[The enigma of pulmonary hypertension of undetermined origin]. / El enigma de la hipertensión arterial pulmonar de origen indeterminado.

The purpose of this review paper is to discuss: A) The differences in the nosological characteristics of this condition. Some authors only accept as primary pulmonary hypertension those patients without any other possible cause. They even exclude those with familiar pulmonary hypertension since its genetical etiology is now well established. It is more generally accepted that the very low incidence of pulmonary hypertension in conditions such as anorexigen use, portal hypertension or others, suggest the coincidence of a permissive genotype, susceptible phenotype (endothelial dysfunction) and a triggering factor. In such a way, pulmonary hypertension may be associated with apparently dissimilar conditions. B) The current interpretation of histologic lesions and their relationship with recent histochemical and immunological findings. The previously proposed hypothesis that some lesions are final and inactive results of prolonged hypertension is difficult to uphold since they were found only months after the clinical beginning of the disease. Moreover cells at the center of the plexiform lesion show histochemical activity patterns. It is also proposed that the anatomically inapparent endothelial dysfunction may be the original event. C) Proposed causal mechanisms such as down-regulation or even absence of K+ voltage channels of the pulmonary vascular smooth muscle cell. This finding would include primary pulmonary hypertension among the simultaneous "channel diseases". The data that justify the possible influence of serotonin plasma levels are also commented.

Breathing control in neurological diseases.

Control of ventilation depends on a brainstem neuronal network that controls activity of the motor neurons innervating the respiratory muscles. This network includes the pontine respiratory group and the dorsal and ventral respiratory groups in the medulla, which contain neurons that fire primarily during inspiration, post-inspiration, or expiration. The ventral respiratory group includes the pre-Bötzinger complex, which contains neurokinin-1 receptor immunoreactive neurons critical for respiratory rhythmogenesis. Structural and degenerative disorders affecting this network produce abnormalities of respiration, including sleep apnea and various patterns of dysrhythmic breathing, not infrequently associated with disturbances of cardiovagal and sympathetic vasomotor control. This emphasizes the important interactions between the respiratory and cardiovascular control networks in the medulla. Common disorders associated with impaired cardiorespiratory control include brainstem stroke or compression, syringobulbia, Chiari malformation, high cervical spinal cord injuries, and multiple system atrophy. This review focuses on the functional organization of the respiratory control network and common causes of impaired control of respiration.

El enigma de la hipertensión arterial pulmonar de origen indeterminado / The enigma of pulmonary hypertension of undetermined origin

The purpose of this review paper is to discuss: A) The differences in the nosological characteristics of this condition. Some authors only accept as primary pulmonary hypertension those patients without any other possible cause. They even exclude those with familiar pulmonary hypertension since its genetical etiology is now well established. It is more generally accepted that the very low incidence of pulmonary hypertension in conditions such as anorexigen use, portal hypertension or others, suggest the coincidence of a permissive genotype, susceptible phenotype (endothelial dysfunction) and a triggering factor. In such a way, pulmonary hypertension may be associated with apparently dissimilar conditions. B) The current interpretation of histologic lesions and their relationship with recent histochemical and immunological findings. The previously proposed hypothesis that some lesions are final and inactive results of prolonged hypertension is difficult to uphold since they were found only months after the clinical beginning of the disease. Moreover cells at the center of the plexiform lesion show histochemical activity patterns. It is also proposed that the anatomically inapparent endothelial dysfunction may be the original event. C) Proposed causal mechanisms such as down-regulation or even absence of K+ voltage channels of the pulmonary vascular smooth muscle cell. This finding would include primary pulmonary hypertension among the simultaneous "channel diseases". The data that justify the possible influence of serotonin plasma levels are also commented

El enigma de la hipertensión arterial pulmonar de origen indeterminado / The enigma of pulmonary hypertension of undetermined origin

The purpose of this review paper is to discuss: A) The differences in the nosological characteristics of this condition. Some authors only accept as primary pulmonary hypertension those patients without any other possible cause. They even exclude those with familiar pulmonary hypertension since its genetical etiology is now well established. It is more generally accepted that the very low incidence of pulmonary hypertension in conditions such as anorexigen use, portal hypertension or others, suggest the coincidence of a permissive genotype, susceptible phenotype (endothelial dysfunction) and a triggering factor. In such a way, pulmonary hypertension may be associated with apparently dissimilar conditions. B) The current interpretation of histologic lesions and their relationship with recent histochemical and immunological findings. The previously proposed hypothesis that some lesions are final and inactive results of prolonged hypertension is difficult to uphold since they were found only months after the clinical beginning of the disease. Moreover cells at the center of the plexiform lesion show histochemical activity patterns. It is also proposed that the anatomically inapparent endothelial dysfunction may be the original event. C) Proposed causal mechanisms such as down-regulation or even absence of K+ voltage channels of the pulmonary vascular smooth muscle cell. This finding would include primary pulmonary hypertension among the simultaneous "channel diseases". The data that justify the possible influence of serotonin plasma levels are also commented

El enigma de la hipertensión arterial pulmonar de origen indeterminado. / [The enigma of pulmonary hypertension of undetermined origin]

The purpose of this review paper is to discuss: A) The differences in the nosological characteristics of this condition. Some authors only accept as primary pulmonary hypertension those patients without any other possible cause. They even exclude those with familiar pulmonary hypertension since its genetical etiology is now well established. It is more generally accepted that the very low incidence of pulmonary hypertension in conditions such as anorexigen use, portal hypertension or others, suggest the coincidence of a permissive genotype, susceptible phenotype (endothelial dysfunction) and a triggering factor. In such a way, pulmonary hypertension may be associated with apparently dissimilar conditions. B) The current interpretation of histologic lesions and their relationship with recent histochemical and immunological findings. The previously proposed hypothesis that some lesions are final and inactive results of prolonged hypertension is difficult to uphold since they were found only months after the clinical beginning of the disease. Moreover cells at the center of the plexiform lesion show histochemical activity patterns. It is also proposed that the anatomically inapparent endothelial dysfunction may be the original event. C) Proposed causal mechanisms such as down-regulation or even absence of K+ voltage channels of the pulmonary vascular smooth muscle cell. This finding would include primary pulmonary hypertension among the simultaneous [quot ]channel diseases[quot ]. The data that justify the possible influence of serotonin plasma levels are also commented.

Respuesta a Broncodilatadores en pacientes ancianos / Bronchodilating response in elderly patients

El asma en el anciano es más severa y ha sido sugerido que la respuesta broncodilatadora dismi- nuida podría contribuir a esta mayor severidad. La forma más adecuada de expresión de la respuesta a broncodilatadores no está uniformemente aceptada. El objetivo del presente estudio fue explorar la respuesta broncodilatadora en pacientes ancianos con diferentes grados de severidad del asma y mediante diferentes formas de expresión de la reversibilidad. Se evaluaron 72 asmáticos (VEF1/CVF < 1.64 SEE del predicho). Fueron considerados dos grupos: Grupo I: 3 65 años (71.0 ñ 11.7 años; VEF1 54.0 ñ 16.7 por ciento del predicho) y Grupo II: < 40 años (23.0 ñ 7.7 años, VEF1 67.6 ñ 16.1 por ciento). La respuesta a broncodilatadores expresada como Dabsoluto, D percent predicho o Delta percent máximo no fue diferente entre los dos grupos. La respuesta como Delta percent inicial fue menor en los pacientes jóvenes (> 65 años: 22.2 ñ 16.6 Delta por ciento vs < 40 años: 11.8 ñ 9.9 por ciento, p = < 0.005) pero esta diferencia no persistió al realizar un análisis de covarianza tomando como cofactor de ajuste el VEF1 basal. Ni Dabsoluto (r = 0.13, p = NS), ni Delta por ciento predicho (r = 0.06, p = NS) ni Dmáximo (r = 0.09, p = NS) mostraron correlación con la edad. Delta percent inicial mostró débil pero significativa correlación con la edad (r = 0.28, p = < 0.05) y marcada dependencia del VEF1 basal (r = 0.47, p = < 0.001). La respuesta a broncodilatadores en los ancianos está conservada. La utilización de Delta por ciento inicial crea diferencias dependientes de la mayor severidad.derada.

Respuesta a Broncodilatadores en pacientes ancianos / Bronchodilating response in elderly patients

El asma en el anciano es más severa y ha sido sugerido que la respuesta broncodilatadora dismi- nuida podría contribuir a esta mayor severidad. La forma más adecuada de expresión de la respuesta a broncodilatadores no está uniformemente aceptada. El objetivo del presente estudio fue explorar la respuesta broncodilatadora en pacientes ancianos con diferentes grados de severidad del asma y mediante diferentes formas de expresión de la reversibilidad. Se evaluaron 72 asmáticos (VEF1/CVF < 1.64 SEE del predicho). Fueron considerados dos grupos: Grupo I: 3 65 años (71.0 ñ 11.7 años; VEF1 54.0 ñ 16.7 por ciento del predicho) y Grupo II: < 40 años (23.0 ñ 7.7 años, VEF1 67.6 ñ 16.1 por ciento). La respuesta a broncodilatadores expresada como Dabsoluto, D percent predicho o Delta percent máximo no fue diferente entre los dos grupos. La respuesta como Delta percent inicial fue menor en los pacientes jóvenes (> 65 años: 22.2 ñ 16.6 Delta por ciento vs < 40 años: 11.8 ñ 9.9 por ciento, p = < 0.005) pero esta diferencia no persistió al realizar un análisis de covarianza tomando como cofactor de ajuste el VEF1 basal. Ni Dabsoluto (r = 0.13, p = NS), ni Delta por ciento predicho (r = 0.06, p = NS) ni Dmáximo (r = 0.09, p = NS) mostraron correlación con la edad. Delta percent inicial mostró débil pero significativa correlación con la edad (r = 0.28, p = < 0.05) y marcada dependencia del VEF1 basal (r = 0.47, p = < 0.001). La respuesta a broncodilatadores en los ancianos está conservada. La utilización de Delta por ciento inicial crea diferencias dependientes de la mayor severidad.derada. (Au)