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The effect of intensive plasma water exchange by hemofiltration on hemodynamics and soluble mediators in canine endotoxemia.

High volume hemofiltration (HVHF) (200 ml/kg/h) improves hemodynamics in experimental septic shock but is difficult to apply clinically. Accordingly, we studied whether less intensive HVHF (80 ml/kg/h) can still improve hemodynamics in experimental septic shock. We also investigated its effect on the serum concentrations of several inflammatory mediators, including endothelin (ET-1), endotoxin (LPS), tumor necrosis factor-alpha (TNF-alpha), and 6-keto prostaglandin F(1alpha) (6-kepto PGF(1alpha)). Sixteen anesthetized dogs were connected to a continuous veno-venous hemofiltration (CVVH) (filtration: 80 ml/kg/h) or sham circuit and endotoxin (0.5 mg/kg) was infused intravenously over 5 min. Hemodynamic variables were measured at baseline and at 15, 45, 90, and 180 min. The major hemodynamic finding was that endotoxin-induced hypotension was significantly attenuated by intensive CVVH (p < 0.04). Changes in cardiac output and right ventricular ejection fraction were equal in both groups. ET-1 levels, but not LPS, TNF-alpha, or 6-keto PGF(1alpha), were lower during CVVH (p = 0.042). Endotoxin or TNF-alpha were not found in the ultrafiltrate. Median clearances of ET-1 and 6-keto PGF(1alpha) during intensive CVVH were 8.8 and 25.9 ml/m, respectively. We conclude that intensive CVVH attenuates the early component of endotoxin-induced hypotension and reduces serum concentrations of endothelin-1. The effect of CVVH on blood pressure is not explained by convective clearance of the mediators in question.

6-Ketoprostaglandin F1 alpha↗

Hemodynamic tolerance of intermittent hemodialysis in critically ill patients: usefulness of practice guidelines.

Poor hemodynamic tolerance of intermittent hemodialysis (IHD) is a common problem for patients in an intensive care unit (ICU). New dialysis strategies have been adapted to chronic hemodialysis patients with cardiovascular insufficiency. To improve hemodynamic tolerance of IHD, specific guidelines were progressively implemented into practice through the year 1996 in our 26-bed medical ICU. To evaluate the efficiency of these guidelines we retrospectively compared all IHD performed during the years before (1995) and after (1997) implementation of these recommendations. Forty-five patients underwent 248 IHD sessions in 1995 and 76 patients underwent 289 IHD sessions in 1997. The two populations were similar for age, sex, chronic hemodialysis (26% versus 17%), and secondary acute renal failure. In 1997, patients were more severely ill with a higher SAPS II (50 +/- 17 versus 59 +/- 24; p = 0.036), and more patients required epinephrine or norepinephrine infusion before dialysis sessions (16% versus 34%; p < 0.0001). The compliance to guidelines was high, inducing a significant change in IHD modalities. As a result, hemodynamic tolerance was significantly better in 1997, with less systolic blood pressure drop at onset (33% versus 21%, p = 0. 002) and during the sessions (68% versus 56%, p = 0.002). IHD with hypotensive episode or need for therapeutic interventions were less frequent in 1997 (71% versus 61%, p = 0.015). The ICU mortality was similar (53.3% in 1995 versus 47.3% in 1997; p = 0.52) but death rate in 1997, but not in 1995, was significantly less than predicted from SAPS II (47.3% versus 65.6%; p = 0.02). Length of ICU stay was also reduced for survivors in 1997 (p = 0.04). Implementation of practice guidelines for intermittent hemodialysis in ICU patients lessens hemodynamic instability and may improve outcome.

Critical Illness↗

Short-term oral administration of L-arginine improves hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

We sought to assess the effects of oral supplementation of L-arginine, the precursor of nitric oxide (NO), on hemodynamics and exercise capacity in patients with pulmonary hypertension. Acute hemodynamic responses to oral L-arginine (0.5 g/10 kg body weight) or placebo were examined in 19 patients with primary or precapillary secondary pulmonary hypertension. Cardiopulmonary exercise tests were performed to measure peak oxygen consumption (peak V O(2)) and the ventilatory response to carbon dioxide production (V E-V CO(2) slope) before and 1 wk after treatment with L-arginine (1.5 g/10 kg body weight/d) or placebo. Oral supplementation of L-arginine significantly increased plasma L-citrulline, which indicated enhancement of NO production. Supplemental L-arginine produced a 9% decrease in mean pulmonary arterial pressure (53 +/- 4 to 48 +/- 4 mm Hg, p < 0.05) and a 16% decrease in pulmonary vascular resistance (14.8 +/- 1.5 to 12.4 +/- 1.4 Wood units, p < 0.05). L-arginine modestly decreased mean systemic arterial pressure (92 +/- 4 to 87 +/- 3 mm Hg, p < 0.05). A 1-wk supplementation of L-arginine resulted in a slight increase in peak V O(2) (831 +/- 88 to 896 +/- 92 ml/min, p < 0.05) and a significant decrease in the V E- V CO(2) slope (43 +/- 4 to 37 +/- 3, p < 0.05) without significant systemic hypotension. Hemodynamics and exercise capacity remained unchanged during placebo administration. These results suggest that oral supplementation of L-arginine may have beneficial effects on hemodynamics and exercise capacity in patients with precapillary pulmonary hypertension.

Administration, Oral↗

Effects of pentoxifylline on pulmonary hemodynamics during acute hypoxia in anesthetized dogs.

The effects of pentoxifylline on pulmonary hemodynamics were studied in anesthetized dogs during acute alveolar hypoxia. In Series A, 7 dogs received pentoxifylline orally (18 mg/kg/day) for 11 wk and 7 untreated dogs served as control animals. During anesthesia and controlled ventilation, acute alveolar hypoxia was induced (10 to 13% inspired O2) and pulmonary and systemic hemodynamic and blood rheologic measurements were compared with normoxia. In control dogs, cardiac index did not change during hypoxia, but pulmonary vascular resistance index (PVRI) increased 79%, erythrocyte filterability decreased significantly (p less than 0.05), and relative viscosity of blood corrected for hematocrit did not change. In the pentoxifylline-treated dogs, cardiac index increased 28% and PVRI increased only 20%; in contrast to the control dogs, relative viscosity of blood was decreased by 18% and no significant changes in filterability were observed. The increase in PVRI in relation to the drop in arterial O2 saturation was significantly larger (p less than 0.05) in the control dogs. Pentoxifylline also increased P50 by 2.8 mm Hg (p less than 0.05). In Series B, hemodynamic measurements were made during variations in blood flow (induced by restricting venous return) in 3 treated (26 mg/kg/day for 3 wk) and 3 control dogs. In these experiments, pulmonary artery pressure was significantly lower at comparable flows during both normoxia and hypoxia. In both studies, the hemodynamic effects of the drug on the systemic circulation were less than on the pulmonary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Pulmonary function before and sequentially after valve replacement surgery with correlation to preoperative hemodynamic data.

Hemodynamic results after valve replacement surgery are well documented, but there are few follow-up studies on pulmonary function. Pulmonary function and hemodynamic studies were made, preoperatively, in 149 patients with predominant, mitral, aortic or combined mitral and aortic stenosis. A sequential postoperative follow-up of the pulmonary function was performed on 88 patients for as long as 125 wk after valve replacement. All patients had reduced preoperative values for forced vital capacity (FVC), single-breath carbon monoxide diffusing capacity (DLCO), forced expiratory volume in one second, peak expiratory flow rate, and maximal flow after exhalation of 75, 50, and 25% of FVC, and increased total airway resistance, resistance during expiration, and residual volume. The aortic group tended toward more normal values. There was significant correlation between the pulmonary function parameters and the hemodynamic data. In the early postoperative period (10 wk), deterioration of pulmonary function was significant in the aortic group and variable in the mitral and the combined groups; these responses correlated with preoperative hemodynamic and pulmonary function status. Between 10 to 125 wk, all patients showed progressive improvement, especially among those in the mitral group. Patients who died during or soon after mitral valve replacement were found to have significantly lower FVC and DLCO and significantly higher peripheral vascular resistance and cardiothoracic ratio. It is concluded that deterioration in pulmonary function is correlated to severity of cardiac dysfunction, and is reversible late after surgery, except in very advanced cases that have poor prognosis.

Adolescent↗

Effects of hematocrit on renal hemodynamics and sodium excretion in hydropenic and volume-expanded dogs.

The effects of hematocrit on renal hemodynamics and sodium excretion were studied in anesthetized dogs during both hydropenia and volume expansion. The hematocrit was decreased by isovolemic exchange with the animal's own previously harvested plasma and increased by isovolemic exchange with fresh, washed red blood cells. Renal perfusion pressure was maintained constant throughout the experiments by the adjustment of a suprarenal aortic clamp. During hydropenia, a decrease in hematocrit was associated with an increase in sodium and potassium excretion and solutefree water reabsorption. These changes were accompained by an increase in renal plasma flow and renal blood flow and a decrease in renal vascular resistance. Glomerular filtration rate was unchanged and filtration fraction was significantly decreased as hematocrit was lowered. Increasing hematocrit during hydropenia had the opposite effects on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics. In another group of animals, hematocrit was lowered during volume expansion with either saline or plasma, then returned to the control level by isovolemic exchange with washed red blood cells. This increase in hematocrit during volume expansion had a similar effect on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics as during hydropenia. These results therefore suggest that acute changes in hematocrit may significantly affect sodium excretion and renal hemodynamics during both hydropenia and volume expansion. The changes in solute-free water reabsorption and potassium excretion suggest that the alterations in hematocrit may affect primarily the reabsorption of sodium in the proximal tubule. The concommitant effects of hematocrit on renal vascular resistance and filtration fraction may mediate this change in sodium reabsorption by altering hydrostatic and oncotic pressures in the peritubular circulation.

Animals↗

Hemodynamic sequelae of regression of experimental atherosclerosis.

Regression of experimental atherosclerosis is characterized by decreased intimal thickness and luminal enlargement, but intimal fibrosis becomes more dense. We tested the hypothesis that fibrosis of arteries during regression might limit vasodilator capacity and restrict hemodynamic improvement despite luminal improvement. We studied limb, coronary, and cerebral hemodynamics in 11 normal cynomolgus monkeys, 10 monkeys given an atherogenic diet for 20 mo and 8 monkeys given a regression diet for an additional 18 mo. The atherogenic diet induced lesions of moderate severity (50-60% stenosis); owing to characteristic vessel growth during the atherogenic period, luminal size did not decrease correspondingly. Regression monkeys showed typical changes of regression with luminal enlargement but increased fibrosis. The iliac artery was perfused at constant blood flow and maximal vasodilatation was produced with papaverine. Blood flow was measured with microspheres during maximal vasodilatation in the coronary bed (adenosine) and cerebral bed (hypercapnia). In normal monkeys, minimal vascular resistances were 1.95 +/- 0.19 mm Hg/ml/min X 100 g (mean +/- SE) (limb), 0.13 +/- 0.01 (coronary), and 0.44 +/- 0.02 (cerebral). In atherosclerotic monkeys minimal resistance increased (P less than 0.05) 108, 62, and 166% in the limb, coronary, and cerebral beds, respectively. In regression monkeys, minimal resistance increased from values found in atherosclerotic animals in the limb (+22%), decreased inconsistently in the coronary bed (-19%), and decreased significantly in the cerebral bed (-44%, P less than 0.05). Thus morphologic regression was accompanied by significant hemodynamic improvement during maximal dilatation only in cerebral vessels. We conclude that increases in luminal size during regression of atherosclerotic lesions may not be associated with increases in vasodilator capacity, as intimal fibrosis may limit physiologically important hemodynamic improvement.

Animals↗

Hemodynamic regulation of myosin heavy chain gene expression. Studies in the transplanted rat heart.

Cardiac work is a major determinant of heart size and growth. Heterotopic cardiac isografts are hemodynamically unloaded and undergo atrophy. To determine the molecular changes that occur as a result of hemodynamic unloading, we have studied the rate of synthesis of total cardiac proteins and myosin heavy chain (MHC) and the expression of the myosin heavy chain gene as reflected in the messenger RNA levels for alpha- and beta-MHC isoforms. 72 h after transplantation there is a significant decrease in left ventricular size accompanied by a 27% decrease in the rate of total cardiac protein synthesis and a 53% decrease in the rate of myosin heavy chain synthesis. In contrast to isografts 14 d after transplantation which have a decrease in protein synthetic capacity, simultaneous measurements of 18S ribosomal RNA and myosin messenger RNA suggest that after 3 d the decrease in synthesis is due to a change in the efficiency of protein translation. While the working in situ heart expresses primarily alpha-MHC mRNA (97%) hemodynamic unloading leads to a 43% decrease in alpha-MHC mRNA concentration and the de novo expression of the beta-MHC mRNA. Total MHC mRNA (alpha plus beta) concentration analyzed by a quantitative S1 nuclease protection assay was similar in the two groups of hearts. Thus, in association with hemodynamic unloading there are changes in cardiac myosin heavy chain content as a result of both gene transcription and protein translation mechanisms.

Animals↗

Leukotriene D4 is a mediator of proteinuria and glomerular hemodynamic abnormalities in passive Heymann nephritis.

We assessed the role of leukotrienes (LTs) in Munich-Wistar rats with passive Heymann nephritis (PHN), an animal model of human membranous nephropathy. 10 d after injection of anti-Fx1A antibody, urinary protein excretion rate (Upr) in PHN was significantly higher than that of control. Micropuncture studies demonstrated reduced single nephron plasma flow and glomerular filtration rates, increased transcapillary hydraulic pressure difference, pre- and postglomerular resistances, and decreased ultrafiltration coefficient in PHN rats. Glomerular LTB4 generation from PHN rats was increased. Administration of the 5-LO activating protein inhibitor MK886 for 10 d markedly blunted proteinuria and normalized glomerular hemodynamic abnormalities in PHN rats. An LTD4 receptor antagonist SK&F 104353 led to an immediate reduction in Upr and to reversal of glomerular hemodynamic impairment. Ia(+) cells/glomerulus were increased in PHN rats. In x-irradiated PHN rats, which developed glomerular macrophage depletion, augmented glomerular LT synthesis was abolished. Thus, in the autologous phase of PHN, LTD4 mediates glomerular hemodynamic abnormalities and a hemodynamic component of the accompanying proteinuria. The synthesis of LTD4 likely occurs directly from macrophages or from macrophage-derived LTA4, through LTC4 synthase in glomerular cells.

Animals↗

Effects of anesthetic technique on the hemodynamic response to microlaryngeal surgery.

Our aim was to study the attenuation of the hemodynamic response to microlaryngeal surgery by beta-blocking agents used as support drugs to the anesthetic technique. The study was carried out in 30 patients randomly allocated to one of three groups. The control group received only anesthetic drugs. The second group received labetalol hydrochloride 0.3 mg/kg 3 minutes before induction and 0.15 mg/ kg 2 minutes prior to the start of suspension of the larynx. The third group received esmolol hydrochloride 500 micrograms/kg 3 minutes prior to induction and a continuous infusion of 300 micrograms/kg during the surgical procedure. Hemodynamic data in the three groups were compared by analysis of variance. A statistically significant difference (p < .05) was found in hemodynamic data among the two groups treated with blocking agents and the control group. The addition of beta-blocking agents to the anesthetic technique attenuates the hemodynamic response to suspension laryngoscopy.

Adrenergic alpha-Antagonists↗

Inhaled nitric oxide improves hemodynamics in patients with acute pulmonary hypertension after high-risk cardiac surgery.

Severe pulmonary hypertension and right-sided circulatory failure (RSCF) represent an increasing cause of morbidity and mortality in patients undergoing high-risk cardiac surgery. Increased pulmonary vascular resistance in the setting of cardiopulmonary bypass (CPB) may further lead to decrease blood flow across the pulmonary vascular bed; thereby decreasing left ventricular filling and cardiac output. Current management techniques for RSCF include both nonspecific vasodilator and inotropic agents (often limited by systemic hypotension) and the placement of right ventricular assist devices (associated with increased perioperative morbidity). Inhaled nitric oxide (NOi) represents a novel, specific pulmonary vasodilator that has been proven efficacious in these clinical settings. We evaluated 34 patients in 38 operations who underwent cardiac surgery at Columbia Presbyterian Medical Center, and who received NOi (20 ppm) through a modified ventilatory circuit for hemodynamically significant elevations in pulmonary vascular resistance. Nine patients underwent cardiac transplantation, three patients bilateral lung transplantation, 16 patients left ventricular assist device placement and 10 patients routine cardiac surgery. Patients receiving NOi exhibited substantial reductions in mean pulmonary artery pressure (mPAP) (34.6 +/- 2.0 to 26.0 +/- 1.7 mmHg, p < 0.0001), with improvements in systemic hemodynamics, mean arterial pressure (68 +/- 3.1 to 75.9 +/- 2.0 mmHg, p = 0.006). In five cases, patients could not be weaned from CPB until NOi was administered. Patients were maintained on NOi from 6 to 240 h postoperatively (median duration 36 h). Inhaled NO induces substantial reductions in mPAP and increases in both cardiac index and systemic blood pressure in patients displaying elevated pulmonary hemodynamics after high-risk cardiac surgery. NO is, therefore, a useful adjunct in these patients in whom acute pulmonary hypertension threatens right ventricular function and hemodynamic stability.

Acute Disease↗

Transcranial Doppler in asymptomatic carotid stenosis representing hemodynamic impairment: correlation study with magnetic resonance imaging.

BACKGROUND AND PURPOSE: Since the benefit of an endarterectomy in an asymptomatic carotid stenosis is not as clear as that in symptomatic stenosis, identifying patients with a high risk of stroke will allow the improved selection of surgical candidates. To evaluate the role of transcranial Doppler (TCD) in assessing an asymptomatic stenosis, this study examined the association of a TCD-detected hemodynamic change with a stenosis-related abnormality on magnetic resonance imaging (MRI). METHODS: Asymptomatic patients with a more than 60% internal carotid artery stenosis were enrolled in this study. The hemodynamic change in the TCD was analyzed in terms of the demographic characteristics, the stroke risk factors, and the stenosis-related MRI abnormalities that are a proven risk factor of a further stroke. RESULTS: Fifty-three patients were retrospectively recruited. While there were no differences in the demographic characteristics or frequency of the stroke risk factors, the proportion of patients with stenosis-related MRI abnormality was significantly higher in patients with a hemodynamic change on TCD (13/19 vs 6/34, P < .01; odds ratio = 10.11; 95% confidence interval = 2.73-37.4). CONCLUSIONS: The TCD-detected hemodynamic changes may provide useful information for assessing the frequency of silent stroke in patients with an asymptomatic carotid stenosis.

Aged↗

The role of the pulmonary afferent receptors in producing hemodynamic changes during hyperinflation and endotracheal suctioning in an oleic acid-injured animal model of acute respiratory failure.

The purpose of this study was to examine the role of the pulmonary afferent receptors in producing hemodynamic changes during hyperinflation and endotracheal suctioning (ETS) in an oleic acid-injured animal model of acute respiratory failure. Previous investigations of hyperinflation as a method to prevent hypoxia-induced sequelae of ETS have demonstrated unrecognized hemodynamic consequences. In this within-subject, repeated-measures study, instrumented, oleic acid-injured dogs had continuous measurements of heart rate (HR), mean aortic blood pressure (MAP), left ventricular pressure (Plv), pulmonary artery pressure (Ppa), right ventricular afterload (Ppa(tm)), right atrial pressure (Pra), and right ventricular filling pressure (Pra(tm)) during hyperinflation and ETS when the vagi were intact and after the pulmonary branches of the vagus nerves had been severed. After severing the vagi, MAP and Plv were decreased and HR and Ppa were increased. With the vagi severed, there was less variation in MAP and Ppa but increased variation in HR. These findings suggest that vagally mediated reflexes from the lungs produce some, but not all, of the hemodynamic effects associated with hyperinflation and ETS. Continued research is necessary to discover a method of hyperoxygenation and suctioning that does not produce potentially harmful hemodynamic effects.

Afferent Pathways↗

Heart rate variability and hemodynamic alterations in canines with normal cardiac function during exposure to pressure support, continuous positive airway pressure, and a combination of pressure support and continuous positive airway pressure.

Variations in intrathoracic pressure generated by different ventilator weaning modes may significantly affect intrathoracic hemodynamics and cardiovascular stability. Although several investigators have attributed cardiovascular alterations during ventilator weaning to augmented sympathetic tone, there is limited investigation of changes in autonomic tone during ventilator weaning. Heart rate variability (HRV), the analysis of beat-to-beat changes in heart rate, is a noninvasive indicator of autonomic tone that might be useful in the identification of patients who are at risk for weaning difficulty due to underlying cardiac dysfunction. The authors describe HRV and hemodynamics in response to 3 ventilatory conditions: pressure support (PS) 10 cmH2O, continuous positive airway pressure (CPAP) 10 cmH2O, and a combination of PS 10 cmH2O and CPAP 10 cmH2O (PS + CPAP) in a group of canines with normal ventricular function. Six canines were studied in the laboratory. Continuous 3-lead electrocardiographic data were collected during baseline (controlled mechanical ventilation) and following transition to each of the ventilatory conditions (PS, CPAP, PS + CPAP) for analysis of HRV. HRV was evaluated using power spectral analysis to define the power under the curve in a very low frequency range (0.0033 to < 0.04 Hz, sympathetic tone), a low frequency range (0.04 to < 0.15 Hz, primarily sympathetic tone), and a high frequency range (0.15 to < 0.40 Hz, parasympathetic tone). A thermodilution pulmonary artery catheter measured cardiac output and right ventricular end-diastolic volume to describe global hemodynamics. There were significant increases in very low frequency power (sympathetic tone) with a concomitant significant reduction in high-frequency power (parasympathetic tone) with exposure to PS + CPAP. These alterations in HRV were associated with significantly increased heart rate and reduced right ventricular end-diastolic volume. Although there was a small but significant increase in cardiac output with exposure to PS, HRV was unchanged. These data indicate that there was a relative shift in autonomic balance to increased sympathetic and decreased parasympathetic tone with exposure to PS + CPAP. The increase in intrathoracic pressure reduced right ventricular end-diastolic volume (preload). This hemodynamic alteration generated a change in autonomic tone, so that cardiac output could be maintained. Individuals with autonomic and/or cardiovascular dysfunction may not be capable of this type of response and may fail to successfully wean from mechanical ventilation.

Analysis of Variance↗

Saphenofemoral junction ligation supplemented by postoperative sclerotherapy: a review of long-term clinical and hemodynamic results.

This review article summarizes information found in the literature concerning long-term results following high ligation supplemented in the postoperative period by sclerotherapy. Subjective complaints, recurrent reflux, and recurrent varicose vein rates as well as changes in venous hemodynamics are reviewed and compared with results after high ligation and stripping. The fate of the greater saphenous vein trunk after high ligation, the question whether it could actually be used as a graft in arterial and coronary artery reconstructions, and the relevance of saphenous vein saving surgery are discussed. The trunk of the greater saphenous vein, when incompetent preoperatively, continues to be patent and incompetent after surgery in most cases. It is not diffusely degenerated and could be used as an arterial substitute. However, ligation of the saphenofemoral junction alone provokes a higher recurrence rate in comparison with high ligation and stripping. The excellent hemodynamic improvement achieved immediately after high ligation deteriorates progressively during the follow-up owing to recurrent reflux. Sclerotherapy can compensate this undesirable feature, because it is itself capable of reducing or even abolishing reflux and improving venous hemodynamics, although only transitorily, but repeated sclerosing injections can restore improvement at any time, if necessary, during the follow-up period. The improvement of venous hemodynamics and subjective symptoms achieved with the combined procedure (high ligation plus sclerotherapy) is comparable with that after high ligation and stripping.

Femoral Vein↗

Renal hemodynamic effects of relaxin in humans.

Rat studies have convincingly demonstrated the essential role of the ovarian hormone relaxin in mediating gestational renal hemodynamic and osmoregulatory changes in that species. We describe a model in nonpregnant volunteers using exogenous hCG to stimulate the production and release of ovarian relaxin in order to assess renal hemodynamic responses. Women (n = 10) were serially studied +/- hCG stimulation during menstrual cycles with measurement of inulin, PAH, and neutral dextran clearances (to determine glomerular filtration rate [GFR], renal plasma flow [RPF], and glomerular porosity, respectively). Controls were women without ovarian function (n = 6) and men (n = 10). GFR and RPF were increased in the luteal phase compared to the follicular phase (15.3% increase in GFR, P < 0.005; 17.8% increase in RPF, P < 0.05). In controls, GFR and RPF were not significantly different between study occasions. Although exogenous hCG did not stimulate relaxin secretion in women without ovarian function or in men, it did so in normal women, but not into the pregnancy range. In no group were renal hemodynamics augmented by administered hCG. In naturally occurring cycles, increased serum relaxin is associated with augmented renal hemodynamics. As luteal stimulation with hCG failed to yield pregnancy relaxin levels, the use of exogenous relaxin for human administration is needed to further elucidate the renal vasodilatory properties of relaxin.

Adolescent↗

Effect of atrial natriuretic peptide on hemodynamics of the stage 21 chick embryo.

Atrial natriuretic peptide (ANP) is important in the modulation of hemodynamics and fluid balance in the mature subject, but its hemodynamic effects at early stages of morphogenesis are not defined. We studied the effect of rat atriopeptin III on hemodynamics in chick embryos at Hamburger-Hamilton stage 21. The cardiovascular system is not yet innervated, nor is the kidney formed in these embryos. The vitelline arterial and venous blood pressures were measured with a servo-null, micro-pressure system and the dorsal aortic blood flow was measured with a 20 MHz pulsed Doppler velocity meter. The peptide was infused into the vitelline vein with a microinjector at doses of 0.1, 1.0, and 10 ng. Doses normalized by body wt of embryos averaged 0.003, 0.035, and 0.32 ng/mg (n = 61), respectively. Vitelline arterial blood pressure decreased in a dose dependent manner [y = 55.8 - 9.9x; r = -0.49; p less than 0.01 (y = % of baseline, x = log ng/mg)], and dorsal aortic blood flow, a measure of cardiac output, decreased similarly (y = 39.6 - 16.2x; r = -0.47; p less than 0.01). Heart rate did not change. Ten ng of ANP increased the vitelline venous diameter, determined directly under a microscope, from 125 +/- 47 (SD) microns to 139 +/- 49 microns (n = 11; p less than 0.01), and decreased vitelline venous pressure from 0.34 +/- 0.05 mm Hg to 0.10 +/- 0.07 mm Hg (n = 5). We conclude that ANP exerts its hemodynamic effect by direct venodilation in the noninnervated and anephric circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pancuronium does not alter the hemodynamic status of piglets after normoxia or hypoxia.

Pancuronium is a neuromuscular blocking agent commonly used to eliminate agitation in sick newborn infants requiring mechanical ventilation. Experimental data supporting this method of intervention are controversial, and hemodynamic studies in newborn infants report conflicting results. This study was designed to determine the hemodynamic effects of pancuronium administered under conditions of normoxia, hypoxia, and preexposure to hypoxia in neonatal piglets with normal lungs. After baseline hemodynamic and blood gas measurements were obtained, pancuronium was administered in two i.v. bolus injections of 0.1 mg/kg. Tidal volume and minute ventilation were maintained constant during the experimental procedure by adjusting ventilator settings. Twenty min after pancuronium, no changes from baseline values were found in arterial blood gases, heart rate, cardiac output, mean arterial pressure, systemic vascular resistance, pulmonary artery pressure, pulmonary vascular resistance, central venous pressure, or pulmonary capillary wedge pressure in any of the three conditions studied. In conclusion, pancuronium administered during normoxia, hypoxia, or after preexposure to hypoxia while controlled ventilation is maintained does not alter systemic or pulmonary hemodynamic status of the newborn piglet.

Animals↗