Biomedical subjects

T G Fernandes

Publications and source records attributed to T G Fernandes.

10 recordsLinked to original sources

PubMed2004

Relationship between cardiovascular dysfunction and hyperglycemia in streptozotocin-induced diabetes in rats.

Streptozotocin (STZ)-induced diabetes in rats is characterized by cardiovascular dysfunction beginning 5 days after STZ injection, which may reflect functional or structural autonomic nervous system damage. We investigated cardiovascular and autonomic function, in rats weighing 166 +/- 4 g, 5-7, 14, 30, 45, and 90 days after STZ injection (N = 24, 33, 27, 14, and 13, respectively). Arterial pressure (AP), mean AP (MAP) variability (standard deviation of the mean of MAP, SDMMAP), heart rate (HR), HR variability (standard deviation of the normal pulse intervals, SDNN), and root mean square of successive difference of pulse intervals (RMSSD) were measured. STZ induced increased glycemia in diabetic rats vs control rats. Diabetes reduced resting HR from 363 +/- 12 to 332 +/- 5 bpm (P < 0.05) 5 to 7 days after STZ and reduced MAP from 121 +/- 2 to 104 +/- 5 mmHg (P = 0.007) 14 days after STZ. HR and MAP variability were lower in diabetic vs control rats 30-45 days after STZ injection (RMSSD decreased from 5.6 +/- 0.9 to 3.4 +/- 0.4 ms, P = 0.04 and SDMMAP from 6.6 +/- 0.6 to 4.2 +/- 0.6 mmHg, P = 0.005). Glycemia was negatively correlated with resting AP and HR (r = -0.41 and -0.40, P < 0.001) and with SDNN and SDMMAP indices (r = -0.34 and -0.49, P < 0.01). Even though STZ-diabetic rats presented bradycardia and hypotension early in the course of diabetes, their autonomic function was reduced only 30-45 days after STZ injection and these changes were negatively correlated with plasma glucose, suggesting a metabolic origin.

Animals↗

PubMed2000

Effects of exercise training on autonomic and myocardial dysfunction in streptozotocin-diabetic rats.

Several investigators have demonstrated that diabetes is associated with autonomic and myocardial dysfunction. Exercise training is an efficient non-pharmacological treatment for cardiac and metabolic diseases. The aim of the present study was to investigate the effects of exercise training on hemodynamic and autonomic diabetic dysfunction. After 1 week of diabetes induction (streptozotocin, 50 mg/kg, iv), male Wistar rats (222 +/- 5 g, N = 18) were submitted to exercise training for 10 weeks on a treadmill. Arterial pressure signals were obtained and processed with a data acquisition system. Autonomic function and intrinsic heart rate were studied by injecting methylatropine and propranolol. Left ventricular function was assessed in hearts perfused in vitro by the Langendorff technique. Diabetes (D) bradycardia and hypotension (D: 279 +/- 9 bpm and 91 +/- 4 mmHg vs 315 +/- 11 bpm and 111 +/- 4 mmHg in controls, C) were attenuated by training (TD: 305 +/- 7 bpm and 100 +/- 4 mmHg). Vagal tonus was decreased in the diabetic groups and sympathetic tonus was similar in all animals. Intrinsic heart rate was lower in D (284 +/- 11 bpm) compared to C and TD (390 +/- 8 and 342 +/- 14 bpm, respectively). Peak systolic pressure developed at different pressures was similar for all groups, but +dP/dt max was decreased and -dP/dt max was increased in D. In conclusion, exercise training reversed hypotension and bradycardia and improved myocardial function in diabetic rats. These changes represent an adaptive response to the demands of training, supporting a positive role of physical activity in the management of diabetes.

Animals↗

PubMed2000

Oxidative stress in the latissimus dorsi muscle of diabetic rats.

The purpose of the present study was to investigate the effects of experimental diabetes on the oxidant and antioxidant status of latissimus dorsi (LD) muscles of male Wistar rats (220 +/- 5 g, N = 11). Short-term (5 days) diabetes was induced by a single injection of streptozotocin (STZ, 50 mg/kg, iv; glycemia >300 mg/dl). LD muscle of STZ-diabetic rats presented higher levels of thiobarbituric acid reactive substances (TBARS) and chemiluminescence (0.36 +/- 0.02 nmol/mg protein and 14706 +/- 1581 cps/mg protein) than LD muscle of normal rats (0.23 +/- 0.04 nmol/mg protein and 7389 +/- 1355 cps/mg protein). Diabetes induced a 92% increase in catalase and a 27% increase in glutathione S-transferase activities in LD muscle. Glutathione peroxidase activity was reduced (58%) in STZ-diabetic rats and superoxide dismutase activity was similar in LD muscle of both groups. A positive correlation was obtained between catalase activity and the oxidative stress of LD, as evaluated in terms of TBARS (r = 0.78) and by chemiluminescence (r = 0.89). Catalase activity also correlated inversely with glutathione peroxidase activity (r = 0.79). These data suggest that an increased oxidative stress in LD muscle of diabetic rats may be related to skeletal muscle myopathy.

Animals↗

PubMed1999

Exercise reverses peripheral insulin resistance in trained L-NAME-hypertensive rats.

Several studies have demonstrated an increase in peripheral resistance to insulin associated with hypertension. To assess the hemodynamic and metabolic effects of exercise training, normotensive and N(omega)-nitro-L-arginine methyl ester (L-NAME)-hypertensive male Wistar rats were submitted to low-intensity treadmill exercise training for 10 weeks and compared with their sedentary controls. Blood pressure signals were obtained and processed with a data acquisition system (CODAS, 1 kHz) to evaluate mean arterial pressure, heart rate, autonomic control of heart rate, and baroreflex sensitivity. Exercise training induced a nonsignificant 6.5-mm Hg decrease in mean arterial pressure in trained hypertensive rats (163+/-9 mm Hg) compared with sedentary hypertensive rats (169.5+/-5. 5 mm Hg). The hypertensive groups showed impairment of baroreflex function in response to changes in arterial pressure compared with sedentary controls. Furthermore, exercise training improved the tachycardic response to decreasing arterial pressure and reduced intrinsic heart rate in trained control rats compared with all other groups. Sedentary hypertensive rats presented a decrease in body weight compared with normotensive animals. Basal evaluation of the glucose/insulin ratio showed increased insulin resistance in sedentary (28.4+/-3) and trained (23.5+/-2.7) hypertensive rats compared with sedentary control rats (40.5+/-3). However, the glucose/insulin ratio evaluated during the exercise session in trained rats showed an improvement in insulin resistance (54.5+/-5 for control rats and 44+/-9 for hypertensive rats). In conclusion, L-NAME-induced hypertension is accompanied by an increase in insulin resistance in rats. The improvement in peripheral insulin sensitivity during exercise and the body weight gain observed in trained hypertensive rats may support the positive role of physical activity in the management of hypertension.

Animals↗

PubMed1997

Exercise training in aging: hemodynamic, metabolic, and oxidative stress evaluations.

The effects of exercise training on hemodynamic and metabolic parameters as well as on responses to oxidative stress in aged individuals are controversial. The aim of the present study was to investigate changes in heart hate, mean arterial pressure, vasoreactivity, and plasma levels of insulin and glucose in male aged Wistar rats submitted to exercise training for 11 weeks (1 h/d; 5 d/wk) in a treadmill. The isolated heart was perfused by H2O2, and oxidative stress was evaluated using thiobarbituric acid reactive substances. Cardiovascular functions were recorded with a data acquisition system (CODAS, 1 kHz). Trained aged rats were bradycardic as compared with sedentary aged rats (298+/-7 versus 336+/-16 bpm) but presented similar mean arterial pressure and vasoreactivity and plasma levels of insulin and of glucose, which were quantified by radioimmunoassay and colorimetric enzymatic test. Plasma levels of insulin and of glucose ratio were increased in trained aged rats (6.9+/-0.7 versus 3.5+/-0.4 in sedentary aged rats), and the response to oxidative stress was decreased (0.4+/-0.1 versus 0.7+/-0.1 nmol/mg protein in sedentary aged rats). These results showed that exercise training produced a lower resting heart rate as well as changes in metabolic and oxidative responses. This suggests a higher myocardium protection of trained than sedentary aged rats.

Aging↗

PubMed1997

Baroreflex and chemoreflex dysfunction in streptozotocin-diabetic rats.

Several investigators have demonstrated that streptozotocin (STZ) diabetes induces changes in the autonomic control of the cardiovascular system. Changes in cardiovascular function may be related to peripheral neuropathy. The aim of the present study was to analyze changes in heart rate (HR) and arterial pressure (AP) as well as baroreflex and chemoreflex sensitivity in STZ-induced diabetic male Wistar rats (STZ, 50 mg/kg, i.v., 15 days). Intra-arterial blood pressure signals were obtained for control and diabetic rats (N = 9, each group). Data were processed in a data acquisition system (CODAS, 1 kHz). Baroreflex sensitivity was evaluated by measuring heart rate changes induced by arterial pressure variation produced by phenylephrine and sodium nitroprusside injection. Increasing doses of potassium cyanide (KCN) were used to evaluate bradycardic and pressor responses evoked by chemoreflex activation. STZ induced hyperglycemia (447 +/- 49 vs 126 +/- 3 mg/dl), and a reduction in AP (99 +/- 3 vs 118 +/- 2 mmHg), resting HR (296 +/- 11 vs 355 +/- 16 bpm) and plasma insulin levels (16 +/- 1 vs 57 +/- 11 microU/ml). We also observed that the reflex bradycardia (-16.8 +/- 0.1 vs -12.5 +/- 0.1 bpm/mmHg, in the diabetic group) and tachycardia (-3.68 +/- 0.5 vs -1.75 +/- 0.3 bpm/mmHg, in the diabetic group) produced by vasopressor and depressor agents were impaired in the diabetic group. Bradycardia evoked by chemoreflex activation was attenuated in diabetic rats (control: -17 +/- 1, -86 +/- 19, -185 +/- 18, -208 +/- 17 vs diabetic: -7 +/- 1, -23 +/- 5, -95 +/- 13, -140 +/- 13 bpm), as also was the pressor response (control: 6 +/- 1, 30 +/- 7, 54 +/- 4, 59 +/- 5 vs diabetic: 6 +/- 1, 8 +/- 2, 33 +/- 4, 42 +/- 5 mmHg). In conclusion, the cardiovascular response evoked by baroreflex and chemoreflex activation are impaired in diabetic rats. The alterations of cardiovascular responses may be secondary to the autonomic dysfunction of cardiovascular control.

Animals↗

PubMed1997

Time course of changes in heart rate and blood pressure variability in streptozotocin-induced diabetic rats treated with insulin.

Autonomic neuropathy is a frequent complication of diabetes associated with higher morbidity and mortality in symptomatic patients, possibly because it affects autonomic regulation of the sinus node, reducing heart rate (HR) variability which predisposes to fatal arrhythmias. We evaluated the time course of arterial pressure and HR and indirectly of autonomic function (by evaluation of mean arterial pressure (MAP) variability) in rats (164.5 +/- 1.7 g) 7, 14, 30 and 120 days after streptozotocin (STZ) injection, treated with insulin, using measurements of arterial pressure, HR and MAP variability. HR variability was evaluated by the standard deviation of RR intervals (SDNN) and root mean square of successive difference of RR intervals (RMSSD). MAP variability was evaluated by the standard deviation of the mean of MAP and by 4 indices (P1, P2, P3 and MN) derived from the three-dimensional return map constructed by plotting MAPn x [(MAPn + 1)-(MAPn)] x density. The indices represent the maximum concentration of points (P1), the longitudinal axis (P2), and the transversal axis (P3) and MN represents P1 x P2 x P3 x 10(-3). STZ induced increased urinary glucose in diabetic (D) rats compared to controls (C). Seven days after STZ, diabetes reduced resting HR from 380.6 +/- 12.9 to 319.2 +/- 19.8 bpm, increased HR variability, as demonstrated by increased SDNN, from 11.77 +/- 1.67 to 19.87 +/- 2.60 ms, did not change MAP, and reduced P1 from 61.0 +/- 5.3 to 51.5 +/- 1.8 arbitrary units (AU), P2 from 41.3 +/- 0.3 to 29.0 +/- 1.8 AU, and MN from 171.1 +/- 30.2 to 77.2 +/- 9.6 AU of MAP. These indices, as well as HR and MAP, were similar for D and C animals 14, 30 and 120 days after STZ. Seven-day rats showed a negative correlation of urinary glucose with resting HR (r = -0.76, P = 0.03) as well as the MN index (r = -0.83, P = 0.01). We conclude that rats with short-term diabetes mellitus induced by STZ presented modified autonomic control of HR and MAP which was reversible. The metabolic control may influence these results, suggesting that insulin treatment and a better metabolic control in this model may modify arterial pressure, HR and MAP variability.

Animals↗

PubMed1995

Autonomic dysfunction in short-term experimental diabetes.

Previous data showed that diabetes induced by streptozotocin for 5 days causes changes in arterial pressure control and baroreflex regulation of heart rate in male Wistar rats. The impairment of baroreflex may be related to autonomic neuropathy as described by several investigators. The aim of this study was to identify autonomic changes in short-term experimental diabetes in rats (induced for 5 days with streptozotocin 65 mg IP). Intra-arterial blood pressure signals were obtained from 6 control group and 7 diabetic group rats and processed in a data acquisition system (CODAS, 1 kHz). Both vagal and sympathetic function were assessed through intravenous injections of methylatropine and propranolol. Streptozotocin induced hyperglycemia (18.9 +/- 1.8 versus 5.8 +/- 0.2 mmol/L) and reductions in mean arterial pressure (102 +/- 2 versus 117 +/- 3 mm Hg) and resting heart rate (298 +/- 14 versus 332 +/- 2 beats per minute). Sodium and potassium levels were not different between groups. The intrinsic heart rate was reduced in the diabetic group (302 +/- 10 versus 398 +/- 6 beats per minute). This group also exhibited depressed vagal and sympathetic tone (50% and 22%, respectively), reduction of vagal effect (42%), and no change in sympathetic effect. In conclusion, early autonomic dysfunction in short-term streptozotocin-induced diabetes seems to be related to changes in arterial pressure and baroreflex control.

Animals↗

PubMed1995

Streptozotocin diabetes modifies arterial pressure and baroreflex sensitivity in rats.

Although an increased prevalence of hypertension is associated with insulin-dependent diabetes, little is known about the effect of streptozotocin (STZ) diabetes on arterial pressure (AP) regulation in rats. Changes in AP induced by STZ, as well as associated factors in blood pressure regulation such as baroreflex sensitivity, plasma renin activity (PRA), plasma glucose and insulin levels and endothelium participation, were studied in male Wistar rats weighing 287 +/- 10 g. The same seven conscious rats were used for all measurements before and after STZ diabetes. AP pulses were stored on a videotape recorder and processed by a data acquisition system. Baroreflex sensitivity was evaluated by measuring heart rate (HR) changes induced by AP variations produced by phenylephrine and sodium nitroprusside injection. The effect of inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg i.v. bolus plus infusion at 20 mg kg-1 h-1) on AP was evaluated in another set of rats (6 normal and 5 submitted to STZ treatment). STZ induced hyperglycemia (306 +/- 19 mg/dl), a reduction in mean arterial pressure (MAP, from 116 +/- 5 to 101 +/- 4 mmHg) and no changes in HR (320 +/- 10 vs 298 +/- 14 bpm). The tachycardic response to arterial pressure decreases was impaired (-2.29 +/- 0.5 vs -4.5 +/- 0.7 bpm/mmHg, in control) while the bradycardic response to arterial pressure increases was unchanged. Pressure responsiveness to phenylephrine was impaired after STZ (3.78 +/- 0.4 vs 6.73 +/- 0.8 mmHg microU-1 ml-1, in control).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Changes in blood pressure control in aged rats.

The aging process is related to several changes in cardiovascular, metabolic and autonomic functions. However, descriptions of changes in arterial pressure (AP), baroreflex sensitivity and associated variations of serum glucose and insulin are controversial. The aim of this paper was to study AP, baroreflex sensitivity and changes in plasma levels of glucose and insulin of young (10 weeks, 239 +/- 4.3 g) and aged (18-24 months, 412 +/- 8.5 g) male Wistar rats. AP pulses were videotaped and processed on a microcomputer, using an analog-to-digital converter (beat-to-beat analysis). Baroreflex sensitivity was evaluated measuring heart rate changes induced by mean arterial pressure (MAP) variations produced by phenylephrine and sodium nitroprusside injections (N = 10 in each group). Plasma glucose (N = 10 in each group) and plasma insulin (N = 6 in each group) were quantified by a colorimetric enzymatic test and radioimmunoassay, respectively. There were no differences in systolic, diastolic or mean AP (110 +/- 5 vs 107 +/- 3 mmHg) between aged and young rats. The tachycardic response to the reduction of AP was impaired in aged compared to young rats (-1.95 +/- 0.29 vs -3.26 +/- 0.49 bpm/mmHg), while the bradycardic response to increases in AP was similar (-1.02 +/- 0.22 vs -1.5 +/- 0.26 bpm/mmHg). Basal levels of glucose (83 +/- 6 vs 62 +/- 4 mg/dl) and insulin (8.3 +/- 2 vs 4 +/- 0.5 microU/ml) were different. Thus, the reflex tachycardia evoked by a fall in AP is depressed in old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗