18 research outputs found
Modulação autonĂ´mica da pressĂŁo arterial e variabilidade da freqĂĽĂŞncia cardĂaca em ratos hipertensos e diabĂ©ticos
OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131±3 mmHg and 276±6 bpm) were lower than in SHR (160±7 mmHg and 330±8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55±0.1 vs. 0.97±0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1±0.2 mmHg) than in SHR (5.7±0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3±0.8 vs. 28.7±7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure.OBJETIVO: O objetivo do presente estudo foi investigar a modulação autonĂ´mica do sistema cardiovascular em ratos espontâneamente hipertensos (SHR) e diabĂ©ticos por estreptozotocina (STZ), avaliando a sensibilidade do reflexo barorreceptor e a variabilidade da pressĂŁo arterial e da freqĂĽĂŞncia cardĂaca. MÉTODOS: Ratos SHR machos foram divididos em grupos controle (SHR) e diabĂ©ticos (SHR+DM, 5 dias apĂłs STZ). A pressĂŁo arterial (PA) e a sensibilidade dos barorreceptores (avaliada pelas respostas taquicárdicas e bradicárdicas a alterações da PA) foram monitoradas. Os sinais de pressĂŁo arterial sistĂłlica (PAS) e o intervalo de pulso (IP) foram analisados no domĂnio do tempo e da freqĂĽĂŞncia pelo mĂ©todo autoregressivo sendo quantificados os componentes oscilatĂłrios de baixa (BF: 0,2-0,6Hz) e alta (AF:0,6-3,0Hz) freqĂĽĂŞncia. RESULTADOS: A PA mĂ©dia e a freqĂĽĂŞncia cardĂaca estavam reduzidas no grupo SHR+DM (131±3 mmHg e 276±6 bpm) em relação ao grupo SHR (160±7 mmHg e 330±8 bpm). A bradicardia reflexa a aumentos de PA estava atenuada no grupo SHR+DM quando comparada ao grupo SHR (0,55±0,1 vs 0,97±0,1 bpm/mmHg). A variabilidade da PAS no domĂnio do tempo (desvio padrĂŁo batimento-a-batimento da sĂ©rie temporal da PAS) foi menor no grupo SHR+DM (3,1±0,2 mmHg) quando comparada ao grupo SHR (5,7±0,6 mmHg). O desvio padrĂŁo do IP foi semelhante entre os grupos. O diabetes reduziu o componente BF da PAS (3,3±0,8 vs 28,7±7,6 mmHg² no SHR), mas nĂŁo alterou o componente AF da PAS. Em relação aos componentes oscilatĂłrios do IP nĂŁo houve diferença entre os grupos. CONCLUSĂ•ES: Estes resultados sugerem que a associação de hipertensĂŁo e diabetes causa uma importante diminuição da modulação simpática cardiovascular perifĂ©rica que poderia, pelo menos em parte, ser responsável pela redução da PA. AlĂ©m disso, este estudo demonstra que o diabetes pode, de fato, piorar a já reduzida função de tamponamento dos barorreceptores ao mesmo tempo em que reduz a pressĂŁo arterial
Cardiac Impairment Evaluated by Transesophageal Echocardiography and Invasive Measurements in Rats Undergoing Sinoaortic Denervation
Background: Sympathetic hyperactivity may be related to left ventricular (LV) dysfunction and baro- and chemoreflex impairment in hypertension. However, cardiac function, regarding the association of hypertension and baroreflex dysfunction, has not been previously evaluated by transesophageal echocardiography (TEE) using intracardiac echocardiographic catheter.Methods and Results: We evaluated exercise tests, baroreflex sensitivity and cardiovascular autonomic control, cardiac function, and biventricular invasive pressures in rats 10 weeks after sinoaortic denervation (SAD). the rats (n = 32) were divided into 4 groups: 16 Wistar (W) with (n = 8) or without SAD (n = 8) and 16 spontaneously hypertensive rats (SHR) with (n = 8) or without SAD (SHRSAD) (n = 8). Blood pressure (BP) and heart rate (HR) did not change between the groups with or without SAD; however, compared to W, SHR groups had higher BP levels and BP variability was increased. Exercise testing showed that SHR had better functional capacity compared to SAD and SHRSAD. Echocardiography showed left ventricular (LV) concentric hypertrophy; segmental systolic and diastolic biventricular dysfunction; indirect signals of pulmonary arterial hypertension, mostly evident in SHRSAD. the end-diastolic right ventricular (RV) pressure increased in all groups compared to W, and the end-diastolic LV pressure increased in SHR and SHRSAD groups compared to W, and in SHRSAD compared to SAD.Conclusions: Our results suggest that baroreflex dysfunction impairs cardiac function, and increases pulmonary artery pressure, supporting a role for baroreflex dysfunction in the pathogenesis of hypertensive cardiac disease. Moreover, TEE is a useful and feasible noninvasive technique that allows the assessment of cardiac function, particularly RV indices in this model of cardiac disease.Conselho Nacional de Desenvolvimento CientĂfico e TecnolĂłgico (CNPq)Univ SĂŁo Paulo, Fac Med, Cardiomyopathy Unit, Heart Inst InCor,Hosp Clin, SĂŁo Paulo, BrazilUniv SĂŁo Paulo, Fac Med, Hypertens Unit, Heart Inst InCor,Hosp Clin, SĂŁo Paulo, BrazilUniversidade Federal de SĂŁo Paulo, Dept Biosci, SĂŁo Paulo, BrazilUniversidade Federal de SĂŁo Paulo, Dept Biosci, SĂŁo Paulo, BrazilWeb of Scienc
Autonomic modulation of arterial pressure and heart rate variability in hypertensive diabetic rats
OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131±3 mmHg and 276±6 bpm) were lower than in SHR (160±7 mmHg and 330±8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55±0.1 vs. 0.97±0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1±0.2 mmHg) than in SHR (5.7±0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3±0.8 vs. 28.7±7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure
Transesophageal echocardiography of spontaneously hypertensive rats showing right ventricle (RV) (A), tricuspid inflow (B) and tissue Doppler imaging of the tricuspid annulus (C).
<p>Transesophageal echocardiography of spontaneously hypertensive rats showing right ventricle (RV) (A), tricuspid inflow (B) and tissue Doppler imaging of the tricuspid annulus (C).</p
Tissue Doppler imaging data of mitral and tricuspid annulus data obtained by transesophageal echocardiography.
<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>S’ = peak velocity of systolic velocity obtained by tissue Doppler imaging; E’ = peak velocity of early diastolic velocity obtained by tissue Doppler imaging; A’ = peak velocity of late diastolic velocity obtained by tissue Doppler imaging.</p>a<p>p<0.05 vs. W, <sup>b</sup>p<0.05 vs. SAD, and <sup>c</sup>p<0.05 vs. SHR.</p
Volumes and ejection fraction of the right ventricle, and biventricular diastolic function data obtained by transesophageal echocardiography.
<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>FE VD = right ventricular ejection fraction; E/A = ratio of peak velocity of E and A waves of mitral or tricuspid inflow; DT = deceleration time of E wave; IVRT = isovolumic relaxation time of LV; AFF = atrial filling fraction.</p>a<p>p<0.05 vs. W, <sup>b</sup>p<0.05 vs. SAD and <sup>c</sup>p<0.05 vs. SHR.</p
Correlations between invasive and noninvasive data in all animals.
<p>Values are mean ± SD.</p><p>AFF = atrial filling fraction; LV = left ventricle; AcT TTE = aceleration time of right ventricular outflow (transthoracic echocardiography); AcT TEE = aceleration time of right ventricular outflow (transesophageal echocardiography); TT = time from the beginning to the end of right ventricular outflow; CI = cardiac index; LVMass = left ventricular mass; MPI = myocardial performance index; EF = ejection fraction; E/E’ =  ratio of peak velocity of E wave of mitral inflow and peak velocity of early diastolic velocity obtained by tissue Doppler imaging; EDP = end-diastolic pressure.</p
Blood pressure, heart rate, baroreflex sensitivity and cardiovascular autonomic modulation of normotensive and hypertensive groups.
<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>HR = heart rate; PI = pulse interval; SD PI = standard deviation of pulse interval; SBP = systolic blood pressure; SD SBP = standard deviation of systolic blood pressure; PIV = pulse interval variance; LF (ms<sup>2</sup>) = low-frequency band of heart rate variability; HF (ms<sup>2</sup>) = high-frequency band of heart rate variability; LF band (%) = low-frequency band of heart rate variability; HF band (%) = high-frequency band of heart rate variability; SBPV = SBP variability; LF SBP (mmHg<sup>2</sup>) = low frequency band of SBPV; BRI = bradycardic response index; TRI = tachycardic response index;</p>a<p>p<0.05 vs. W, <sup>b</sup>p<0.05 vs. SAD, and <sup>c</sup>p<0.05 vs. SHR.</p
Cardiac morphology obtained by M-mode transthoracic echocardiography.
<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; GSHR = spontaneously hypertensive rats; GSHRDSA = spontaneously hypertensive rats with denervation;</p><p>LVd = left ventricular end-diastolic dimension; LVd = left ventricular end-systolic dimension; IVSd = interventricular septum thickness in diastole; PWd = posterior wall thickness in diastole; FS = fractional shortening; CI = cardiac index; LVMass = left ventricular mass; RWT = relative wall thickness; Ao = aortic dimension; LA = left atrium thickness in diastole.</p>a<p>p<0.05 vs. W and <sup>b</sup>p<0.05 vs. SAD.</p
Myocardial performance index, right ventricular outflow by transesophageal, transthoracic echocardiography and invasive data.
<p>Va1ues are mean ± SD.</p><p>W = Wistar; SAD = sinoaortic denervation; SHR = spontaneously hypertensive rats; SHRSAD = spontaneously hypertensive rats with sinoaortic denervation.</p><p>MPI = myocardial performance index; LV = left ventricle; RV = right ventricle; AcT = aceleration time of right ventricular outflow; TT = time from the beginning to the end of right ventricular outflow; EDPRV = end-diastolic pressure of right ventricle; EDPLV = end-diastolic pressure of left ventricle; ESPRV = end-systolic pressure of the right ventricle.</p>a<p>p<0.05 vs. W, <sup>b</sup>p<0.05 vs. SAD, and <sup>c</sup>p<0.05 vs. SHR.</p