RESUMEN
This study aimed to characterize the role played by baroreceptors and chemoreceptors in the hypertensive response to bilateral carotid occlusion (BCO) in conscious C57BL mice. On the day before the experiments the animals were implanted with pneumatic cuffs around their common carotid arteries and a femoral catheter for measurement of arterial pressure. Under the same surgical approach, groups of mice were submitted to aortic or carotid sinus denervation or sham surgery. BCO was performed for 30 or 60 s, promoting prompt and sustained increase in mean arterial pressure and fall in heart rate. Compared with intact mice, the hypertensive response to 30 s of BCO was enhanced in aortic-denervated mice (52 ± 4 vs. 41 ± 4 mmHg; P < 0.05) but attenuated in carotid sinus-denervated mice (15 ± 3 vs. 41 ± 4 mmHg; P < 0.05). Suppression of peripheral chemoreceptor activity by hyperoxia [arterial partial pressure of oxygen (Pa(O(2))) > 500 mmHg] attenuated the hypertensive response to BCO in intact mice (30 ± 6 vs. 51 ± 5 mmHg in normoxia; P < 0.05) and abolished the bradycardia. It did not affect the hypertensive response in carotid sinus-denervated mice (20 ± 4 vs. 18 ± 3 mmHg in normoxia; P < 0.05). The attenuation of the hypertensive response to BCO by carotid sinus denervation or hyperoxia indicates that the hypertensive response in conscious mice is mediated by both baro- and chemoreceptors. In addition, aortic denervation potentiates the hypertensive response elicited by BCO in conscious mice.
Asunto(s)
Barorreflejo , Presión Sanguínea , Arteria Carótida Común/inervación , Seno Carotídeo/inervación , Células Quimiorreceptoras , Frecuencia Cardíaca , Hipertensión/fisiopatología , Presorreceptores/fisiopatología , Animales , Aorta/inervación , Arteria Carótida Común/cirugía , Seno Carotídeo/cirugía , Células Quimiorreceptoras/metabolismo , Constricción , Desnervación , Modelos Animales de Enfermedad , Hiperoxia/metabolismo , Hiperoxia/fisiopatología , Hipertensión/etiología , Hipertensión/metabolismo , Hipertensión/prevención & control , Masculino , Ratones , Ratones Endogámicos C57BL , Oxígeno/sangre , Presión Parcial , Presorreceptores/metabolismo , Factores de TiempoRESUMEN
Devido ao número crescente de pessoas idosas que são candidatas à estimulação, os fatores relacionados ao uso de marcapassos em idades avançadas têm importantes implicações clínicas. Neste estudo prospectivo, descrevemos nossa experiência com o implante e o seguimento de 66 pacientes com idade igual ou superior a 70 anos (média de 76 anos) e com marcapassos DDD, com a finalidade de avaliar a ocorrência de complicações, a estabilidade da estimulação DDD e a qualidade de vida. O tempo médio até o último seguimento foi de 10,5 meses, com variação de 326 meses. Na maioria dos casos, a qualidade de vida dos pacientes melhorou significantemente após o implante. Dois marcapassos (3,3por cento) foram reprogramados para o modo VVI em decorrência de fibrilação atrial. Cinco pacientes (7,5por cento) tiveram complicações relacionadas ao eletrodo atrial, sendo que em dois foi necessária a reoperação. Sessenta e um dos 66 pacientes (92,5por cento), cujo estado era minuciosamente conhecido em fevereiro de 2000, permaneceram funcionalmente no modo DDD até o último seguimento. Concluímos que a estimulação de dupla-câmara é estável, apresenta baixo risco e pode melhorar a qualidade de vida em um grande espectro de pacientes idosos.
Asunto(s)
Humanos , Masculino , Femenino , Anciano , Estimulación Cardíaca Artificial , Marcapaso Artificial , Bloqueo Cardíaco/cirugía , Calidad de Vida , Seno Carotídeo/cirugía , Seno Carotídeo/patologíaRESUMEN
The relationship between an acute increase in arterial pressure and renal sympathetic nerve activity produced in rats under chloralose anesthesia after carotid and sinoaortic denervation was analyzed by quantifying the nerve activity associated with arterial pressure changes. After sinus denervation there was no change in arterial pressure (125 +/- 2.3 vs 124.6 +/- 5 mmHg, N = 6), but the renal sympathetic nerve activity (10.8 +/- 0.9 vs 8.0 +/- 1.1 bars s-1 cycle-1, N = 6) was significantly decreased. In spite of this, baroreflex control of renal sympathetic nerve activity was the same as during the control period. After sinoaortic denervation, there were simultaneous increases in arterial pressure (from 124 +/- 2.3 to 188 +/- 6 mmHg, N = 6) and renal sympathetic nerve activity (from 10.8 +/- 0.9 to 13.7 +/- 2.9 bars s-1 cycle-1) with marked attenuation of the baroreflexes. Spectral analysis of arterial blood pressure after sinus denervation showed a shift of a 1-Hz peak to 0.7 Hz, probably related to a decrease in respiratory frequency. The results suggest that after sinoaortic denervation the acute increase in arterial pressure is only due to aortic denervation.
Asunto(s)
Seno Carotídeo/cirugía , Riñón/inervación , Presorreceptores/fisiología , Seno Aórtico/cirugía , Sistema Nervioso Simpático/fisiología , Animales , Presión Sanguínea , Desnervación , Frecuencia Cardíaca , RatasRESUMEN
The relationship between an acute increase in arterial pressure and renal sympathetic nerve activity produced in rats under chloralose anesthesia after carotid and sinoaortic denervation was analyzed by quantifying the nerve activity associated with arterial pressure changes. After sinus denervation there was no change in arterial pressure (125 ñ 2.3 vs 124.6 ñ 5 mmHg, N +6), but the renal sympathetic nerve activity (10.8 ñ 0.9 vs 8.0 ñ 1.1 bars s-1 cycle-1, N+6) was significantly decreased. In spite of this, baroreflex control of renal sympathetic nerve activity was the same as during the control period. After sinoaortic denervation, there were simultaneous increases in arterial pressure (from 124 ñ 2.3 to 188 ñ 6m Hg, N +6) and renal sympathetic nerve activity (from 10.8 ñ 0.9 to 13.7 ñ 2.9 bars s-1 cycle-1) with marked attenuation of the baroreflexes. Spectral analysis of arterial blood pressure after sinus denervation showed a shift of a 1-Hz peak to 0.7 Hz, probably related to a respiratory frequency. The results suggest that after sinoaortic denervation the acute in arterial pressure is only due to aortic denervation