual volume was increased in 9 out of 14 patients (64%) (RV = 0.51 +/- 0.06 L.) and bronchial obstruction was a feature in 11/14 patients (78%) (MMEF = 53 +/- 4%). In all cases a low Pa02 was observed (44 +/- 2 mmHg) and in six an increase in PaC02 was detected. The vital capacity did not correlate with the degree of inflammation or fibrosis observed by LB. A significant negative correlation was found between Pa02 and the degree of inflammation (r = 0.68, p X 0.05) as well as with fibrosis + inflammation degrees (r = -0.63, p less than 0.05). In general, initial LFT and clinical improvement occur simultaneously. Lung function tests support the diagnosis of EAA-P, but are not capable of separating inflammation from lung fibrosis.

Adolescent↗
PubMedDate not supplied

[Pneumonitis caused by hypersensitivity to pigeons. (I). Clinical value of counterimmunoelectrophoresis for detection of specific antibodies in the serum].

Hypersensitivity pneumonitis due to pigeon's exposure (pigeon's breeder disease) is a interstitial lung disease caused by immune mechanisms after sensitization to pigeon serum antigens. An immunological test, counterimmunoelectrophoresis (CIE), has been developed to recognize the humoral immune response against pigeon serum and dropping antigens, in a simple, low cost and fast test than other cumbersome tests presently in use. The CIE has high sensibility and specificity (X2 = 35.8 p 0.001) that guarantee its clinical usefulness. When Pigeon breeder's disease is suspected on clinical grounds, the CIE test is indicated to confirm diagnosis.

Adult↗