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At least 1,135 records · Page 63Linked to original sources
PubMed1996

Lorazepam and midazolam in the intensive care unit: a randomized, prospective, multicenter study of hemodynamics, oxygen transport, efficacy, and cost.

OBJECTIVES: To evaluate and compare the clinical efficacy, impact on hemodynamic and oxygen transport variables, safety profiles, and cost efficiency of sedation and anxiolysis with lorazepam vs. continuous infusion of midazolam in critically ill, intensive care unit patients. DESIGN: Multicenter, prospective, randomized, open-label study. SETTING: Teaching hospitals. PATIENTS: Ninety-five critically ill, mechanically ventilated patients with fiberoptic pulmonary artery catheters in place were randomly assigned to receive short-term (8 hrs) sedation with either intermittent intravenous injection lorazepam (group A, n = 50) or continuous intravenous infusion midazolam (group B, n = 45) titrated to clinical response. MEASUREMENTS AND MAIN RESULTS: The severity of illness, demographic characteristics, levels of anxiety and agitation, hemodynamic parameters, oxygen transport variables, quality of sedation, nursing acceptance, and laboratory chemistries reflecting drug safety were recorded. There were no significant differences with regard to demographic data, hemodynamic and oxygen transport variables, or levels of anxiety/agitation between the two groups at baseline, 5 mins, 30 mins, and 4 and 8 hrs after administration of sedation. There were no significant differences in the quality of sedation or anxiolysis. Midazolam-treated patients used significantly larger amounts of drug for similar levels of sedation and anxiolysis (14.4 +/- 1.2 mg/8 hrs vs. 1.6 +/- 0.1 mg/8 hrs, p = .001). Both drugs were safely administered and patient and nurse satisfaction was similar. CONCLUSIONS: Sedation and anxiolysis with lorazepam and midazolam in critically ill patients is safe and clinically effective. Hemodynamic and oxygen transport variables are similarly affected by both drugs. The dose of midazolam required for sedation is much larger than the dose of lorazepam required for sedation, and midazolam is therefore less cost-efficient.

Adolescent↗
PubMed1996

Evaluation of the effects of autotransfusion of unprocessed blood on hemodynamics and oxygen transport in anesthetized pigs.

OBJECTIVE: To examine the hemodynamic effects and the oxygen transport pattern of autotransfusion of unprocessed blood on hemodynamics and oxygen transportation. DESIGN: Prospective, observational study. SETTING: Research laboratory of a university medical center. SUBJECTS: Six healthy, domestic pigs (20 - 33 kg). INTERVENTIONS: A left thoracotomy was performed and a 5-mm incision was created in the descending aorta, resulting in a controlled hemorrhage of 30 mL/kg (approximately 40% of blood volume) into the thoracic cavity over a 45-min time period. During that period, mean arterial pressure (MAP) was maintained slightly > 50 mm Hg, using intravenous lactated Ringers' solution. The blood sample was collected from the open thorax with compresses soaked in citric acid solution and then extracted by manual squeezing, filtered through several layers of gauzes, and stored in glass bottles. Repeat measurements were performed after hemorrhage, after retransfusion of the harvested blood, and thereafter every 15 mins up to 60 mins. The animals were supported for 2 more hrs and were observed for the following 48 hrs. MEASUREMENTS AND MAIN RESULTS: All animals survived and were in good condition 48 hrs after the experimental hemorrhage. The circulatory and oxygen transport response at the end of hemorrhage and concomitant maintenance of blood pressure at > 50 mm Hg resulted in: significant reductions of cardiac index, MAP, and oxygen transport (DO2) (46%, 50%, and 64% reductions, respectively, p < .01, in an increase of heart rate (HR) (+21%, not significant), pulmonary vascular resistance index (+112%, p < .05), and oxygen extraction (+105%, p < .01), as well as in a nonsignificant decrease of systemic vascular resistance index (-8%). After autotransfusion, the basic hemodynamic variables, MAP and HR were corrected, remaining near baseline (not significant) afterward. Cardiac index and DO2 increased after autotransfusion, but remained below the baseline until the end of the study protocol (p < .05). A significant increase was noticed for pulmonary arterial pressure and pulmonary vascular resistance index immediately after autotransfusion (p < .01). These values were corrected in part after 15 to 30 mins, but remained higher throughout the observaton period compared with baseline (29.5% and 89.8%, respectively, p < .05). The recently introduced relationship between cardiac index and oxygen extraction has been proposed to avoid problems of mathematical coupling between oxygen consumption and DO2 measurements. This relationship followed a similar course in all experiments throughout each phase. A shift downward and to the right represented the endpoint of the hemorrhagic phase. After autotransfusion, a shift toward baseline was noticed. Prothrombin time and partial thromboplastin time remained unchanged after autotransfusion. Free hemoglobin concentrations increased immediately after autotransfusion (+33%, p < .05), but returned to baseline values 48 hrs later. Histologic examination showed no changes in the examined organs. CONCLUSIONS: Reinfusion of large amounts of unprocessed blood (up to 40% of blood volume), collected with compresses from a noncontaminated surgical field is a cheap method, which may be of potential benefit in trauma patients, when more sophisticated autotransfusion devices are lacking. In the present study, this method resulted in transient but significant hemodynamic changes in the pulmonary circulation. Impairment of oxygen transport was noticed after the end of hemorrhage, but this impairment cannot be attributed to the autotransfusion technique alone, but also to factors such as hemorrhagic shock, surgical trauma, etc.

Animals↗
PubMed1996

Hormonal and hemodynamic changes in a validated animal model of brain death.

OBJECTIVE: To examine the hormonal and hemodynamic changes in a validated animal model of brain death. DESIGN: Prospective, controlled study. SETTING: Experimental research laboratory. SUBJECTS: Adult male mongrel dogs (n = 10). INTERVENTIONS: Brain death was induced by inflation of a subdural balloon in ten mongrel dogs weighing 23 to 30 kg and validated neuropathologically. The hearts were instrumented with micromanometers and ultrasonic flow probes to measure cardiovascular changes. No inotropic or vasoactive support was given. Hemodynamic stability was maintained with intravenous fluids. Blood samples and hemodynamic readings were collected before and after the induction of brain death. MEASUREMENTS AND MAIN RESULTS: A Cushing reflex, followed by a hyperdynamic response and diabetes insipidus, occurred in every animal following brain death. Mean arterial pressure, heart rate, contractility, and cardiac output increased to > 350 mm Hg, 230 beats/min, 4200 mm Hg/sec, and 2.8 L/min, respectively, at the peak of this phenomenon before returning to baseline. A plasma catecholamine surge was observed in every animal 15 mins after brain death, while the circulating concentrations of the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 mins of brain death, respectively, and continued to decrease throughout the experiments. Circulating triiodothyronine, thyroxine, and glucagon concentrations decreased significantly (p < .01) from 0.58 +/- 0.05 ng/mL, 2.20 +/- 0.15 micrograms/dL, and 49.7 +/- 9.1 pg/mL, respectively, to 0.34 +/- 0.03 ng/mL, 1.14 +/- 1.14 micrograms/dL, and 6.9 +/- 1.4 pg/mL, respectively, 420 mins after brain death. The hematocrit increased significantly 15 mins after brain death and then gradually decreased throughout the duration of the experiments. CONCLUSIONS: In a validated animal model of brain death, significant decreases in the circulating concentrations of stress hormones, as well as hemodynamic instability, occurred after brain death. Measurements of plasma adrenocorticotrophic hormone and vasopressin values may be useful as diagnostic predictors of brain death. Furthermore, the observed changes may contribute to organ dysfunction after brain death and may necessitate hormonal as well as inotropic and vasoactive support to maintain donor organ function in the clinical setting.

Adrenocorticotropic Hormone↗
PubMed1999

Gas exchange and hemodynamics in experimental pleural effusion.

OBJECTIVE: To investigate the cardiorespiratory effects of graded bilateral pleural effusions in the anesthetized pig. DESIGN: Prospective, randomized, controlled, laboratory study. SETTING: Animal laboratory. SUBJECTS: Eleven male Yorkshire pigs. INTERVENTIONS: Animals were anesthetized using inhaled isoflurane. Orotracheal intubation was followed by mechanical ventilation. Bilateral chest tubes were inserted, and graded increasing pleural effusions were created using saline of 0, 20, 40, and 80 mL/kg, divided equally between each side. At each pleural volume, intravascular volume was randomly altered (by phlebotomy or transfusion of colloid) to normal (unchanged), low (decreased by 10 mL/kg), or high (increased by 10 mL/kg). MEASUREMENTS AND MAIN RESULTS: Hemodynamic parameters, intrapleural pressures, hemoglobin, and blood gases were measured. At the lowest volume of pleural fluid, PaO2 was reduced by approximately 50% vs. baseline, whereas systemic hemodynamics were unchanged. PaO2 was reduced in a dose-dependent fashion as pleural volume increased but was not affected by alterations in intravascular volume. Intrapulmonary shunt was increased both by intrapleural volume in a dose-dependent fashion and by increases in intravascular volume at high levels of pleural volume. Cardiac output and systemic mean arterial pressure increased with elevated intravascular volume but were not influenced by lower levels of intrapleural volume. Mean pulmonary arterial pressure, central venous pressure, and pulmonary artery occlusion pressure were increased by elevations in both intrapleural volume and intravascular volume. Intrapleural pressure and pulmonary vascular resistance were related to intrapleural volume only. CONCLUSIONS: Hypoxemia occurs as an early event in acute bilateral pleural effusions and precedes hemodynamic decompensation. Oxygenation is independent of intravascular filling pressures, but hemodynamics are preserved with elevated filling pressures. Clinical studies should be undertaken to examine the risks/benefits of careful removal of pleural fluid in patients with pleural effusions, when oxygenation is impaired during mechanical ventilation.

Anesthesia, Inhalation↗
PubMed2000

Effect of acute moderate changes in PaCO2 on global hemodynamics and gastric perfusion.

OBJECTIVE: To describe global hemodynamics and splanchnic perfusion changes in response to acute modifications in Paco2 in hemodynamically stable patients. DESIGN: Prospective, randomized crossover study. SETTING: Medical-surgical intensive care unit at a community hospital (400,000 inhabitants). PATIENTS: Ten critically ill patients who were sedated, paralyzed, and mechanically ventilated. INTERVENTIONS: Hypercapnia and hypocapnia were obtained by increasing and reducing instrumental deadspace in random order. After each intervention, patients returned to the basal condition. Each period lasted 80 min: 20 min to achieve stable Paco2 and 60 min for tonometer equilibration. In each period, global hemodynamic variables and tonometric data were collected. The periods were compared using analysis of variance. MEASUREMENTS AND MAIN RESULTS: Acute hypercapnia (Paco2 from 40+/-3 to 52+/-3 torr, p<.05) increased cardiac index (3.43+/-0.37 vs. 3.97+/-0.43 mL/min/m2, p<.05), heart rate (95+/-6 vs. 105+/-3 beats/min, p<.05), and mean pulmonary artery pressure (21+/-1 vs. 24+/-1 mm Hg, p<.05) and reduced systemic vascular resistance (992+/-98 vs. 813+/-93 dyne x sec/ cm5, p<.05) and oxygen extraction ratio (27+/-3% vs. 22+/-2%, p<.05). Standardized intramucosal Pco2 increased from 49+/-2 to 61+/-3 torr (p<.05) with an associated decrease in calculated intramucosal pH ([pHi] 7.35+/-0.03 vs. 7.25+/-0.02, p<.05), but the gastro-arterial Pco2 gradient (deltaPco2) did not change. Acute hypocapnia (Paco2 from 41+/-3 to 34+/-3 torr, p<.05; pH 7.41+/-0.01 to 7.47+/-0.02, p<.05) induced slight increments in systemic vascular resistance (995+/-117 vs. 1088 +/- 160 dyne x sec/cm5, p<.05) and oxygen extraction ratio (28+/-2% vs. 30+/-2%, p<.05). Standardized intramucosal Pco2 decreased (50+/-4 vs. 44+/-3 torr, p<.05), pHi increased (7.33+/-0.03 vs. 7.36+/-0.02; p<.05), but deltaPco2 did not change. CONCLUSIONS: In this small group of stable patients, moderate acute variations in Paco2 had a significant effect on global hemodynamics, but splanchnic perfusion, assessed by deltaPco2, did not change. In these conditions, the use of pHi to evaluate gastric perfusion appears unreliable.

Acute Disease↗
PubMed2000

Systemic hemodynamics, gastric intramucosal PCO2 changes, and outcome in critically ill burn patients.

OBJECTIVES: To define the hemodynamic and gastric intramucosal PCO2 (PiCO2) changes during the first 48 hrs after burn trauma and to analyze their relationship with outcome. DESIGN: Prospective, observational study in a cohort of consecutively admitted critically ill burn patients. SETTING: Intensive care burn unit in a university hospital. PATIENTS: Forty-two patients with burns covering >20% of body surface area or inhalation injury. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients were monitored with an oximetric pulmonary arterial catheter and a gastric tonometer to measure PiCO2. The difference between arterial and gastric mucosal PCO2 (P[i-a]CO2) was considered indicative of gastric mucosal hypoxia. Hemodynamic and PiCO2 measurements were performed during the first 48 hrs after admission. Patients suffered burns covering 36.1% +/- 14.3% (mean +/- SD) and 45.3% +/- 21.9% of body surface area (survivors and nonsurvivors, respectively). All patients were successfully resuscitated by conventional standards. Nonsurvivors (n = 16) died a median of 17 days after admission. In univariate analysis, the presence of shock during the resuscitation phase, age, mixed venous pH, P[i-a]CO2, right atrial pressure, pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, systemic and pulmonary vascular resistance, left ventricular stroke work index, mixed venous oxygen saturation, and systemic oxygen delivery, consumption, and extraction ratio, measured over the first 12 hrs after admission, were significantly (p < .05) different between survivors and nonsurvivors. These differences disappeared after 12 hrs after admission. Multivariate analysis identified age, percentage body surface area burned, and oxygen delivery index (6 hrs after admission) as factors independently associated with a poor outcome. P[i-a]CO2 (12 hrs after admission) was significantly greater in patients with than in those without inhalation injury (17 +/- 13 torr [2.26 +/- 1.73 kPa] vs. 6 +/- 10 torr [0.79 +/- 1.33 kPa]; p = .005). Patients with a P[i-a]CO2 difference (6 hrs after admission) > or =10 torr (1.33 kPa) had a mortality rate of 56% vs. 25% of those patients with <10 torr (p = .044). CONCLUSIONS: Our data indicate that there are hemodynamic and biochemical changes that occur early after burn trauma that are associated with prognosis after an apparently successful resuscitation. Particularly, a hemodynamic profile characterized by systemic acidosis, low systemic blood flow, and systemic and pulmonary vasoconstriction early after trauma is associated with a poor outcome. Additionally, intestinal mucosal acidosis occurs after burn trauma, is influenced by inhalation injury, and is a variable related to outcome.

Adolescent↗
PubMed2000

Effects of positive end-expiratory pressure on hemodynamics and indocyanine green kinetics in patients after orthotopic liver transplantation.

OBJECTIVE: To determine the impact of positive end-expiratory pressure (PEEP) ventilation on hemodynamics and a clinical test for assessment of dynamic liver performance in patients undergoing orthotopic liver transplantation (OLT). DESIGN: Prospective, descriptive patient study. SETTING: University hospital intensive care unit. PATIENTS: A total of 25 patients after OLT. INTERVENTIONS: All patients were intubated and mechanically ventilated with biphasic positive airway pressure. The effects of three different randomly chosen levels of PEEP (0 cm H2O, 5 cm H2O, and 10 cm H2O) were studied in the immediate postoperative period. MEASUREMENTS AND MAIN RESULTS: Systemic hemodynamics, arterial and venous blood gas analyses, and plasma disappearance rate of indocyanine green (ICG(PDR)), using the transpulmonary indicator dilution technique, were obtained simultaneously. For data evaluation, patients were grouped retrospectively according to their hemodynamic response to PEEP (Group A and Group B). In Group A (n = 13), PEEP did not alter cardiac index. In Group B (n = 11), PEEP levels of 5 cm H2O and 10 cm H2O significantly reduced cardiac index and oxygen delivery. ICG(PDR) remained statistically unchanged in both groups. CONCLUSIONS: Short-term pressure-controlled ventilation with PEEP levels of up to 10 cm H2O does not exert detrimental effects on systemic hemodynamics in OLT patients and does not interfere with ICG(PDR). However, it remains to be determined whether these findings could be confirmed under the application of higher PEEP levels over a longer period of time and whether they could be of clinical relevance for the use of indocyanine green as a dynamic liver function test.

Coloring Agents↗
PubMedDate not supplied

Third level hemodynamics: guiding clinical decisions.

Hemodynamic monitoring is one of the most frequently used technologies in critical care nursing. But how often do critical care practitioners consider the underlying reason for monitoring these variables? What really is the oxygen balance in the cell? How does oxygen supply and demand figure into the hemodynamic equation? This article demonstrates how the imbalance of oxygen supply and demand at the cellular level is important to understanding the patient's hemodynamic status. It is followed by a continuing education packet you can use to teach the cellular principles of hemodynamics.

Cardiac Output↗
PubMed1994

Cardiac and hemodynamic tolerability of iopromide with or without sodium or iloprost and of ioversol in the anesthetized rat.

RATIONALE AND OBJECTIVES: In this study, the cardiac and hemodynamic effects of iopromide alone were compared with those of two combination preparations (iopromide plus sodium and iopromide plus the prostacyclin analog iloprost) and with ioversol after left ventricular bolus administration in rats. METHODS: The tracheae of anesthetized male Wistar rats were cannulated to facilitate spontaneous respiration. The animals were set up to allow recording or calculation of the following parameters: femoral arterial blood pressure (systolic, mean, and diastolic), left ventricular end-diastolic pressure, heart rate, and contractility. Iopromide (330 mg iodine/mL; 2 g iodine/kg) with or without sodium chloride (20 mmol/L) or iloprost (approximately 50 ng/mL; dose: 300 ng/kg) was injected into the left ventricle within 30 seconds. Ioversol (320 mg iodine/mL) was used at the same dose and injection rate. RESULTS: Iopromide and ioversol induced transient changes in blood pressure (decrease followed by an increase), left ventricular end-diastolic pressure (increase), heart rate (decrease), contractility (increase followed by decrease), and electrocardiogram (extrasystoles, ST depression). Ioversol exhibited more pronounced effects on contractility and ST depression. The differences were statistically significant. The addition of sodium to iopromide resulted in a slight, but not significant influence on cardiac or hemodynamic parameters. The addition of iloprost improved ST depression slightly and hemodynamics significantly resulting in less mean and end-diastolic blood pressure change and less heart rate decrease. Contractility was significantly increased compared with iopromide with or without sodium. CONCLUSIONS: The addition of sodium or iloprost to nonionic contrast media might be useful in the alleviation of cardiac and hemodynamic side-effects.

Anesthesia, General↗
PubMed1998

Hemodynamic profile of corticotropin-induced hypertension in the rat.

OBJECTIVES: To examine hemodynamic variables in corticotropin-induced hypertension in rats and the effects of reversal of the hypertension by L-arginine on the hemodynamic profile. METHODS: Sixty male Sprague-Dawley rats were randomly divided into four groups: sham treatment (0.9% NaCl, injected subcutaneously); 0.5 mg/kg corticotropin per day, subcutaneously; 0.6% L-arginine in food plus sham; and L-arginine plus corticotropin. Systolic blood pressure, water and food intakes, urine volume, and body weight were measured every second day. After 10 days mean arterial blood pressure was measured by intra-arterial cannulation, and cardiac output, and renal, mesenteric, and hindquarter blood flows were determined using transonic small animal flowmeters. RESULTS: Injection of corticotropin increased blood pressure, water intake, urine volume, and plasma sodium concentration, and decreased body weight and plasma potassium concentration. It increased cardiac output (P < 0.01), mesenteric blood flow (P < 0.05), and renal vascular resistance (P < 0.05), and decreased renal blood flow (P < 0.05), but did not change calculated total peripheral resistance, hindquarter blood flow, mesenteric or hindquarter vascular resistance. L-arginine prevented corticotropin-induced rises in blood pressure (P < 0.001) and renal vascular resistance (P < 0.05), and a fall in renal blood flow (P < 0.05), but did not affect other hemodynamic variables. CONCLUSION: The hemodynamic profile of corticotropin-induced hypertension in the rat is characterized by a rise in cardiac output and renal vascular resistance, a fall in renal blood flow, but no change in total peripheral resistance, hindquarter blood flow, mesenteric vascular resistance, or hindquarter vascular resistance. L-arginine prevented corticotropin-induced rises both in blood pressure and in renal vascular resistance in the rat. These data suggest that the increase in renal vascular resistance might play a role in corticotropin-induced hypertension in the rat.

Adrenocorticotropic Hormone↗
PubMed1998

Coronary hemodynamics in aging spontaneously hypertensive and normotensive Wistar-Kyoto rats.

OBJECTIVE: To delineate hypertension-related and age-related changes in coronary hemodynamics and to assess the role of myocardial (i.e. left ventricular) hypertrophy and cardiac fibrosis in inducing progressive deterioration of coronary flow reserve associated both with hypertension and with aging. METHODS: Systemic and coronary hemodynamics (using radionuclide-labeled microspheres), right ventricular, left ventricular, and aortic mass indexes, and ventricular hydroxyproline concentrations (an estimate of collagen) in normotensive Wistar-Kyoto and spontaneously hypertensive rats aged 22, 35, and 65 weeks were determined. RESULTS: Spontaneously hypertensive rats of all ages had greater left ventricular and aortic masses, greater collagen concentrations in both ventricles, a lower coronary flow reserve, and greater minimal coronary vascular resistance after administration of dipyridamole than did Wistar-Kyoto rats. Despite spontaneously hypertensive rats having only left ventricular hypertrophy, coronary hemodynamics were impaired to the same extent in both ventricles. Progressive increases in myocardial collagen concentration, decreases in coronary flow reserve, and increases in minimal coronary vascular resistance were observed in rats of both strains with aging. A positive correlation and linear regression between myocardial collagen concentration and minimal vascular resistance were found for both ventricles of rats of both strains. CONCLUSIONS: Both aging and hypertension adversely affected the coronary circulation; furthermore, these effects appeared to be additive. Cardiac fibrosis, but not hypertrophy, might play a role in progressive deterioration of coronary hemodynamics in aging and hypertension and could provide an explanation for the diastolic dysfunction encountered clinically in older patients with hypertension.

Aging↗
PubMed2002

Cilnidipine improves spontaneously hypertensive rat coronary hemodynamics without altering cardiovascular mass and collagen.

OBJECTIVE: The present study was designed to determine the effects of prolonged treatment with cilnidipine, a novel dihydropyridine calcium antagonist which blocks both L-type and N-type calcium channels, on systemic, regional and coronary hemodynamics, cardiovascular mass and collagen content in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. METHODS: Male 23-week-old WKY and SHR rats were divided into two groups for each strain. One group received cilnidipine (10 mg/kg per day), whereas their respective controls were given no therapy. Systemic and regional hemodynamics (radionuclide-labeled microspheres), left and right ventricular and aortic mass, and hydroxyproline concentration were determined after 12 weeks treatment. RESULTS: The data demonstrated that cilnidipine neither affected systemic hemodynamics nor cardiovascular mass and collagen content in WKY rats. The same treatment in the SHR reduced arterial pressure and total peripheral resistance without changes in heart rate and cardiac index. Ventricular and aortic mass indices as well as ventricular collagen content remained unchanged. There were no differences in organ blood flows between two SHR groups, whereas renal, liver and left ventricular coronary vascular resistances were reduced by cilnidipine. After dipyridamole infusion left ventricular minimal coronary vascular resistance decreased further in cilnidipine-treated SHR as compared with control SHR rats. CONCLUSION: These data suggest that cilnidipine, an L- and N- type calcium channel antagonist, exerted beneficial effects on coronary hemodynamics without altering cardiovascular mass or collagen content in SHR.

Animals↗
PubMed2003

Protective effects of dietary potassium chloride on hemodynamics of Dahl salt-sensitive rats in response to chronic administration of sodium chloride.

BACKGROUND: Dietary potassium supplementation decreases blood pressure and prevents strokes in humans, and prevents strokes and renal damage in Dahl salt-sensitive (DSS) rats. OBJECTIVE: To study the effects of various concentrations of dietary potassium chloride (KCl) on the hemodynamics of Dahl salt-resistant (DSR) and DSS rats receiving a 1% sodium chloride (NaCl) diet for 8 months, to determine whether there is an optimal dietary concentration of KCl that minimizes increases in blood pressure and causes least impairment of blood flow in the brain and kidneys. METHODS AND RESULTS: We found a biphasic effect on hemodynamic parameters as a function of dietary KCl in DSS rats of the Rapp strain fed 1% NaCl with increasing dietary KCl (0.7, 2.6, 4 and 8%). After 8 months receiving a diet containing 1% NaCl and 0.7% KCl, DSS rats had mean arterial pressures (MAP), plasma volumes, cardiac outputs and renal and cerebral vascular resistances that were significantly increased compared with those of DSR rats receiving the same diet. With a 2.6% KCl diet, all these parameters were significantly reduced compared with those in DSS rats fed the 0.7% KCl diet and were similar to those in DSR rats fed 2.6% KCl. Total peripheral resistance in DSR and DSS rats was similar on all diets. When KCl was increased to 4 and 8%, MAP, plasma volume, cardiac output and renal vascular resistance progressively increased in DSR and DSS rats, without changing total peripheral resistance. These changes paralleled increases in plasma aldosterone, which resulted from adrenocortical stimulation by the increasing dietary KCl; however, cerebral vascular resistance of DSR and DSS rats decreased significantly with a 4% KCl diet, despite increased aldosterone and sodium retention. Only DSS rats fed a 2.6% KCl diet had hemodynamics similar to those of DSR control rats fed the same diet, and hyperaldosteronism, sodium retention and increased plasma volume did not occur. CONCLUSION: 'Optimal' dietary KCl (2.6%) prevents hypertension and preserves cerebral and renal hemodynamics in DSS rats fed a diet containing 1% NaCl for 8 months, which causes hypertension when dietary KCl is limited or excessive.

Aldosterone↗
PubMedDate not supplied

Hemodynamic effects of antagonists of the vasoconstrictor action of vasopressin in conscious dogs.

Two antagonists of the pressor action of arginine-vasopressin (AVP) were studied in conscious, normally hydrated dogs: 1-deaminopenicillamine-4-valine-8-D-arginine-vasopressin, or dPVDAVP, and 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid)2-(O-methyl)tyrosine arginine-vasopressin, or d(CH2)5Tyr(Me)AVP. We first examined the hemodynamic effects of these antagonists when given alone. The infusion of dPVDAVP, 200 ng/kg/min, increased cardiac output (measured with an aortic electromagnetic flowmeter) by 23% and heart rate by 27%, leaving arterial pressure unchanged. Most of the change in cardiac output reflected a large increase in skeletal muscle blood flow, as determined by radioactive microspheres. The injection of d(CH2)5Tyr(Me)AVP, 10 micrograms/kg, had little effect on cardiac output, arterial pressure, and heart rate. We then examined the ability of the two antagonists to block the hemodynamic responses to injections of AVP. In the absence of the antagonists, AVP induced dose-related increases in mean arterial pressure and total peripheral resistance, as well as decreases in heart rate and cardiac output. The antagonist dPVDAVP shifted the dose-response curves to the right without changing their slope. On the contrary, the hemodynamic response to AVP was strikingly modified following blockade with d(CH2)5Tyr(Me)AVP. Cardiac output and heart rate increased, whereas total peripheral resistance decreased, for doses of AVP between 25 and 400 ng/kg. It is concluded that some antagonists of the pressor action of vasopressin may influence hemodynamics of conscious dogs by effects other than competitive antagonism at the level of vascular receptors.

Animals↗
PubMed1986

Effects of bisoprolol in relation to metoprolol and bufuralol on left ventricular hemodynamics at rest and during exercise in chronic ischemic heart disease.

To assess acute hemodynamic effects of bisoprolol on left ventricular hemodynamics at rest and during exercise, 16 patients with documented chronic ischemic heart disease were studied and compared with patients after administration of metoprolol and bufuralol. Simultaneous right heart catheterization and radionuclide angiocardiography were performed at rest and during exercise before and after drug administration. Bisoprolol was given orally to 16 patients, six receiving 5 mg, and 10 patients receiving 20 mg. Metoprolol was injected intravenously in a dose of 0.15 mg/kg to another 16 patients, and 30 mg bufuralol were given orally to 10 patients. The hemodynamic profiles of all three compounds were similar to that previously described after acute beta-blockade. All three drugs tested and compared showed a marked negative chronotropic effect, while there were slight differences in the negative inotropic and blood pressure lowering effect. Bisoprolol induced only mild negative inotropic changes, which were barely detectable after the 5 mg dose. The negative inotropic changes were more pronounced after metoprolol, and were partly balanced by the vasodilating properties of bufuralol. Thus, bisoprolol showed a significantly reduced rate pressure product with only a relatively mild negative inotropic effect. Based on these observations, even the higher dose of 20 mg bisoprolol seems to be hemodynamically safe for clinical application.

Adrenergic beta-Antagonists↗
PubMed1986

Hemodynamic patterns in the natural history of borderline hypertension.

This paper gives a review of cross-sectional and long-term hemodynamic studies in mild and borderline hypertension at different ages. Since the term borderline and mild are frequently used rather loosely, the selection criteria and blood pressure during the hemodynamic study should be noted. For two decades it has been assumed that subjects below 40 years of age with mild or borderline hypertension usually have a higher resting cardiac index (CI) and heart rate (HR) than normotensive age-matched controls. This assumption is supported by numerous previous and recent invasive studies in young males. However, a true hyperkinetic circulatory system with abnormally low arteriovenous oxygen difference is not typical. The whole-body oxygen consumption is increased, and cardiac output is normal when related to the oxygen uptake. Thus, the so-called whole-body autoregulation theory should not be applied to explain the chain of hemodynamic events including a fall in cardiac index and an increase in total peripheral resistance over time. Recent noninvasive studies in children and adolescents with mild or borderline hypertension have generally not demonstrated higher cardiac indexes in mildly hypertensive groups, and blood pressure increases have been due to increased total peripheral resistance. Possible explanations for these different findings in subjects supposed to be in the initial phase of essential hypertension are discussed. Our laboratory performed invasive long-term follow-up studies of central hemodynamics at rest and during exercise at 10 years and 17 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Central and regional vascular hemodynamics following intravenous milrinone in the conscious rat: comparison with dobutamine.

This study examined the hemodynamic and regional vascular profile of intravenous (i.v.) milrinone during increasing doses (3, 6, 12 micrograms/kg/min, n = 8) and by intraindividual comparison of milrinone and dobutamine (n = 10) in normal conscious rats. At 3 micrograms/kg/min, Milrinone increased coronary and cerebral blood flow (radioactive microspheres 15 +/- 5 microns) (7.7-9.8 and 1.05-1.27 ml/min/g respectively, both p less than 0.05) without significant changes in systemic hemodynamics. At 6 micrograms/kg/min milrinone increased skeletal muscle blood flow (0.19-0.24 ml/min/g, p less than 0.05) along with increases in cardiac output, stroke volume, and stroke work (all p less than 0.05), while systemic vascular resistance decreased (-51%, p less than 0.05). When compared with dobutamine, milrinone caused a greater increase in cardiac output (+26% vs. +17%) and a greater reduction in systemic vascular resistance. Milrinone and dobutamine increased renal, intestinal, cerebral, and coronary flow to a similar extent, but only milrinone enhanced hepatic arterial blood flow (+26%, p less than 0.05) and tended to increase flow to skeletal muscle (+35%, p = 0.07). We conclude that milrinone exerts significant regional vasodilating effects in a conscious rat model, being most prominent in the coronary and cerebral circulations at a dosage that does not alter central hemodynamics. At higher doses, milrinone causes a balanced increase in regional blood flow including enhanced flow to skeletal muscle. The hemodynamic (particularly as compared with dobutamine) and regional vascular profile of milrinone suggests a predominant vasodilating effect in the rat. Given a similar limited response of rat and diseased human myocardium to milrinone, these findings may have important clinical implications.

Animals↗
PubMed1988

Hemodynamic effects of prolonged intravenous therapy with enoximone in patients with severe congestive heart failure.

The hemodynamic differences between bolus administration and constant intravenous infusion over a 48-h period with enoximone, a new positive inotropic/vasodilator agent, were evaluated. Twenty-four patients were studied, 15 patients in the bolus group (Group A) and nine patients in the constant infusion group (Group B). The overall hemodynamic results were similar in both groups. Cardiac output increased in Group A from 3.1 +/- 0.71 to 5.5 +/- 1.3 L/min and in Group B from 3.6 +/- 1.0 to 5.9 +/- 1.2 L/min. Significant decreases occurred in pulmonary capillary wedge pressure (30 +/- 7 to 20 +/- 8 mm Hg and 37 +/- 5 to 21 +/- 11 mm Hg) and systemic vascular resistance (2184 +/- 456 to 1300 +/- 305 dyn.s.cm-5 and 1752 +/- 415 to 1035 +/- 130 dyn.s.cm-5). Group A required repeat drug boluses every 3-5 h to maintain these hemodynamic effects. The terminal blood half-life of enoximone derived following the continuous infusion in Group B was 10.6 +/- 7.0 h. In conclusion, intravenous enoximone produces acute salutary hemodynamic effects in patients with severe congestive heart failure that can be sustained for at least 48 h by intermittent boluses or a continuous infusion.

Adult↗