Chemical sympathectomy restores baroreceptor-heart rate reflex and heart rate variability in rats with chronic nitric oxide deficiency.

Nitric oxide (NO) plays a crucial role not only in regulation of blood pressure but also in maintenance of cardiac autonomic tone and its deficiency induced hypertension is accompanied by cardiac autonomic dysfunction. However, underlying mechanisms are not clearly defined. We hypothesized that sympathetic activation mediates hemodynamic and cardiac autonomic changes consequent to deficient NO synthesis. We used chemical sympathectomy by 6-hydroxydopamine to examine the influence of sympathetic innervation on baroreflex sensitivity (BRS) and heart rate variability (HRV) of chronic N(G)-nitro-L-arginine methyl ester (L-NAME) treated adult Wistar rats. BRS was determined from heart rate responses to changes in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. Time and frequency domain measures of HRV were calculated from 5-min electrocardiogram recordings. Chronic L-NAME administration (50 mg/kg per day for 7 days orally through gavage) in control rats produced significant elevation of blood pressure, tachycardia, attenuation of BRS for bradycardia and tachycardia reflex and fall in time as well as frequency domain parameters of HRV. Sympathectomy completely abolished the pressor as well as tachycardic effect of chronic L-NAME. In addition, BRS and HRV improved after removal of sympathetic influence in chronic L-NAME treated rats. These results support the concept that an exaggerated sympathetic activity is the principal mechanism of chronic L-NAME hypertension and associated autonomic dysfunction.

Effect of losartan, an angiotensin II type 1 receptor antagonist on cardiac autonomic functions of rats during acute and chronic inhibition of nitric oxide synthesis.

We studied the effect of losartan on baroreflex sensitivity (BRS) and heart rate variability (HRV) of adult Wistar rats during acute and chronic inhibition of nitric oxide synthesis by N(G)-nitro-L-arginine methyl ester (L-NAME). Chronic L-NAME administration (50 mg/kg per day for 7 days, orally through gavage) increased mean arterial pressure (MAP), heart rate but significantly decreased BRS. In addition, a significant fall of standard deviation of normal RR intervals, total spectral power, high frequency spectral power and a rise of low frequency to high frequency (LF: HF) ratio was seen. Acute L-NAME administration (30 mg/kg, i.v. bolus dose) also raised MAP and impaired HRV but it was associated with augmented BRS for bradycardia reflex. Losartan treatment (10 mg/kg, i.v.) in both acute and chronic L-NAME treated rats, decreased MAP but the difference was not significant. On the other hand, losartan administration normalized depressed BRS for bradycardia reflex and significantly reduced LF to HF ratio in chronic L-NAME treated rats. But this improvement was not observed in acute L-NAME group. These results indicate importance of mechanisms other than renin-angiotensin system in the pressor response of both acute as well as chronic L-NAME. However, autonomic dysregulation especially following chronic L-NAME appears to be partly angiotensin dependent.

Brainstem auditory evoked potentials among rubber factory workers.

The study was conducted on 27 rubber factory workers for the functional assessment of brainstem auditory pathway. Neurobehavioural questionnaire was administered to the workers and the personal sampler was used to evaluate the respirable particulate load inhaled per day of each worker along with qualitative analysis for PAH compounds. Evoked potential recording was carried out for brainstem auditory responses. Chest X-rays of workers exhibited varied abnormal features. Multiple regression analysis of data showed definite prolongation of latencies with increasing concentration of respirable particulate load though it was not statistically significant. Comparison with normative data indicated prolongation of latencies of rubber factory workers.

Ventilatory functions in stone quarry workers of Rajasthan.

Ninety two stone quarry workers from nearby villages of Jodhpur town were, assessed for their lung functions which included measurement of Forced vital capacity (FVC), Forced expiratory volume in Ist second (FEV1), and Peak expiratory flow rate (PEFR). A detailed questionnaire was administered to all the workers, who were divided into group I (cutting the stone) and group II (loading and unloading the stone) depending on the nature of their Job. The presenting complaints included cough with sputum (55%), chest pain (79%), bodyache (31%) and 21% gave the history as suffering from tuberculosis. Comparison of the lung function results between two groups indicated a significant decrement of FEV1 and PEFR in group II as compared to group I workers. The observed lung functions were also found to be lower on comparison with the normative data from Rajasthan. However, no difference in observed lung function results of smokers and nonsmokers were obtained. Thus the reported lower values of lung functions independent of smoking habits, may be due to occupational stone dust exposure.

Behavioural parameters in hypertensives on atenolol therapy.

Behavioural responses which included psychological tests and cold pressor test as a stress test were studied in 20 mild to moderate hypertensives of both sexes, excluding smokers, alcoholics, secondary hypertensives and patients of chronic obstructive pulmonary diseases. Subjects were put on 2 weeks of placebo washout period followed by 6 weeks of treatment with atenolol. Following treatment with atenolol they showed no significant alteration in the scores of psychological tests which included Weschler adult intelligence scale for orientation, while showing significant depression in the rise of heart rate, systolic blood pressure and diastolic blood pressure following cold pressor test. On further analysis, the results showed that hypertensives on placebo had lower scores of memory and attention test as compared to normotensive controls. Besides this, hypertensives on placebo had higher rise of heart rate and systolic blood pressure as compared to normotensive controls after cold pressor test.

A study of pulmonary profile of hypertensive patients--comparison of atenolol vs amlodipine.

Two groups of drugs commonly used for the treatment of hypertension are atenolol and amlodipine. These drugs are reported to have conflicting changes on pulmonary responses. In order to study the effect of hypertension and antihypertensive treatment on pulmonary responses, 40 patients with essential hypertension having diastolic blood pressure between 90-114 mmHg on three consecutive weekly visits were taken. Pulmonary responses were tested at the end of 2 weeks of placebo washout period and then at the end of 6 weeks of treatment with either atenolol or amodipine. Using a computerized autospiror along with the weekly recordings of heart rate and blood pressure, the various pulmonary and cardiac parameters were taken. Analysis of the result showed that atenolol treatment resulted in significant decline of forced vital capacity (FVC), % forced vital capacity (%FVC), and forced expiratory volume in first second (FEV1) whereas amlodipine did not show any significant change on pulmonary parameters.