Systemic Hemodynamic Values Research Articles

The regulatory effects of mesedin and beditin alpha2-adrenoblockers on the functional activity of the nervous, cardiovascular, and endocrine systems in rats under the hypoxic conditions.

One of the reasons of the development of pathologies causing death is hypoxia. The purposes of this study were (1) to study some physiological and biochemical mechanisms of α2-adrenoblockers, which ensure the tissue resistance increase to hypoxia; (2) to offer new drugs contributing to the increase of tissues' stability towards the hypoxic affection; and (3) to submit new medications to surpass by their anti-hypoxic activity of those already used in modern medicine and have some advantages. The reactivity of postsynaptic vascular α2-adrenoceptors was determined on the damaged spinal cord expressed by the blood pressure increase in response to intravenous administration of azepexole that selectively binds to α2-adrenoceptors. Determination of the systemic hemodynamic values and the vascular resistance to the blood flow was performed by the method with plastic microspheres of marked isotopes. pO2 in the blood and the oxygen-transporting function were determined in a sample of 0.1ml of blood in 30, 90, and 180min after the α2-adrenoblockers' injections. It has been found that one of the major hemodynamic effects of mesedin and beditin was an improvement in cardiac output, as well as a prolonged increase in coronary blood flow and vasodilation of the heart vessels. Some anti-hypoxic mechanisms of the studied α2-adrenoblockers are an improvement of blood oxygen-transporting function followed by tissue oxygenation and the increased level of corticosterone and resistance to hypoxia. Revealing the mechanisms of action of the postsynaptic α2-adrenoceptors suggests that mesedin and beditin are potentially effective therapeutic means for many hypoxic conditions.

Pulse waveform analysis in the optic nerve head circulation reflects systemic vascular resistance obtained via a Swan-Ganz catheter.

To determine whether a pulse waveform analysis in the optic nerve head (ONH) circulation as determined by laser speckle flowgraphy (LSFG) can provide systemic hemodynamic values - the systemic vascular resistance (SVR) in particular - similar to those obtained by using a Swan-Ganz catheter, which is an invasive method. Sixteen consecutive subjects were examined. Hemodynamic monitoring was obtained from right heart catheterization with a Swan-Ganz catheter and coronary angiography without an intracoronary nitroglycerin administration. Direct blood pressure was measured with a trans-radial approach. Single regression analyses were used to determine the relationship between the blowout score and blowout time, which are the items of the pulse waveform analysis in the ONH, by using LSFG and the hemodynamic parameters. The blowout time was significantly and negatively correlated with the SVR (r = -0.52, p = 0.04), the ocular perfusion pressure with the mean arterial blood pressure of the radial artery (r = -0.52, p = 0.04) and the radial artery pulse pressure (r = -0.52, p = 0.04).The pulmonary capillary wedge pressure (r = -0.44, p = 0.09) and the mean arterial blood pressure of the radial artery (r = -0.44, p = 0.09) tended to be correlated with the blowout time, but did not reach significance. The blowout score was significantly and negatively correlated with the radial artery blood pressure (r = -0.51, p = 0.046). A pulse waveform analysis in the ONH by LSFG may be one of the useful methods for understanding the SVR.

Interactions macro- et microcirculatoires dans le choc

Microcirculatory alterations, frequently observed in shock states, are associated with the development of multiple organ failure and death. These microcirculatory alterations occur even when systemic hemodynamic variables are within resuscitation goals. In this review, we discuss the link between the microcirculation and systemic hemodynamics. Several studies suggested that microvascular perfusion may be dependent from systemic hemodynamics in severely hypotensive patients. However, the threshold of blood pressure at which this occurs is not well defined and it is difficult to define which mean arterial pressure target should be reached. The microcirculation is usually independent of systemic hemodynamics in the usual range of systemic hemodynamic values encountered when resuscitation targets are met. Fluids and vasoactive agents affect the microcirculation independently of their systemic effects.

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure

The aim of the study is to evaluate the effect of a single treatment with the molecular adsorbents recirculating system (MARS) on systemic hemodynamics and oxygen consumption (VO(2)) in patients with hyperacute liver failure (HALF). In a controlled design, eight patients with HALF were assigned to a 6-hour MARS treatment, and five patients, to a control group that was mechanically cooled to match the MARS group. Systemic hemodynamic variables were determined hourly during the study period. In the MARS group, systemic vascular resistance index increased by 46% from 1,215 +/- 437 to 1,778 +/- 710 dynes x s x cm(-5) x m(-2) (P <.0001), which significantly exceeded a 6% increase in the control group. Mean arterial pressure increased from 69 +/- 5 to 83 +/- 11 mm Hg in the MARS group (P <.0001) and was unchanged in the control group. Cardiac index decreased by 20% from 4.6 +/- 1.8 to 3.7 +/- 1.1 L/min x m(-2) (P =.0007) in the MARS group and by 7% in the control group. Heart rate decreased from 105 +/- 21 to 85 +/- 15 beats/min in the MARS group (P <.0001) and was unchanged in the control group. In the MARS group, oxygen delivery decreased from 621 +/- 198 to 486 +/- 141 mL/min x m(-2) (P <.05), and VO2, from 142 +/- 31 to 112 +/-21 mL/min x m(-2) (P <.05). Arterial lactate and pH levels were unchanged. In conclusion, systemic hemodynamic values tend to normalize, whereas systemic VO(2) decreases during MARS treatment in patients with HALF. These effects cannot be explained by the degree of cooling associated with MARS.

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: A prospective controlled trial

The aim of the study is to evaluate the effect of a single treatment with the molecular adsorbents recirculating system (MARS) on systemic hemodynamics and oxygen consumption (VO2) in patients with hyperacute liver failure (HALF). In a controlled design, eight patients with HALF were assigned to a 6-hour MARS treatment, and five patients, to a control group that was mechanically cooled to match the MARS group. Systemic hemodynamic variables were determined hourly during the study period. In the MARS group, systemic vascular resistance index increased by 46% from 1,215 ± 437 to 1,778 ± 710 dynes · s · cm−5 · m−2 (P < .0001), which significantly exceeded a 6% increase in the control group. Mean arterial pressure increased from 69 ± 5 to 83 ± 11 mm Hg in the MARS group (P < .0001) and was unchanged in the control group. Cardiac index decreased by 20% from 4.6 ± 1.8 to 3.7 ± 1.1 L/min · m−2 (P = .0007) in the MARS group and by 7% in the control group. Heart rate decreased from 105 ± 21 to 85 ± 15 beats/min in the MARS group (P < .0001) and was unchanged in the control group. In the MARS group, oxygen delivery decreased from 621 ± 198 to 486 ± 141 mL/min · m−2 (P < .05), and VO2, from 142 ± 31 to 112 ±21 mL/min · m−2 (P < .05). Arterial lactate and pH levels were unchanged. In conclusion, systemic hemodynamic values tend to normalize, whereas systemic VO2 decreases during MARS treatment in patients with HALF. These effects cannot be explained by the degree of cooling associated with MARS. (Liver Transpl 2003;9:290-297.)

Effects of octreotide on central hemodynamics and systemic oxygen use in patients with viral cirrhosis

OBJECTIVE: Octreotide has potentially beneficial effects in patients with cirrhosis. However, the effects of octreotide on central hemodynamics and oxygen use have not been established. The present study was undertaken to evaluate the effect of octreotide on central hemodynamics and oxygen use in patients with viral cirrhosis. METHODS: Twenty-five patients with cirrhosis were enrolled in the study. They were randomly assigned to receive either placebo (n = 10) or a continuous infusion of 100 μg/h of octreotide after an initial 100-μg bolus (n = 15). Hemodynamic measurements and oxygenation values were obtained before and 60 min after octreotide or placebo administration. RESULTS: Placebo administration did not have any effect on hemodynamic and oxygenation values. In patients who received octreotide, systemic hemodynamic values including cardiac index, mean arterial pressure, and systemic vascular resistance were not affected. The mean pulmonary arterial pressure tended to increase after octreotide administration but was statistically insignificant. There was a significant increase in pulmonary arterial vascular resistance, whereas the pulmonary capillary wedge pressure and right atrial pressure were significantly decreased. Arterial oxygen tension, systemic oxygen uptake, and oxygen extraction ratio were significantly decreased after octreotide administration, whereas oxygen transport as well as arterial and mixed venous oxygen contents remained unchanged. CONCLUSIONS: In patients with viral cirrhosis, octreotide administration exerted a significant effect on pulmonary circulation. It also resulted in a decrease in systemic oxygen uptake and oxygen extraction ratio. These results suggested that octreotide may impair tissue oxygenation in patients with viral cirrhosis.

Inhalation of the nitric oxide synthase cofactor tetrahydrobiopterin in healthy volunteers.

Pulmonary endothelial dysfunction is the hallmark of acute lung injury. Impaired pulmonary endothelial nitric oxide (NO) production in this event has been described. Tetrahydrobiopterin (BH4) is an essential cofactor for NO synthase and modulator of its activity. At high local concentrations, BH4 provokes local vasodilation in vivo in healthy individuals. At lower concentrations, BH4 selectively and locally restores disturbed NO-dependent vasodilation in patients with endothelial dysfunction. In this preliminary study, we therefore investigated the feasibility of BH4 inhalation in five healthy human volunteers. Inhalation of buffered, aqueous BH4-dihydrochloride solution was well tolerated; despite the buffer, BH4 stability was completely preserved. Resorption of inhaled BH4 was demonstrated by significantly increased BH4 levels in plasma and urine. Inhaled BH4 did not alter pulmonary function and had no effect on systemic hemodynamic values. Our data demonstrate that inhalation is a novel method for local BH4 administration, offering a basic therapeutic tool for investigation of restoration of impaired NO-dependent vasodilation due to pulmonary endothelial dysfunction.

Effects of octreotide on postprandial systemic and hepatic hemodynamics in patients with postnecrotic cirrhosis

The effects of octreotide on postprandial hemodynamic responses were evaluated in 20 patients with postnecrotic cirrhosis. They were randomly assigned to receive either a 100-micrograms bolus with a 100-micrograms/h infusion of octreotide or a placebo. Placebo administration did not affect any of the hemodynamic values. However, after a liquid meal of 500 kcal, postprandial increases in the hepatic venous pressure gradient and hepatic blood flow were observed in patients receiving placebo, while the systemic hemodynamic values remained unchanged. In contrast, in patients receiving octreotide, the hepatic blood flow was significantly decreased 30 min after administration, while the hepatic venous pressure gradient and the systemic hemodynamic values were not affected. After ingestion of a meal, the mean values of the hepatic blood flows were not significantly different from basal values. Moreover, the wedged hepatic venous pressure, the hepatic venous pressure gradient and the systemic hemodynamic values were not affected by meal ingestion. However, during octreotide infusion, hepatic blood flow 30 min after the meal had a tendency to increase compared to before the meal. In conclusion, octreotide inhibited the postprandial increase in portal pressure in patients with postnecrotic cirrhosis. In addition, octreotide decreased hepatic blood flow in the fasting state. When given before a meal, the increase in blood flow induced by the meal restored the hepatic blood flow to basal levels.

Octreotide decreased liver metabolic activity in patients with hepatitis B surface antigen-positive cirrhosis.

The influence of octreotide and somatostatin on liver metabolic activity were studied in 16 patients with cirrhosis that was positive for hepatitis B surface antigen (HBsAg). In patients receiving a 50 micrograms bolus and a 50 micrograms/hr infusion of octreotide, the hepatic blood flow, hepatic clearance, and the maximum velocity/metabolic elimination rate constant (Vmax/km) were significantly reduced after octreotide infusion compared with basal values. Similarly, the hepatic blood flow, hepatic clearance, and Vmax/km were significantly decreased in patients receiving a 250 micrograms bolus and a 250 micrograms/hr infusion of somatostatin. The extraction ratio and the systemic hemodynamic values, including cardiac index, heart rate, mean arterial pressure, and systemic vascular resistance, showed no significant changes in patients receiving either octreotide or somatostatin. These findings suggest that, as with somatostatin, octreotide reduced hepatic blood flow and impaired liver metabolic activity in patients with HBsAg-positive cirrhosis. These effects may have important clinical implications in the management of bleeding esophageal varices in patients with cirrhosis.

Hemodynamic evaluation of octreotide in patients with hepatitis B-related cirrhosis

The hemodynamic effects of octreotide were studied in 20 patients with hepatitis B-related cirrhosis. In patients receiving a 100-μg bolus and a 100-μg/h infusion, heart rate, cardiac index, and systemic vascular resistance showed no significant changes, whereas right atrial pressure, pulmonary capillary wedge pressure, and inferior vena cava pressure decreased significantly after octreotide infusion compared with basal values. In contrast, in patients receiving a 50-μg bolus and a 50-μg/h infusion, all the systemic hemodynamic values were unaffected. In both groups of patients receiving two different doses of octreotide, the estimated hepatic blood flow, hepatic indocyanine green clearance, and wedge hepatic venous pressure were significantly reduced at 60 minutes after octreotide administration compared with basal values, whereas the hepatic venous pressure gradient remained unchanged. It is concluded that the two different doses of octreotide administration result in the reduction of the wedge hepatic venous pressure and the hepatic blood flow of a similar magnitude, whereas the hepatic venous pressure gradient is unaffected. Octreotide induces discrepant systemic hemodynamic response; this effect is dose related.

Regional sympathetic activity, severity of liver disease and hemodynamics in patients with cirrhosis

One hundred and eight patients with cirrhosis (23 grade A, 46 grade B and 39 grade C, according to Pugh's classification) underwent hemodynamic studies and plasma catecholamine concentration measurements. Blood samples were withdrawn from the pulmonary artery (n = 108), the hepatic vein (n = 108), the azygos vein (n = 59), the right renal vein (n = 66), the right jugular vein (n = 34) and the femoral vein (n = 33). Plasma noradrenaline concentrations in the pulmonary artery and the hepatic vein were more elevated in grade B (607 +/- 52 and 402 +/- 42 pg/ml, respectively) and C patients (630 +/- 59 and 475 +/- 53 pg/ml, respectively) than in grade A patients (411 +/- 51 and 243 +/- 40 pg/ml, respectively). Plasma noradrenaline concentrations from these two vessels were negatively correlated with indocyanine green clearance. These results indicate that both overall and splanchnic sympathetic activities are dependent on altered hepatic function. Significant correlations were found between the wedged hepatic venous pressure and plasma noradrenaline concentrations from either the pulmonary artery, the hepatic vein or the azygos vein. These correlations indicate that both overall and splanchnic sympathetic activities are dependent on the degree of portal hypertension. Moreover, significant correlations were found between hepatic venous plasma noradrenaline concentrations and systemic hemodynamic values, suggesting that splanchnic sympathetic nervous activity could either play a role in the systemic hyperkinetic syndrome or be a consequence of this hyperkinetic syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial and Systemic Hemodynamics During Isovolemic Hemodilution Alone and Combined With Nitroprusside-Induced Controlled Hypotension

Myocardial and systemic effects of isovolemic hemodilution alone and combined with controlled hypotension induced with sodium nitroprusside (SNP) were studied in halothane-anesthetized, open-chest dogs. Regional blood flow was measured with radioactive microspheres and used to compute regional oxygen (O2) supply. Values for regional blood flow in myocardium were used to compute myocardial O2 (MVO2) and lactate uptake (MVLAC) using the Fick equation. Hemodilution to hematocrit 50% of baseline increased aortic blood flow and decreased systemic vascular resistance, although other systemic hemodynamic values were not changed. Twofold increases in myocardial blood flow were accompanied by no change in MVO2, MVLAC, or coronary sinus PO2. Hemodilution increased regional blood flow sufficiently in the pancreas, liver, duodenum, skeletal muscle, skin, and brain to preserve O2 supply whereas unchanged blood flow in the spleen and kidney reduced O2 supply. Under hemodilution, 15 min of intravenous SNP sufficient to reduce mean arterial pressure by 50% caused parallel reductions in aortic blood flow, dP/dt max, and left ventricular end-diastolic pressure; systemic vascular resistance was unaffected. Myocardial blood flow and MVO2 decreased proportionally, whereas MVLAC and coronary sinus PO2 did not change. Regional blood flow and O2 supply decreased in the kidney, spleen, liver, and skin. Extending SNP infusion to 60 min increased myocardial blood flow and MVO2, but other hemodynamic values were unchanged. Comparing previous results with adenosine-induced hypotension inferred that coronary vasodilator reserve was greatly reduced at this time. In conclusion, although myocardial O2 supply versus demand balance was well maintained during SNP-induced hypotension under hemodiluted conditions, diminished coronary vasodilator reserve suggests increased vulnerability to ischemia if stresses of augmented cardiac work demand or impaired arterial oxygenation were superimposed. The decrease in O2 supply in the kidney during combined hemodilution and SNP-induced hypotension also warrants concern. These latter findings suggest the need for extensive clinical monitoring when SNP is used for controlled hypotension under hemodiluted conditions.

Lethal ischemia due to intracoronary endothelin in pigs.

Endothelin is a recently discovered endothelium-derived peptide with potent coronary constrictor properties in vitro. To evaluate endothelin's cardiac actions in vivo, we measured coronary flow and regional myocardial shortening when intracoronary porcine endothelin was given to anesthetized open-chested pigs. Bolus adminstration into the left anterior descending (LAD) coronary artery of six pigs caused dose-related rapidly reversing depression of LAD flow and local shortening. Marked reductions in flow [-71 +/- 8 (SE) %] and shortening (-83 +/- 2%) after 30 pmol/kg demonstrated endothelin's potency in cardiac tissues. Systemic hemodynamic values were unaltered except for transient rises in left ventricular end-diastolic pressure. Endothelin-induced decrement in LAD flow was accompanied by electrocardiographic signs of myocardial ischemia and net release of local myocardial lactate. Intracoronary infusion of endothelin, 15 pmol.kg-1.min-1, caused progressive decline in LAD flow and local shortening followed by severe persistent hypotension and terminal ventricular fibrillation in four of five pigs. Unlike intracoronary delivery of other potent coronary constrictors, intracoronary administration of endothelin did not lead to rapid escape from the peptide's deleterious influence. Coronary exposure to endothelin under pathophysiological circumstances could result in uniquely persistent decrements in myocardial perfusion and contractile function.

Comparison of selective (beta 1) and nonselective (beta 1 and beta 2) beta-adrenergic blockade on systemic and coronary hemodynamic findings in angina pectoris

To investigate the influence of selective β 1-adrenergic blockade, in contrast to β 1- and β 2-adrenergic blockade, systemic and coronary hemodynamics were studied. Measurements were made at rest and during exercise in 23 patients with suspected coronary artery disease (CAD) before and after either metoprolol or propranolol, given in doses to provide comparable β 1-receptor blockade. Quantitative coronary angiography was performed at rest. Using a randomized, double-blind protocol, either β 1 and β 2 blockade was produced by propranolol (0.1 mg/kg intravenously), or selective β 1 blockade was produced by metoprolol (0.15 mg/kg intravenously). As expected, at these doses both drugs produced a comparable decrease in heart rate at rest and during exercise, averaging 9% and 14% after propranolol and 10% and 16% after metoprolol. Exercise duration to ischemia was prolonged in most patients with severe CAD after either propranolol (5 of 7) or metoprolol (6 of 10) treatment. The effects of these 2 β-blocking drugs on systemic hemodynamic values at rest and during exercise were similar. Additionally, coronary sinus flow was usually unchanged by both drugs at rest (−5% after propranolol and −4% after metoprolol, differences not significant) and decreased a similar amount during exercise (−15% after propranolol and −9% after metoprolol, both p <0.05). Coronary resistance did not change significantly with either drug (0% after propranolol and 3% after metoprolol), and during exercise (11% after propranolol and 3% after metoprolol), suggesting that decreases in flow were secondary to reduced demand. Furthermore, neither drug produced detectable changes in coronary artery size. For example, the average change in the minimal diameter of 29 coronary stenoses was −2% after propranolol and 0% after metoprolol (difference not significant).

Endogenous catecholamine levels in chronic heart failure. Relation to the severity of hemodynamic abnormalities

Plasma free epinephrine, norepinephrine, and dopamine concentrations were determined in 48, 63, and 45 patients, respectively, with overt congestive heart failure, and compared with those in 26 patients with stable angina but without heart failure. Systemic hemodynamic values were determined to assess the severity of heart failure. Arterial epinephrine levels were not different between patients with heart failure (73 ± 92 pg/ml) and patients without heart failure (55 ± 73 pg/ml). In patients with congestive heart failure, norepinephrine (665 ± 510 pg/ml, mean ± SD) and dopamine (407 ± 405 pg/ml) levels were significantly higher than in patients with stable angina without heart failure (norepinephrine 184 ± 136 pg/ml, p <0.001, and dopamine 197 ± 259 pg/ml, p <0.02). However, in patients with congestive heart failure, the plasma norepinephrine levels did not correlate with cardiac Index (r = 0.21, p = NS), pulmonary capillary wedge pressure (r = 0.11, p = NS), mean arterial pressure (r = 0.11, p = NS), or systemic vascular resistance (r = 0.18, p = NS). Similarly, there was no correlation between dopamine levels and the hemodynamic abnormalities In patients with congestive heart failure. These findings suggest that although endogenous norepinephrine and dopamine levels are frequently elevated In patients with heart failure, reflecting enhanced sympathetic activity, catecholamine levels do not reflect the severity of heart failure.

Patterns of Left Ventricular Adaptation in Borderline and Mild Essential Hypertension: Echocardiographic Findings

To assess patterns of left ventricular adaptation, 38 patients with borderline and 38 with sustained mild essential hypertension, all lacking electrocardiographic and roentgenographic criteria for left ventricular hypertrophy, were compared using systemic hemodynamic values and M-mode echocardiograms. All patients had normal left ventricular function and measurements of wall thickness. Those with borderline hypertension showed no asymmetric increase in the ratio of septal to posterior wall thickness. The ratio of the left ventricular radius to wall thickness remained normal in both groups, indicating no disproportionate hypertrophy or dilatation of chambers during the phase of normal left ventricular function. Neither finding substantiates asymmetric septal hypertrophy in early hypertension. Those with mild essential hypertension demonstrated an augmented mean circumferential fiber shortening rate compared to those with borderline hypertension (P < 0.005), suggesting an early stage of left ventricular hyperfunction in the development and elaboration of hypertensive heart disease.