Biomedical subjects

V M Farah

Publications and source records attributed to V M Farah.

3 recordsLinked to original sources

PubMed1992

Vagal function impairment after exercise training.

The present investigation was undertaken to evaluate the vagal function of trained (T) and sedentary (S) rats by use of different approaches in the same animal. After 13 wk of exercise training (treadmill for 1 h 5 times/wk at 26.8 m/min and 15% grade), T rats had a resting heart rate (HR) slightly but significantly lower than S rats (299 +/- 3 vs. 308 +/- 3 beats/min). T rats had marked reduction of the intrinsic HR (329 +/- 4 vs. 369 +/- 5 beats/min) after blockade by methylatropine and propranolol. They also exhibited depressed vagal and sympathetic tonus. Baroreflex bradycardia (phenylephrine injections) was reduced, bradycardic responses produced by electrical stimulation of the vagus were depressed, and responses to methacholine injection were decreased in T rats. Therefore several evidences of vagal function impairment were observed in T rats. The resting bradycardia after exercise training is more likely to be dependent on alterations of the pacemaker cells, inasmuch as the intrinsic HR was markedly reduced.

Animals↗

PubMed1990

Influence of general anesthetics on baroreflex control of circulation.

1. The effects of sodium pentobarbital and alpha-chloralose anesthesia on the baroreflex control of circulation were studied in groups of 7 to 11 rats. The tests were performed in conscious undisturbed rats and repeated after anesthesia. 2. Pentobarbital (15 min) depressed the initial peak of the pressor response produced by carotid occlusion by 68% (15 +/- 1 vs 47 +/- 3 mmHg) and the maintained response by 52% (13 +/- 1 vs 27 +/- 4). Depression by chloralose was 48% (26 +/- 5 vs 50 +/- 3) and 21% (19 +/- 2 vs 24 +/- 3), respectively. The inhibition progressively declined at 30, 60, 90 and 120 min after pentobarbital but was unchanged up to 120 min after chloralose. 3. The baroreflex sensitivity index for bradycardic responses (phenylephrine injection) diminished by 50% after pentobarbital (-1.1 +/- 0.3 vs -2.2 +/- 0.3 beats/min per mmHg) and remained unaltered after chloralose. 4. The baroreflex sensitivity index for tachycardic responses (nitroprusside injection) was depressed by 61% after pentobarbital (-1.5 +/- 0.5 vs -3.8 +/- 0.5 beats/min per mmHg) and 35% after chloralose (-2.5 +/- 0.2 vs -3.9 +/- 0.5). 5. In general the depression of reflex control of circulation was more severe after pentobarbital than after chloralose anesthesia, while the resting control arterial pressure was not affected by either. The inhibition of the baroreflex tachycardic responses was more intense than that of the bradycardic responses and represented a better index of the depression exerted on the pressure responses to carotid occlusion.

Animals↗

PubMed1989

Attenuation of neurogenic hypertension by chronic converting enzyme inhibition.

We compared the effects produced by acute and chronic administration of captopril in sinoaortic denervated rats. In conscious undisturbed rats acute administration of captopril (10 mg/kg intravenously) produced acute transient reductions in mean arterial pressure of 16 and 26%, 6 h (mean arterial pressure 148 +/- 4 mmHg) and 24 h (133 +/- 3 mmHg) after the sinoaortic denervation, respectively. Chronic captopril treatment (30 mg/day orally) produced a permanent attenuation of the hypertension induced by sino-aortic denervation, as shown by a beat-to-beat analysis of arterial pressure for 80 min. The attenuation was 11% (131 +/- 7 versus 148 +/- 4 mmHg) and 24% (103 +/- 9 versus 133 +/- 3 mmHg) in rats studied 6 and 24 h after the sinoaortic denervation, respectively. Chronic captopril administration produced no alteration in the tachycardia, nor in the heart rate variability of the sinoaortic denervated rats; the latter was lower than that of normotensive rats. These data show that while acute administration of captopril in sinoaortic denervated rats produced a rapid hypotensive response, chronic administration produced a long-lasting attenuation of hypertension, presumably by interference with sympathetic cardiovascular control.

Animals↗