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Biomedical subjects

E M Krieger

Publications and source records attributed to E M Krieger.

At least 55 records · Page 3Linked to original sources

Alterations in the cardiovascular control by the chemoreflex and the baroreflex in old rats.

The aging process is associated with alterations in the autonomic control of cardiovascular function. In the present study, we observed that reflex bradycardia and tachycardia produced by pressor and depressor agents were attenuated in old (24 mo) rats [70 and 56% of responses in young rats (4 mo), respectively]. In contrast, the bradycardia induced by chemoreflex activation with increasing doses of KCN (60, 100, 140, and 180 micrograms/kg) was greater in old [-30 +/- 19, -155 +/- 32, -198 +/- 15, and -204 +/- 24 beats/ min (bpm)] than in young rats [-13 +/- 6, -75 +/- 20 (P < 0.05), -99 +/- 26 (P < 0.05), and -103 +/- 20 (P < 0.05) bpm]. The chemoreflex-pressor responses tended to be greater in old (12 +/- 6, 47 +/- 6, 54 +/- 7, and 55 +/- 5 mmHg) than in young rats (4 +/- 2, 32 +/- 8, 42 +/- 6, and 44 +/- 4 mmHg), but the differences between both groups were not statistically significant. However, pressor responses were higher in old rats after the chemoreflex-activated bradycardia was attenuated by atropine (4 mg/kg iv) [old (17 +/- 9(1) P < 0.05; 57 +/- 4, P < 0.05; 61 +/- 4; and 64 +/- 5 mmHg) vs. young (3 +/- 2, 29 +/- 9(1) 50 +/- 5, and 58 +/- 7 mmHg)]. Administration of the alpha 1-blocker prazosin (1 mg/kg iv) blunted pressor responses but did not change the bradycardia induced by chemoreflex in both groups. In conclusion, our data indicate that the bradycardia and pressor responses to chemoreflex activation were exaggerated, whereas the heart rate responses (bradycardia and tachycardia) to baroreflex were depressed in old rats.

Aging↗

Arterial blood pressure and left ventricular hypertrophy in haemodialysis patients.

OBJECTIVE: To test the hypothesis that there is an association between arterial blood pressure and left ventricular hypertrophy and patterns of ventricular geometry, defined echocardiographically, in a group of stable haemodialysis patients with a low prevalence of extrarenal diseases. DESIGN AND METHODS: Patients with end-stage renal failure treated by regular haemodialysis (aged 44.3 +/- 12.9 years, n = 103, among whom 52 men and 23 blacks, dialysis duration 49.8 +/- 35.3 months) were subjected to echocardiographic evaluation (M-mode, bidimensional and Doppler) on the day preceding dialysis. The average of all predialysis blood pressure determinations during the 3 months preceding the tests (34-38 determinations in each patient) were used as baseline data. Univariate and multivariate tests were used to assess the main variables associated with echocardiographically defined cardiac alterations and with patterns of ventricular geometry. RESULTS: The systolic blood pressure was significantly associated with the left ventricular mass index and was significantly and independently correlated with left ventricular hypertrophy, posterior wall hypertrophy, left ventricle dilation and increased relative wall thickness. Other significant correlations were between the haematocrit level and left ventricular hypertrophy and between age and altered systolic and diastolic functions. Concentric ventricular hypertrophy was observed only in patients with a history of hypertension, whereas the prevalence of normal geometry was higher in patients without a history of hypertension. CONCLUSION: The systolic blood pressure is an important factor influencing the occurrence of left ventricular hypertrophy in haemodialysis patients and also affects the left ventricle geometry in this population.

Adult↗

Plasma lipid profile and coronary artery disease in Brazilian hemodialysis patients.

We studied the prevalence of lipid disorders and of coronary artery disease and the main factors affecting plasma lipids in a cohort of Brazilian hemodialysis patients. The investigation comprised 75 adult hemodialysis patients and 200 normal controls matched for age, sex, race and body mass index. Mean values for plasma lipids were within normal limits in the dialysis group. Total cholesterol (184 +/- 44 vs. 201 +/- 46 mg/dl), LDL (110 +/- 36 vs. 131 +/- 44 mg/dl) and HDL (40 +/- 13 vs. 47 +/- 12 mg/dl) were significantly lower in the dialysis patients (P < 0.01), whereas VLDL (32 +/- 14 vs. 21 +/- 12 mg/dl) and triglyceride (161 +/- 71 vs. 111 +/- 70 mg/dl) were increased (P < 0.01). Increased triglyceride was observed in 24% of the dialysis patients, a prevalence two to three times lower than that reported in the literature. In the dialysis group, the variables positively related to total cholesterol were hypertension (P < 0.05) and gender (female) (P < 0.05); to LDL and HDL, hypertension (P < 0.05 and P < 0.01, respectively); and to triglyceride, use of propranolol (P < 0.01). Age, race, duration of hemodialysis, body mass index and plasma creatinine did not affect plasma lipids. The prevalence of coronary artery disease, established by invasive and noninvasive methods, was 10.7% while in the literature 20-35% of the unselected hemodialysis patients present obstructive coronariopathy. We conclude that the plasma lipid profile of Brazilian hemodialysis patients is similar to those reported in American and European literature, whereas the prevalence of hypertriglyceridemia and of coronary artery disease appears to be reduced.

Adult↗

A biometrical genome search in rats reveals the multigenic basis of blood pressure variation.

A genome-wide search for multiple loci influencing salt-loaded systolic blood pressure (NaSBP) variation among 188 F2 progeny from a cross between the Brown-Norway and spontaneously hypertensive rat strains was pursued in an effort to gain insight into the polygenic basis of blood pressure regulation. The results suggest that loci within five to six genomic regions collectively explain approximately 43% of the total NaSBP variation exhibited among the 188 F2 progeny. Many of these loci are in regions that previous studies have not implicated in blood pressure regulation. Ultimately, however, this study not only sheds light on the multigenic basis of blood pressure but provides further evidence that the identification of the genetic determinants of polygenic traits in mammals is possible with modern biometrical and molecular genetic tools in controlled settings (i.e., breeding paradigm and model organism).

Animals↗

Comparison of echocardiographic changes associated with hemodialysis and renal transplantation.

Long-term hemodialysis has been reported to cause progression of left ventricular (LV) hypertrophy with a tendency toward asymmetric septal hypertrophy. Renal transplantation is believed to reverse some of these changes. The aim of this prospective study was to compare the effects of long-term hemodialysis and of successful renal transplantation on cardiac structure and function assessed by echocardiography. Fifty-three patients were submitted to two echocardiographic evaluations separated by a 30 +/- 8 month interval. At the first control, all patients were on hemodialysis; at the second, 36 patients remained on dialysis while 17 had been submitted to renal transplantation. Age (44 +/- 13 vs. 40 +/- 10 years), gender (male, 50% vs 53%), and duration of dialysis at the initiation of the study (43 +/- 34 vs. 47 +/- 32 months) were comparable in the 2 groups. The prevalence of LV hypertrophy were 83% (first control) and 69% (second control) in the dialysis group and 82% and 71% in the transplant group. Comparisons between the two periods within each group showed that hemodialysis was associated with a significant reduction of the E/A ratio (1.25 +/- 0.4 vs. 1.02 +/- 0.4, p < 0.001) and systolic (155 +/- 28 vs. 137 +/- 26 mm Hg, p < 0.001) and diastolic (94 +/- 21 vs. 84 +/- 16 mm Hg, p < 0.05) blood pressure, and no change in LV mass index (171 +/- 51 vs. 156 +/- 43 g/m2, NS). In the transplanted group, there were reductions in the E/A ratio (1.42 +/- 0.6 vs 1.10 +/- 0.4, p < 0.05) and in LV diastolic dimension (50 +/- 7 vs. 46 +/- 5 mm, p < 0.05), but not in systolic (155 +/- 27 vs. 152 +/- 31 mm Hg, NS) or diastolic (97 +/- 11 vs. 97 +/- 20 mm Hg, NS) blood pressure. The LV mass index also did not change significantly (157 +/- 51 vs. 133 +/- 31 g/m2, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Viscoelastic behavior of "in situ" aortic wall during hemorrhagic hypotension.

Viscoelastic and electrophysiological mechanisms have been implicated in resetting of baroreceptors in hypertension, but resetting in response to hypotension has been less exhaustively studied. To assess the importance of viscoelastic mechanisms in hypotension, we examined the behavior of the "in situ" aorta during hemorrhage. Fifteen minutes of hemorrhage in anesthetized Wistar rats produced stable hypotension (30 mmHg) and a progressive contraction of the mean aortic caliber (-93.8 +/- 18.0 microns, P < 0.05) compared with control measurements. Contraction was not altered by sinoaortic denervation, vagotomy, nephrectomy, adrenalectomy, hexamethonium (30 mg/kg), losartan (10 mg/kg), V1 antagonist (10 micrograms/kg), arterial pH and blood gas control, or indomethacin (3.0 mg/kg). Aortic contraction was greater in rats treated with N omega-nitro-L-arginine (-164.0 +/- 43.0 microns, P < 0.05) than in those treated with sodium nitroprusside (-54.1 +/- 7.5 microns, P < 0.05). The results indicate that aortic contraction is compatible with viscoelastic contraction and suggest that shortening of viscoelastic elements in series with baroreceptor endings increases stress at the baroreceptor membrane and contributes to the development of baroreceptor resetting to hypotension.

Animals↗

Changes of renal sympathetic activity in acute and chronic conscious sinoaortic denervated rats.

The arterial pressure level attained in sinoaortic denervated rats depends on the net effect of eliminating excitatory and inhibitory influences (chemoreceptor and baroreceptor elimination, respectively). After sinoaortic denervation is completed, the hypertension usually observed within the first few days is followed by normotension at the chronic stages. In this work renal sympathetic nerve activity was measured in conscious, unrestrained rats 6 hours (acute) and 20 days (chronic) after sinoaortic denervation. Increased arterial pressure (154 +/- 10 versus 114 +/- 3 mm Hg in controls) and renal sympathetic nerve activity (32 +/- 5 versus 13 +/- 2 bars per cycle in controls) with no changes in heart rate (404 +/- 17 vs 380 +/- 26 beats per minute) were observed in rats with acute sinoaortic denervation. In rats with chronic sinoaortic denervation, arterial pressure (119 +/- 8 mm Hg) and renal sympathetic nerve activity (13 +/- 6 bars per cycle) returned to control levels. Bradycardiac and tachycardiac responses to changes in blood pressure were reduced to 88% and 89%, respectively, in rats with acute sinoaortic denervation and 76% and 74%, respectively, in rats with chronic sinoaortic denervation. The reflex control of renal sympathetic nerve activity after acute and chronic sinoaortic denervation showed an impairment of sympathoinhibition (0.13 +/- 0.02 and 0.25 +/- 0.1 bars per cycle, respectively, versus 0.9 +/- 0.17 bars per cycle in controls). Sympathoexcitatory responses also were impaired in rats with acute and chronic sinoaortic denervation (0.08 +/- 0.03 and 0.37 +/- 0.1 bars per cycle, respectively, compared with 0.98 +/- 0.2 bars per cycle in controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Low-intensity exercise training attenuates cardiac beta-adrenergic tone during exercise in spontaneously hypertensive rats.

Acute and chronic exercise decrease peripheral sympathetic nerve activity, but the effect of exercise training of varying intensity on the sympathetic control of heart rate of spontaneously hypertensive rats has not yet been described. The effect of low and high intensities of exercise training on the vagal and sympathetic activities that control heart rate at rest and during dynamic exercise at 0.5, 0.8, and 1.0 mph for 4 minutes per stage was investigated in sedentary (SED, n = 11), high-intensity (HT, n = 12), and low-intensity exercise-trained (LT, n = 13) spontaneously hypertensive rats. Exercise training was performed on a treadmill for 60 minutes, 5 days per week for 18 weeks, at 55% maximum oxygen consumption for the LT group and 85% for the HT group. Vagal and sympathetic activities were studied after administration of methylatropine (3 mg/kg) and propranolol (4 mg/kg), respectively. The LT group had a significantly lower heart rate (at 0.5, 0.8, 1.0 mph versus rest: 410 +/- 7, 464 +/- 9, and 295 +/- 6 beats per minute [bpm], respectively) than the HT (440 +/- 6, 453 +/- 7, 474 +/- 5, and 315 +/- 4 bpm) and the SED (474 +/- 11, 500 +/- 11, 523 +/- 10, and 327 +/- 3 bpm) groups. Sympathetic effect (LT: 84 +/- 10, 88 +/- 12, 105 +/- 12, and 9 +/- 4; HT: 123 +/- 8, 125 +/- 7, 133 +/- 7, and 34 +/- 7; SED: 130 +/- 13, 143 +/- 12, 150 +/- 10, and 38 +/- 7 bpm) and sympathetic tonus (LT: 125 +/- 6, 121 +/- 5, 112 +/- 6, and 91 +/- 6; HT: 145 +/- 9, 136 +/- 6, 142 +/- 8, and 118 +/- 7; SED: 136 +/- 6, 129 +/- 6, 132 +/- 7, and 118 +/- 8 bpm) were significantly decreased by low-intensity exercise training. In conclusion, low- but not high-intensity exercise training causes resting bradycardia and attenuation of tachycardiac response during progressive dynamic exercise in spontaneously hypertensive rats. This effect can be attributed to a significantly decreased beta-adrenergic tone that controls heart rate.

Animals↗

Blood pressure influences the occurrence of complex ventricular arrhythmia in hemodialysis patients.

We investigated the relationship between blood pressure and the occurrence of complex ventricular arrhythmias (multiform, couplets, or runs) as assessed by 48-hour Holter monitoring in 74 stable long-term hemodialysis patients (44.5 +/- 12 years old; 54% men; 74% whites; dialysis duration, 51.3 +/- 36.1 months; systolic pressure, 146.6 +/- 19.3 mm Hg; diastolic pressure, 89.2 +/- 12.1 mm Hg; prevalence of arterial hypertension, 33.8%). Systolic and diastolic pressures represented the average of all predialysis determinations during the 3 months preceding the tests. Hemodialysis was performed midway through the Holter monitoring period. M-mode and bidimensional echocardiograms and myocardial perfusion tests were also obtained from all patients. Complex arrhythmias were observed in 37 individuals (50%). Univariate analysis showed that systolic pressure (P < .001), diastolic pressure (P < .05), age (P < .001), left ventricular posterior wall thickness (P < .01), left ventricular mass index (P < .05), and ischemic alterations on myocardial perfusion tests (P < .005) were significantly associated with complex arrhythmias. With the use of a multivariate model (stepwise logistic regression analysis) only systolic pressure (P < .01) and age (P < .05) were independently associated with complex arrhythmias. Sex; angina; dialysis duration; New York Heart Association functional class; use of digitalis; plasma levels of creatinine, sodium, potassium, calcium, and phosphate; hematocrit; left ventricular fractional shortening; left ventricular diastolic diameter; and ST segment deviation were not correlated with complex arrhythmias. The severity and frequency of complex arrhythmias were not influenced by hemodialysis. At follow-up (5 to 80 months) 5 patients had died of sudden death, 4 of whom were hypertensive and older than 45 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Malignant hypertension is accompanied by marked alterations in chylomicron metabolism.

Malignant hypertension (MH) is a severe complication of untreated arterial hypertension that damages the vascular system. It is often accompanied by disturbances in lipid metabolism that could contribute to its pathophysiology. We examined chylomicron metabolism in MH patients using a triglyceride-rich emulsion known to mimic natural chylomicrons when injected into the bloodstream. The emulsion was labeled with [3H]triolein and [14C]cholesteryl oleate and injected intravenously into 15 normolipidemic MH patients aged 29 to 56 years (8 men) for comparison with 17 healthy control subjects. Consecutive plasma samples were taken at regular intervals during 1 hour for determination of the disappearance curves of the labels. The fractional clearance rate of the [3H]triolein emulsion in MH patients was twice as small as that of control subjects (0.061 +/- 0.012 and 0.141 +/- 0.074 min-1, respectively). On the other hand, [14C]cholesteryl oleate fractional clearance rate was not statistically different in MH patients and control subjects (0.032 +/- 0.004 and 0.056 +/- 0.014 min-1, respectively). These results indicate that in MH, lipolysis (measured by the fractional clearance rate of [3H]triolein) is pronounced diminished, whereas the removal of the remnant particles (measured by the fractional clearance rate of [14C]cholesteryl oleate) is not importantly affected. In conclusion, there is an alteration in the circulatory transport of dietary lipids that may be an important component in the vascular disease associated with MH.

Adult↗

Predictors of mortality in long-term haemodialysis patients with a low prevalence of comorbid conditions.

BACKGROUND: Total and cardiovascular mortality rates for haemodialysis patients are still high despite the continuous improvement of dialysis technology. This trend may be a consequence of the increased number of elderly patients and patients with concurrent systemic diseases admitted to dialysis programmes. The objective of the present investigation was to determine the predictors of mortality more closely related to uraemic status and to dialysis treatment by studying relatively young haemodialysis patients with a low prevalence of comorbid conditions using the Cox proportional hazards model. METHODS: Seventy-four haemodialysis patients with a low prevalence of extrarenal diseases (mean age 44.5 +/- 12.1 years, mean dialysis duration 51.3 +/- 36.1 months) were submitted to extensive cardiological and clinical evaluation and followed prospectively for a median period of 60.8 months (range: 5.1-79.8). There were only three diabetics and all patients denied previous myocardial infarction. RESULTS: At follow-up 23 patients had died, 10 of cardiac causes. Five-year survival rates were 70% for overall mortality and 83% for cardiac mortality. Age over 44 years (relative risk 3.73; 95% confidence interval 1.35-10.26) and serum creatinine (inverse correlation) (relative risk 0.73; 95% confidence interval 0.57-0.94) were shown to be independently associated with global mortality by the Cox proportional hazards analysis. Gender, race, dialysis duration, interdialytic weight gain, angina, NYHA classification, hypertension, LV hypertrophy, LV systolic and diastolic dysfunction, complex ventricular arrhythmias and altered myocardial perfusion tests were not significant predictors of overall mortality. There were crude associations between cardiac mortality and cardiothoracic and Sokolow indices (P < 0.01) and age, NYHA classification, systolic hypertension, LV wall and septum hypertrophy, LV dilatation and complex ventricular arrhythmias (P < 0.05). CONCLUSION: In the absence of serious comorbid conditions, the survival of patients on long-term haemodialysis is influenced by nutritional status (as indicated by lower serum creatinine) and age.

Adult↗

Restoration of arterial blood oxygen tension increases arterial pressure in sinoaortic-denervated rats.

The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypoxemia and hypercapnia were observed in acute (1 day) and chronic (20 days) SAD rats [arterial PO2 (PaO2) = 65 +2- 1.6 and 71 +2- 2.2 mmHg and arterial PCO2 (PaCO2) = 46 +/- 1.3 and 37 +/- 1.8 mmHg, respectively] compared with control rats (PaO2 = 85 +/- 1.6 mmHg, PaCO2 = 31 +/- 1.07 mmHg). Increasing inspired PO2 (PIO2) from 138 mmHg (room air) to 155 mmHg restored the PaO2 of SAD rats to control levels (acute = 81 +/- 2.21 mmHg, chronic = 85 +/- 2.35 mmHg). PaO2. restoration produced pronounced elevation of mean arterial pressure (MAP) of acute (from 121 +/- 4 to 147 +/- 3.5 mmHg) and chronic (from 121 +/- 3 to 134 +/- 3.5 mmHg) SAD rats. Progressive stepwise increase of PIO2 (from 138 to 175, 210, and 235 mmHg) produced no additional elevation of MAP of acute (113 +/- 4, 137 +/- 5, 143 +/- 5, and 147 +/- 5 mmHg) and chronic (111 +/- 3.6, 131 +/- 7.4, 130 +/- 8.7, and 130 +/- 7 mmHg) SAD rats. Otherwise, the arterial pressure of control rats remained unchanged to progressive stepwise increase of PIO2 (118 +/- 5, 117 +/- 4, 118 +/- 4, 116 +/- 4 mmHg). These data suggest that the elimination of chemoreceptors in SAD rats produces hypoxemia responsible for hypotensive influences that counteract the pressor effects produced by baroreceptor elimination.

Animals↗

DuP 753 is more effective than captopril on baroreceptor function in high-renin hypertension.

High-renin hypertensive rats exhibit a general impairment of the baroreceptor reflexes. In the present study we compared the effect of the angiotensin converting enzyme inhibitor captopril (10 mg/kg per day) with the effect of the selective angiotensin subtype 1 receptor blocker DuP 753 (10 mg/kg per day) on the baroreceptor reflex bradycardia (progressive doses of phenylephrine) and baroreceptor reflex tachycardia (progressive doses of nitroprusside) in conscious rats 7 days after aortic ligation. Arterial pressure was markedly reduced after both acute (15-minute) treatment with captopril (123 +/- 6 versus 184 +/- 23 mm Hg) and DuP 753 (140 +/- 10.5 versus 181 +/- 5.4 mm Hg), but the depressed baroreceptor reflex bradycardia increased only after DuP 753 (1.13 +/- 0.22 versus 0.75 +/- 0.60 beats per minute [bpm]/mm Hg) and remained attenuated after captopril (0.54 +/- 0.086 versus 0.30 +/- 0.07 bpm/mm Hg). After a 2-day treatment, captopril reduced arterial pressure (95 +/- 5 versus 184 +/- 2.3 mm Hg) to lower levels than DuP 753 (119 +/- 6 versus 172 +/- 4.6 mm Hg), whereas the depressed baroreceptor reflex bradycardia remained unchanged with captopril (0.46 +/- 0.13 versus 0.31 +/- 0.076 bpm/mm Hg) and increased with DuP 753 (1.13 +/- 0.19 versus 0.38 +/- 0.12 bpm/mm Hg). Neither DuP 753 nor captopril administered acutely (15 minutes) or for 2 days significantly altered the depressed baroreceptor reflex tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

[The role of hypertrophy and left ventricular function on the occurrence of ventricular arrhythmias in arterial hypertension].

PURPOSE: To evaluate the role of left ventricular hypertrophy (LVH), left ventricular systolic function an other clinical parameters on prevalence and complexity of ventricular arrhythmias in hypertension. METHODS: Ventricular arrhythmias were studied in 39 hypertensives by 24 hours ambulatory electrocardiographic monitoring. Frequency and complexity of ventricular arrhythmias were compared among 3 groups: A and B, respectively without and with LVH, both with normal left ventricular function; and C with LVH and systolic dysfunction. LVH and systolic dysfunction were established echocardiographically. Linear regression analysis was performed in order to identify an independent correlation between clinical parameters and presence of arrhythmias. RESULTS: Group C patients were older and had significantly higher systolic and diastolic blood pressures, greater mass index, diastolic posterior wall thickness and end-systolic stress and increased prevalence of electrocardiographic strain. Left ventricular diastolic diameter in C group patients was increased only when compared to A group. Frequencies of cases with more than 10 ectopic ventricular beats/hour, pairs and nonsustained ventricular tachycardia episodes were all significantly increased in C when compared to B and to A. However, only left ventricular mass index or diastolic posterior wall thickness identified independently patients with ventricular arrhythmias. CONCLUSION: Left ventricular hypertrophy is the main predictor of potential high risk rhythm disturbances in hypertension.

Adult↗

[Role of blood pressure in rest and exercise conditions and importance of clinical factors in left ventricular hypertrophy in arterial hypertension].

PURPOSE: To evaluate the role of casual and exercise blood pressure as well as the importance of clinical factors on the presence and degree of left ventricular hypertrophy in hypertension. METHODS: Fifteen normotensives (control group) and 30 hypertensives, 14 of them with and 16 without left ventricular hypertrophy (groups with LVH and without LVH, respectively) were studied. LVH diagnosis was established when mass index was higher than 2 standard-deviations of the mean values calculated for each sex in control group. Resting, casual determined, and bicycle exercise systolic and diastolic blood pressures along with age, body surface area, sex and race distribution were compared between groups. In addiction, their relation with mass index as independent variables were also tested. RESULTS: Hypertensives in group with LVH had higher diastolic septal, posterior wall, and relative wall thicknesses. No significant statistical difference was observed neither in sex and race distribution, nor in age and body surface area between groups. Otherwise, there were significant differences in both resting and exercise blood pressure. In the entire population studied, left ventricular mass index significantly correlated with age (r=0,33, p=0,03) as well as with both casual (systolic - r=0,72, p=0,0001; diastolic - r=0,69, p=0,0001) and exercise (systolic - r=0,62, p=0,0001; diastolic - r=0,66, p=0,0001) blood pressures. However, linear regression analysis demonstrated that only resting systolic (p=0,0001) and exercise diastolic (p=0,0303) blood pressures were significant and independent determinants of mass index. CONCLUSION: Resting and exercising blood pressures are the main determinants of left ventricular hypertrophy in hypertension.

Adult↗

[Hypertension and complex ventricular arrhythmias. Evolution following a long-term blood pressure treatment].

PURPOSE: To evaluate the effects of long-term antihypertensive treatment in the frequency as well as in the complexity of ventricular arrhythmias in arterial hypertension. METHODS: Twenty three patients, 14 males and 11 whites, with mean age of 46 years, were submitted to 24 hours ambulatory electrocardiographic monitoring and echocardiographic studies before and 9 months after antihypertensive treatment. RESULTS: There was no significant serum potassium level alteration, but significant reductions of both systolic (from 192 +/- 29mmHg to 161 +/- 25mmHg) and diastolic (from 122 +/- 17mmHg to 99 +/- 16mmHg) blood pressure. Left ventricular percent of fiber shortening significantly increased, even though only from 26 +/- 9% to 30 +/- 9%, and end-systolic wall stress did not change at all (before 258 +/- 94 10(3) dyn/cm2, after 255 +/- 101 10(3) dyn/cm2). Left ventricular mass index showed significant but also a discrete reduction from 211 +/- 75g/m2 to 196 +/- 70g/m2. Ambulatory electrocardiographic monitoring did not show any significant decrease in neither ventricular ectopic beats nor in couplets. Non-sustained ventricular tachycardia episodes remained unchanged too. Four out of 8 patients with more than 30 ventricular ectopic beats per hour reduced it by more than 70%. On the other hand, the number of patients with couplets was reduced from 10 to 8 whilst those with non-sustained ventricular tachycardia increased from 5 to 7. Furthermore, in 7 patients reevaluated 24 months thereafter results were not expressively dissimilar. CONCLUSION: In hypertensive patients with either severe degree of left ventricular hypertrophy or myocardial dysfunction, long-term blood pressure treatment that produce no impressive changes in these abnormalities also do not modify complex ventricular arrhythmias, in spite of a great reduction in the increase blood pressure.

Adolescent↗

Cardiovascular responses of conscious rats to carotid body chemoreceptor stimulation by intravenous KCN.

In the present study we analyzed the cardiovascular, respiratory and behavioral responses evoked in rats by KCN. Hypertension, hyperpnea and alerting behavior were characteristic responses in unanesthetized animals. Selective denervation of aortic and carotid bifurcation areas confirmed the carotid body chemoreceptor (CBC) origin of these responses. Sino-aortic denervation, as well as selective carotid sinus denervation abolished the responses, while, after selective aortic denervation, the responses were not different from those of the control rats. The administration of prazosin abolished the hypertensive response but did not change the bradycardic response, whereas the administration of atropine eliminated the bradycardic response and potentiated the hypertensive response to KCN. Increasing doses of KCN (10-80 micrograms/rat) produced proportionally larger bradycardia, hypertension and hyperventilation. Slight attenuation of bradycardic responses to KCN were observed in rats under chloralose anesthesia, while marked depression of bradycardic responses were observed under pentobarbitone anesthesia. Both anesthetics changed the hypertensive responses to hypotensive responses. In conclusion, the cardiovascular, respiratory and behavioral responses to intravenous KCN are a good functional test to CBC stimulation in unanesthetized rats, producing simultaneously intense bradycardia with hyperventilation and behaviour responses.

Animals↗

Effect of exercise training on RSNA, baroreflex control, and blood pressure responsiveness.

The effect of exercise training (ET) on renal sympathetic nerve activity (RSNA), baroreflex control of RSNA and heart rate (HR), and arterial pressure (AP) responsiveness to phenylephrine and angiotensin II (ANG II) was studied in six trained (T) and six sedentary (S) male Wistar rats. ET was performed on a motor treadmill for 13 wk. The RSNA signals of unanesthetized rats were processed by an analog-to-digital converter to quantify the nerve discharges associated with changes in AP and HR. The reflex control of RSNA and HR were evaluated during progressive injections of phenylephrine and sodium nitroprusside. Mean arterial pressure (MAP) was similar in both groups. RSNA was significantly lower in T rats (28 +/- 2 vs. 36 +/- 3%). T rats had an impairment of baroreflex control of RSNA in response to nitroprusside (4.9 +/- 0.89 vs. 12.3 +/- 1.2 bars.cycle-1.mmHg-1). ET decreased AP responsiveness for phenylephrine and ANG II. Therefore ET produces 1) no change in resting MAP but a significant decrease in RSNA and AP responsiveness and 2) partial impairment of baroreflexes, i.e., bradycardic responses and RSNA during MAP decrease.

Angiotensin II↗