Search

Background: Even if sodium sensitivity represents a risk factor at any blood pressure (BP) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives. Methods and Results: We evaluated the Sodium-Sensitivity Index (SS-Index) in 71 white normotensives after 5 days of high- and low-sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate (HR) and BP variability. According to the SS-Index distribution, we defined 1 sodium-sensitive group (SS, with SS-Index >15 mm Hg/[mmol·day]), 1 sodium-resistant group, (unresponsive to sodium load with -15≤ SS-Index ≤+15), and 1 inverse sodium-sensitive group, responsive to sodium by decreasing BP, with SS-Index <-15). We compared the effects of the diets among groups, and correlated autonomic/hemodynamic indices with the SS-Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR, spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium-sensitive group but not in SS normotensives. Moreover, the highest SS-Indices were associated with the lesser vagal HR decelerations. Conclusions: Our data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

Background: Even if sodium sensitivity represents a risk factor at any blood pressure (BP) level, limited evidence is available that it may influence cardiovascular control in normotensives, particularly in white individuals. Therefore, the aim of the study was to investigate whether sodium sensitivity alters hemodynamic or autonomic responses to salt in normotensives. Methods and Results: We evaluated the Sodium-Sensitivity Index (SS-Index) in 71 white normotensives after 5 days of high- and low-sodium diets. We measured BP continuously at the end of each period, estimating hemodynamic indices from BP waveform analysis, and autonomic indices from heart rate (HR) and BP variability. According to the SS-Index distribution, we defined 1 sodium-sensitive group (SS, with SS-Index >15 mm Hg/[mmol·day]), 1 sodium-resistant group, (unresponsive to sodium load with -15≤ SS-Index ≤+15), and 1 inverse sodium-sensitive group, responsive to sodium by decreasing BP, with SS-Index <-15). We compared the effects of the diets among groups, and correlated autonomic/hemodynamic indices with the SS-Index. After sodium loading, a significant decrease in systemic peripheral resistances, HR, spectral indices of BP modulation, and a significant increase of indices of HR vagal modulation were found in the inverse sodium-sensitive group but not in SS normotensives. Moreover, the highest SS-Indices were associated with the lesser vagal HR decelerations. Conclusions: Our data suggest that salt sensitivity in white normotensive individuals is associated with impaired vasodilation and altered autonomic response to dietary salt. Such dysfunction may critically contribute to induce a BP response to dietary salt.

The low incidence of cardiovascular disease in Mediterranean countries leads to an increased interest of the scientific community for the Mediterranean diet. Our aim was to evaluate total phenol and flavonoid contents, antioxidant capacity, free radical scavenging activity and potential antihypertensive effect of aqueous extract obtained from Thymus serpyllum L. (wild thyme, TE), an aromatic herb from the Lamiaceae family (highly present in Mediterranean diet), in spontaneously hypertensive rats (SHR) and in normotensive Wistar rats. Total phenol content of TE was 2008.33 +/- 10.6 mg/L GAE, and rosmarinic and caffeic acids were predominant phenolic compounds. The ferric reducing/antioxidant power and antioxidant capacity analysis revealed strong antioxidative properties of TE. In vitro nitric oxide-scavenging activity of 1 mg/l TE was 63.43 % with the IC50 value of 122.36 mu g/ml. Bolus injection of TE (100 mg/kg body weight i.v.) induced significant decrease of systolic and diastolic blood pressure and total peripheral resistance in SHR, without effects on these parameters in normotensive Wistar rats. Cardiac index remained unchanged after TE treatment in all experimental rats. Given dose of TE did not show significant nitric oxide-scavenging activity in vivo. Our results indicate that TE may protect against hypertension in experimental model of essential hypertension.

The low incidence of cardiovascular disease in Mediterranean countries leads to an increased interest of the scientific community for the Mediterranean diet. Our aim was to evaluate total phenol and flavonoid contents, antioxidant capacity, free radical scavenging activity and potential antihypertensive effect of aqueous extract obtained from Thymus serpyllum L. (wild thyme, TE), an aromatic herb from the Lamiaceae family (highly present in Mediterranean diet), in spontaneously hypertensive rats (SHR) and in normotensive Wistar rats. Total phenol content of TE was 2008.33 +/- 10.6 mg/L GAE, and rosmarinic and caffeic acids were predominant phenolic compounds. The ferric reducing/antioxidant power and antioxidant capacity analysis revealed strong antioxidative properties of TE. In vitro nitric oxide-scavenging activity of 1 mg/l TE was 63.43 % with the IC50 value of 122.36 mu g/ml. Bolus injection of TE (100 mg/kg body weight i.v.) induced significant decrease of systolic and diastolic blood pressure and total peripheral resistance in SHR, without effects on these parameters in normotensive Wistar rats. Cardiac index remained unchanged after TE treatment in all experimental rats. Given dose of TE did not show significant nitric oxide-scavenging activity in vivo. Our results indicate that TE may protect against hypertension in experimental model of essential hypertension.

Objectives: The objectives of this study were to estimate fetal blood pressure non-invasively from two-dimensional color Doppler-derived aortic blood flow and diameter waveforms, and to compare the results with invasively derived human fetal blood pressures available from the literature. Methods: Aortic pressures were calculated from digitally recorded color Doppler cineloops of the fetal descending aorta by applying the Womersley model in combination with the two-element Windkessel model, assuming constant pulse wave velocity during the second half of pregnancy. The results were compared with invasively derived human fetal blood pressures obtained from the literature. Results: In 21 normal pregnancies the estimated mean aortic pressure regression line increased linearly from 28 mmHg at 20 weeks of gestation to 45 mmHg at 40 weeks of gestation. The pulse pressure based on the regression line increased linearly from 21 mmHg at 20 weeks of gestation to 29 mmHg at 40 weeks of gestation. The aortic compliance exhibited a log linear relationship with the gestational age and a statistically significant eightfold increase was observed between 20 and 40 weeks. The aortic downstream peripheral resistance exhibited an exponentially decaying relationship across the same gestational age range. Non-invasively derived aortic systolic and diastolic aortic pressures were comparable with previously reported invasively derived systolic and diastolic umbilical arterial pressures; however, the mean pressures differed significantly from those reported in the umbilical artery in a separate study. The aortic systolic pressures calculated in this study were significantly higher than invasively derived left ventricular systolic pressures that have been previously reported in the literature. Conclusions: This study demonstrates the feasibility of estimating arterial blood pressure in the human fetus. The method described is of potential use in assessing fetal blood pressure non-invasively, p

Recovery from exercise can be an important factor in performance during repeated bouts of exercise. In a tournament situation, where athletes may compete numerous times over a few days, enhancing recovery may provide a competitive advantage. One method that is gaining popularity as a means to enhance post-game or post-training recovery is immersion in water. Much of the literature on the ability of water immersion as a means to improve athletic recovery appears to be based on anecdotal information, with limited research on actual performance change. Water immersion may cause physiological changes within the body that could improve recovery from exercise. These physiological changes include intracellular-intravascular fluid shifts, reduction of muscle oedema and increased cardiac output (without increasing energy expenditure), which increases blood flow and possible nutrient and waste transportation through the body. Also, there may be a psychological benefit to athletes with a reduced cessation of fatigue during immersion. Water temperature alters the physiological response to immersion and cool to thermoneutral temperatures may provide the best range for recovery. Further performance-orientated research is required to determine whether water immersion is beneficial to athletes.

type:text, We analyzed the vasoconstrictor effects of arginine vasopressin (AVP) on regional arteries before and after ganglionic blockade with hexamethonium. Simultaneous measurements of mean arterial pressure and regional flows were obtained in conscious rats, using chronically implanted electromagnetic flow probes. Regional vascular resistance was calculated as mean arterial pressure divided by regional flow. AVP was applied intravenously as a bolus, at doses ranging from 5×10-11 to 5×10-8 g/kg. AVP increased mean arterial pressure, decreased superior mesenteric, renal and terminal aortic flows (supplied mainly for the hindquarter vascular area), and increased superior mesenteric, renal and terminal aortic (hindquarter) resistances in a dose-dependent manner. Ganglionic blockade decreased mean arterial pressure and renal resistance significantly, whereas there were no significant differences between changes in resistance before and after ganglionic blockade in superior mesenteric or terminal aortic areas. This suggested the presence of basal sympathetic vasoconstrictor tone in the renal area. After ganglionic blockade, the pressor effect of AVP was enhanced significantly. The increase in renal resistance induced by AVP was augmented after ganglionic blockade, whereas increases in superior mesenteric or terminal aortic resistance remained unchanged following ganglionic blockade. Our data suggest that the vasoconstrictor effect of AVP on renal vascular area is reduced by a mechanism which inhibits renal sympathetic basal tone.

We analyzed the vasoconstrictor effects of arginine vasopressin (AVP) on regional arteries before and after ganglionic blockade with hexamethonium. Simultaneous measurements of mean arterial pressure and regional flows were obtained in conscious rats, using chronically implanted electromagnetic flow probes. Regional vascular resistance was calculated as mean arterial pressure divided by regional flow. AVP was applied intravenously as a bolus, at doses ranging from 5×10-11 to 5×10-8 g/kg. AVP increased mean arterial pressure, decreased superior mesenteric, renal and terminal aortic flows (supplied mainly for the hindquarter vascular area), and increased superior mesenteric, renal and terminal aortic (hindquarter) resistances in a dose-dependent manner. Ganglionic blockade decreased mean arterial pressure and renal resistance significantly, whereas there were no significant differences between changes in resistance before and after ganglionic blockade in superior mesenteric or terminal aortic areas. This suggested the presence of basal sympathetic vasoconstrictor tone in the renal area. After ganglionic blockade, the pressor effect of AVP was enhanced significantly. The increase in renal resistance induced by AVP was augmented after ganglionic blockade, whereas increases in superior mesenteric or terminal aortic resistance remained unchanged following ganglionic blockade. Our data suggest that the vasoconstrictor effect of AVP on renal vascular area is reduced by a mechanism which inhibits renal sympathetic basal tone.

We analyzed the vasoconstrictor effects of arginine vasopressin (AVP) on regional arteries before and after ganglionic blockade with hexamethonium. Simultaneous measurements of mean arterial pressure and regional flows were obtained in conscious rats, using chronically implanted electromagnetic flow probes. Regional vascular resistance was calculated as mean arterial pressure divided by regional flow. AVP was applied intravenously as a bolus, at doses ranging from 5×10-11 to 5×10-8 g/kg. AVP increased mean arterial pressure, decreased superior mesenteric, renal and terminal aortic flows (supplied mainly for the hindquarter vascular area), and increased superior mesenteric, renal and terminal aortic (hindquarter) resistances in a dose-dependent manner. Ganglionic blockade decreased mean arterial pressure and renal resistance significantly, whereas there were no significant differences between changes in resistance before and after ganglionic blockade in superior mesenteric or terminal aortic areas. This suggested the presence of basal sympathetic vasoconstrictor tone in the renal area. After ganglionic blockade, the pressor effect of AVP was enhanced significantly. The increase in renal resistance induced by AVP was augmented after ganglionic blockade, whereas increases in superior mesenteric or terminal aortic resistance remained unchanged following ganglionic blockade. Our data suggest that the vasoconstrictor effect of AVP on renal vascular area is reduced by a mechanism which inhibits renal sympathetic basal tone.

type:text, Utilizing the standard Wiggers' method, hemorrhagic shock was induced in ten anesthetized dogs by bleeding to a mean arterial pressure (MAP) of 50 mmHg for 2 hr and then to 30 mmHg for 1 hr, followed by reinfusion of the shed blood. The experimental protocol was designed to evaluate the effect of hemorrhagic shock on sequential pulmonary hemodynamic changes in relation to those of cardiac and systemic circulation. All selected cardiopulmonary hemodynamic parameters were recorded throughout the experiment on a multi-channel poly-oscillograph monitor. Total pulmonary resistance (TPuR) started rising early in hemorrhagic shock and was found to rise to a level that was 10-fold greater than pulmonary arteriolar resistance (PAR). This meant that, 90% of TPuR came from the venous side of the pulmonary vascular bed. Persistently raised TPuR even after reinfusion was linked to early death of the experimental animals. Myocardial contractility (max dp/dt mmHg/sec) which is one of the indices for cardiac performance was found to be severely depressed at terminal stage (p<0.001). Both total pulmonary and peripheral resistances were found to have an inverse relationship to ventricular performance which was measured by left ventricular stroke work (LVSW) and right ventricular stroke work (RVSW). There is a high suspicion that reinfusion or resuscitation following prolonged hypovolemic shock may aggrevate the hemorrhagic shock effects by facilitating the distribution of accumulated blood-borne toxic substances to various target organs and that, this has been linked with the early and sustained pulmonary hemodynamic disturbance found in these experiments.

Utilizing the standard Wiggers' method, hemorrhagic shock was induced in ten anesthetized dogs by bleeding to a mean arterial pressure (MAP) of 50 mmHg for 2 hr and then to 30 mmHg for 1 hr, followed by reinfusion of the shed blood. The experimental protocol was designed to evaluate the effect of hemorrhagic shock on sequential pulmonary hemodynamic changes in relation to those of cardiac and systemic circulation. All selected cardiopulmonary hemodynamic parameters were recorded throughout the experiment on a multi-channel poly-oscillograph monitor. Total pulmonary resistance (TPuR) started rising early in hemorrhagic shock and was found to rise to a level that was 10-fold greater than pulmonary arteriolar resistance (PAR). This meant that, 90% of TPuR came from the venous side of the pulmonary vascular bed. Persistently raised TPuR even after reinfusion was linked to early death of the experimental animals. Myocardial contractility (max dp/dt mmHg/sec) which is one of the indices for cardiac performance was found to be severely depressed at terminal stage (p<0.001). Both total pulmonary and peripheral resistances were found to have an inverse relationship to ventricular performance which was measured by left ventricular stroke work (LVSW) and right ventricular stroke work (RVSW). There is a high suspicion that reinfusion or resuscitation following prolonged hypovolemic shock may aggrevate the hemorrhagic shock effects by facilitating the distribution of accumulated blood-borne toxic substances to various target organs and that, this has been linked with the early and sustained pulmonary hemodynamic disturbance found in these experiments.

Utilizing the standard Wiggers' method, hemorrhagic shock was induced in ten anesthetized dogs by bleeding to a mean arterial pressure (MAP) of 50 mmHg for 2 hr and then to 30 mmHg for 1 hr, followed by reinfusion of the shed blood. The experimental protocol was designed to evaluate the effect of hemorrhagic shock on sequential pulmonary hemodynamic changes in relation to those of cardiac and systemic circulation. All selected cardiopulmonary hemodynamic parameters were recorded throughout the experiment on a multi-channel poly-oscillograph monitor. Total pulmonary resistance (TPuR) started rising early in hemorrhagic shock and was found to rise to a level that was 10-fold greater than pulmonary arteriolar resistance (PAR). This meant that, 90% of TPuR came from the venous side of the pulmonary vascular bed. Persistently raised TPuR even after reinfusion was linked to early death of the experimental animals. Myocardial contractility (max dp/dt mmHg/sec) which is one of the indices for cardiac performance was found to be severely depressed at terminal stage (p<0.001). Both total pulmonary and peripheral resistances were found to have an inverse relationship to ventricular performance which was measured by left ventricular stroke work (LVSW) and right ventricular stroke work (RVSW). There is a high suspicion that reinfusion or resuscitation following prolonged hypovolemic shock may aggrevate the hemorrhagic shock effects by facilitating the distribution of accumulated blood-borne toxic substances to various target organs and that, this has been linked with the early and sustained pulmonary hemodynamic disturbance found in these experiments.

We analyzed the vasoconstrictor effects of arginine vasopressin (AVP) on regional arteries before and after ganglionic blockade with hexamethonium. Simultaneous measurements of mean arterial pressure and regional flows were obtained in conscious rats, using chronically implanted electromagnetic flow probes. Regional vascular resistance was calculated as mean arterial pressure divided by regional flow. AVP was applied intravenously as a bolus, at doses ranging from 5×10-11 to 5×10-8 g/kg. AVP increased mean arterial pressure, decreased superior mesenteric, renal and terminal aortic flows (supplied mainly for the hindquarter vascular area), and increased superior mesenteric, renal and terminal aortic (hindquarter) resistances in a dose-dependent manner. Ganglionic blockade decreased mean arterial pressure and renal resistance significantly, whereas there were no significant differences between changes in resistance before and after ganglionic blockade in superior mesenteric or terminal aortic areas. This suggested the presence of basal sympathetic vasoconstrictor tone in the renal area. After ganglionic blockade, the pressor effect of AVP was enhanced significantly. The increase in renal resistance induced by AVP was augmented after ganglionic blockade, whereas increases in superior mesenteric or terminal aortic resistance remained unchanged following ganglionic blockade. Our data suggest that the vasoconstrictor effect of AVP on renal vascular area is reduced by a mechanism which inhibits renal sympathetic basal tone.

Utilizing the standard Wiggers' method, hemorrhagic shock was induced in ten anesthetized dogs by bleeding to a mean arterial pressure (MAP) of 50 mmHg for 2 hr and then to 30 mmHg for 1 hr, followed by reinfusion of the shed blood. The experimental protocol was designed to evaluate the effect of hemorrhagic shock on sequential pulmonary hemodynamic changes in relation to those of cardiac and systemic circulation. All selected cardiopulmonary hemodynamic parameters were recorded throughout the experiment on a multi-channel poly-oscillograph monitor. Total pulmonary resistance (TPuR) started rising early in hemorrhagic shock and was found to rise to a level that was 10-fold greater than pulmonary arteriolar resistance (PAR). This meant that, 90% of TPuR came from the venous side of the pulmonary vascular bed. Persistently raised TPuR even after reinfusion was linked to early death of the experimental animals. Myocardial contractility (max dp/dt mmHg/sec) which is one of the indices for cardiac performance was found to be severely depressed at terminal stage (p<0.001). Both total pulmonary and peripheral resistances were found to have an inverse relationship to ventricular performance which was measured by left ventricular stroke work (LVSW) and right ventricular stroke work (RVSW). There is a high suspicion that reinfusion or resuscitation following prolonged hypovolemic shock may aggrevate the hemorrhagic shock effects by facilitating the distribution of accumulated blood-borne toxic substances to various target organs and that, this has been linked with the early and sustained pulmonary hemodynamic disturbance found in these experiments.