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Acute effects of the oral administration of midodrine, an alpha-adrenergic agonist, on renal hemodynamics and renal function in cirrhotic patients with ascites.

The effects of the acute administration of arterial vasoconstrictors on renal plasma flow (RPF) and urinary sodium excretion (UNaV) in cirrhotic patients with ascites with or without hepatorenal syndrome (HRS) are still controversial. As a consequence, vasoconstrictors are not actually used in the treatment of renal sodium retention or HRS in these patients, regardless of the several lines of evidence suggesting that these renal functional abnormalities are related to a marked arterial vasodilation. The lack of an orally available effective arterial vasoconstrictor probably represents a further reason for this omission. Consequently, the present study was made to evaluate the acute effects of the oral administration of midodrine, an orally available -mimetic drug, on systemic and renal hemodynamics and on UNaV in cirrhotic patients with ascites. Mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), systemic vascular resistance (SVR), left forearm blood flow (LFBF), left leg blood flow (LLBF), RPF, glomerular filtration rate (GFR), UNaV, plasma renin activity (PRA), plasma concentration of antidiuretic hormone (ADH), and the serum levels of nitrite and nitrate (NOx) were evaluated in 25 cirrhotic patients with ascites (17 without HRS and 8 with type 2 HRS) before and during the 6 hours following the oral administration of 15 mg of midodrine. During the first 3 hours after the drug administration, a significant increase in MAP (89.6 +/- 1.7 vs. 81.80 +/- 1.3 mm Hg; P < .0001) and SVR (1, 313.9 +/- 44.4 vs. 1,121.2 +/- 60.1 dyn . sec . cm-5; P < .0001) accompanied by a decrease in HR (69 +/- 2 vs. 77 +/- 3 bpm; P < .005) and CI (2,932.7 +/- 131.4 vs. 3,152.5 +/- 131.4 mL . min-1 . m2 BSA; P < .0025) was observed in patients without HRS. No change was observed in LFBF and LLBF. The improvement in systemic hemodynamics, which was also maintained during the the 3- to 6-hour period after midodrine administration, was accompanied by a significant increase in RPF (541.5 +/- 43.1 vs. 385.7 +/- 39.9 mL . min-1; P < .005), GFR (93.1 +/- 6.5 vs. 77.0 +/- 6.7 mL . min-1; P < .025), and UNaV (92.7 +/- 16.4 vs. 72.2 +/- 10.7 microEq . min-1; P < .025). In addition, a decrease in PRA (5.33 +/- 1.47 vs. 7.74 +/- 2.17 ng . mL-1 . h; P < .05), ADH (1.4 +/- 0.2 vs. 1.7 +/- 0.2 pg . mL-1; P < .05), and NOx (33.4 +/- 5.0 vs. 49.3 +/- 7.3 micromol-1; P < .05) was found. In patients with HRS, the effects of the drug on the systemic hemodynamics was smaller and shorter. Accordingly, regardless of a significant decrease in PRA (15.87 +/- 3.70 vs. 20.70 +/- 4.82 ng . mL-1 . h; P < .0025) in patients with HRS, no significant improvement was observed in RPF, GFR, or UNaV. In conclusion, the acute oral administration of midodrine is associated with a significant improvement in systemic hemodynamics in nonazotemic cirrhotic patients with ascites. As a result, renal perfusion and UNaV also improve in these patients. By contrast, midodrine only slightly improves systemic hemodynamics in patients with type 2 HRS, with no effect on renal hemodynamics and renal function.

Administration, Oral↗

Improving the reliability of obtaining tumor hemodynamic parameters in the presence of contrast agent extravasation.

A new approach to improve the reliability of dynamic susceptibility contrast MRI for the evaluation of brain tumor hemodynamics in the presence of contrast agent extravasation is described. This model-based technique simultaneously estimates the voxel-wise tumor residue function and the temporal extravascular T(1) changes following contrast agent leakage. With these estimates the model corrects the measured MRI signal, which is then used to calculate tumor hemodynamic parameters. The feasibility of this technique is demonstrated with computer simulations that cover a wide range of hemodynamic conditions and by application to eight tumor-bearing rats. The simulations demonstrate that the corrected hemodynamic parameters precisely matched the actual values with a maximum percentage error of 4.2% compared to 68.6% for the uncorrected parameters. The corrected parameters are also essentially independent of the tumor hemodynamic state and degree of contrast extravasation. Consistent with these improvements, significant differences between corrected and uncorrected parameters, calculated from a gradient-echo sequence, are shown in a rat 9L gliosarcoma model. This method combined with the hemodynamic parameters derived from GE and SE sequences shows promise as a new tool to evaluate tumor angiogenesis and its therapy.

Animals↗

Evidence for a refractory period in the hemodynamic response to visual stimuli as measured by MRI.

We investigated the effects of paired presentations of visual stimuli upon the evoked hemodynamic response of visual cortex measured by magnetic resonance imaging (MRI). Stimuli were identical 500-ms high-contrast checkerboard patterns, presented singly or with an interpair interval (IPI) of 1, 2, 4, or 6 s (onset-to-onset), followed by an intertrial interval of 16-20 s. Images were acquired at 1.5 Tesla using a gradient-echo echoplanar imaging sequence sensitive to blood-oxygenation-level dependent (BOLD) contrast. Single checkerboards evoked a hemodynamic response from visual cortex characterized by a rise at 3 s, peak activation at 5 s, and return to baseline by 10 s. We subtracted subjects' single-stimulus hemodynamic response from their paired-stimulus responses to isolate the contribution of the second stimulus. If the hemodynamic responses were fully additive, the residual should be a time-shifted replica of the single stimulus response. However, the amplitude of the hemodynamic response to the second checkerboard was smaller, and the peak latency was longer, than for the first. Furthermore, the amplitude decrement was dependent upon IPI, such that the response to the second stimulus at 1 s IPI was only 55% of that to a single stimulus, with recovery to 90% at a 6 s IPI. Peak latency was similarly dependent upon IPI with longer latencies observed for shorter IPIs. These results demonstrate an extended refractory period in the hemodynamic response to visual stimuli consistent with that shown previously for neuronal activity measured electrophysiologically.

Adult↗

Central hemodynamic effects of diuretic therapy in chronic heart failure.

In chronic heart failure diuretic drugs improve central hemodynamic variables and cardiac pumping secondary to altered plasma and extracellular volumes; humoral markers of these changes include increased plasma renin and aldosterone levels. The latter increases are maximal over the first week but decline with chronic therapy. The plasma alpha-ANP levels show a reciprocal effect; these data are compatible with a rapid contraction of the plasma volume which is sustained during chronic therapy. The acute hemodynamic actions of diuretic agents reflect both immediate and direct vascular actions and also effects secondary to diuresis (volume redistribution). At rest substantial reductions in pulmonary "wedge" pressure (-29%), with a consequent fall in cardiac output (-10%), are described. Total systemic vascular resistance initially increases but "reverse autoregulation" over subsequent weeks returns this elevation gradually towards control values. Tolerance to these initial hemodynamic effects does not occur with maintained therapy; moreover, echocardiographic markers of contractility and exercise capacity may increase. The early venodilator effects of diuretic drugs can be attributed to prostaglandin release and the initial pressor actions to activation of the renin angiotensin system; these vascular actions may have limited relevance to long-term beneficial effects on hemodynamics. Direct pulmonary vasodilation and improved pulmonary compliance remain an interesting finding. Although most patients are both symptomatically and hemodynamically improved at rest, the actions during exercise are more varied. Some individuals with severely impaired left ventricular function show little hemodynamic improvement, whereas those with milder dysfunction usually benefit; in the main this is probably related to the latter being on a steeper cardiac function curve.(ABSTRACT TRUNCATED AT 250 WORDS)

Bumetanide↗

Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris.

The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.

Adrenergic beta-Antagonists↗

[Problems of clinical evaluation of hemodynamics at rest and during exercise in chronic heart disease. Value of cardiac catheterization and problems of clinical classification].

BACKGROUND: NYHA classification is mostly used for graduation of clinical limitation due to cardiac failure. Right heart catheterization is not generally used to evaluate hemodynamics and to define the effects of drugs in patients with chronic cardiac failure. Clinical data and results from echocardiography, stress tests or nuclear cardiology seem to be sufficient. Our aim was to demonstrate subjectivity of a classification system (NYHA) comparing the graduation done by physicians and by patients and to represent the difficulty to prognosticate hemodynamic data of patients with heart failure. PATIENTS AND METHODS: Limitation of 53 patients with heart diseases was classified by physicians and patients using NYHA classification. Pulmonary capillary wedge pressure (PCWP), stroke volume (SV) and cardiac output were predicted by physicians; they were allowed to utilize all examination data they could get. Predicted hemodynamic data were compared with the results of measurement at rest and during exercise. RESULTS: Patients classified themselves significantly worse than physicians did: 2.68 +/- 0.64 vs. 2.23 +/- 0.74 (p = 0.0012). Similarity in NYHA classification was found in 29/53 cases. Correlation of predicted and measured hemodynamic data was low: PCWP (at rest) r = 0.346; PCWP (during exercise) r = 0.232; SV (at rest) r = 0.476; SV (during exercise) r = 0.445; HMV (at rest) r = 0.412; HMV (during exercise) r = 0.538. CONCLUSION: Clinical classification systems like NYHA are subjective, classification by physicians differs significantly from classification by patients. Prediction of hemodynamics is not possible despite all examination data had been available. Right heart catheterization is necessary to define hemodynamics at rest and during exercise.

Cardiac Catheterization↗

Effect of prone position on hepato-splanchnic hemodynamics in acute lung injury.

OBJECTIVE: To evaluate the effects of prone position on hepato-splanchnic hemodynamics, metabolism and gut mucosal energy balance. DESIGN: Prospective clinical study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: Eleven hemodynamically stable patients with acute lung injury (ALI) requiring mechanical ventilation. INTERVENTION: Patients were studied in the supine position, after 90 min in the prone position and after 90 min of supine repositioning. MEASUREMENTS AND RESULTS: In addition to global hemodynamics we measured intra-abdominal pressure (IAP, bladder), hepato-splanchnic blood flow (HSBF, steady state indocyanine green technique using a hepatic vein catheter) and gastric mucosal-arterial PCO(2) gap (PCO(2) gap, automated air tonometry). Systemic hemodynamics did not change during the whole study. Prone positioning did not significantly affect IAP. HSBF as well as splanchnic oxygen consumption remained unaltered, too. Similarly, neither liver lactate uptake nor indocyanine green extraction were influenced by positional changes. Finally, stable regional hemodynamics were accompanied by an unchanged PCO(2) gap. CONCLUSION: We conclude that if IAP and systemic hemodynamics remain unaffected, the prone position in ALI patients compromises neither hepato-splanchnic perfusion nor gastric mucosal energy balance.

Acute Disease↗

Antagonization of TNF attenuates systemic hemodynamic manifestations of envenomation in a rat model of Vipera aspis snakebite.

OBJECTIVES: Tumor necrosis factor (TNF) has been reported as a mediator of local tissue injury following snake envenomation in an intact rat model. We investigated whether systemic release of TNF occurs following Vipera aspis envenomation. We further analyzed the possible connection between envenomation-related hemodynamic depression and TNF antagonization (TNF antibodies or soluble TNF receptor). DESIGN: A prospective, randomized, controlled experimental study using a rat model for snake envenomation. SETTINGS: A medical university hospital research laboratory. INTERVENTION: Eighty rats (300-400 g) were divided into four groups (n = 20): control and three experimental groups. Intramuscular injection of V. asis 500 microg/kg was administered to the three experimental groups: venom only (group 1), venom and 40 microg anti-TNF antibodies (group 2), venom and 250 microg soluble TNF receptor (p55-R; group 3). Hemodynamic parameters were monitored up to 4 h following venom injection. MEASUREMENTS AND RESULTS: A significant hemodynamic deterioration (reduction in heart rate and blood pressure) occurred 30 min following venom injection in group 1 compared to groups 2 and 3, where hemodynamic parameters remained stable throughout the 4 h observation period. Serum levels of TNF were detected 15 min after venom injection and peaked after 2 h at 485+/-12 pg/ml. CONCLUSIONS: The hemodynamic consequences of intramuscular injection of V. aspis venom can be blunted in a rat by systemic antagonization of TNF activity prior to venom injection. The poisonous hemodynamic effects of the V. aspis venom might be caused by systemic release of TNF.

Animals↗

The effects of elevated intraabdominal pressure, hypercarbia, and positioning on the hemodynamic responses to laparoscopic colectomy in pigs.

BACKGROUND: This study investigated three factors postulated to be sources of physiological stress in laparoscopic surgery: hypercarbia, elevated intraabdominal pressure, and the steep Trendelenburg position. Our research was designed to define the effects of each of these potential stressors on hemodynamic responses observed during laparoscopic colectomy in pigs. METHODS: Twenty-four pigs were randomized into the following four groups, based on the method for obtaining surgical exposure while a colectomy or laparoscopic-assisted colectomy was performed: Open surgery (n = 6), CO2 pneumoperitoneum (n = 6), Helium pneumoperitoneum (n = 6), and abdominal wall Lifter (n = 6). The animals were paralyzed with minute ventilation adjusted. All animals underwent extensive pulmonary and hemodynamic monitoring with measurements of the following parameters: RR, Vt, minute ventilation, O2, sat, ETCO2, PVR, HR, MAP, CO, PAP, CVP, PCWP, SV, LVSWI, DO2, and VO2. The laparoscopic pigs were placed in the steep Trendelenburg position during surgery. RESULTS: The effect of a CO pneumoperitoneum was to increase PaCO2 PVR and cause an acidemia that could not be prevented by an increase in minute ventilation. Elevated intraabdominal pressure decreased UO. Both pneumoperitoneum groups had a fourfold increase in IVCP, a measure of intraabdominal pressure. Some of this increase was due to placement into the Trendelenburg position; IVCP increased to a lesser degree in the Lifter group. The steep Trendelenburg position caused significant increases in PAP, CVP, and PCWP; however, a contributory effect of elevated intraabdominal pressure cannot be ruled out. None of these procedures had any significant effect on the HR or MAP. There was a significant increase in CO in the CO2 and Lifter groups; however, when CO was controlled for HR effects, there was no significant effect on SV from any of these different procedures. LVSWI, DO2, and VO2 were not affected by any of the different exposure methods. CONCLUSIONS: The effects of laparoscopic surgery and open surgery on hemodynamic responses are minimal, and no one method is superior to another when performed in pigs that are healthy, hydrated, and hyperventilated to keep ETCO2 < 40. However, since elderly and sick patients have a lower threshold for physiologic decompensation, we can infer that the small hemodynamic changes noted in this study might become significant factors when surgery is performed on compromised patients. The finding that an abdominal wall lifting device causes the fewest metabolic and hemodynamic effects makes its use an important consideration when performing laparoscopic surgery in patients with cardiopulmonary compromise, hemodynamic instability, or any preexisting renal insufficiency.

Abdomen↗

Hemodynamic effects of moricizine at rest and during supine bicycle exercise: results in patients with ventricular tachycardia and left ventricular dysfunction.

To evaluate the hemodynamic effects of moricizine, 20 patients with frequent nonsustained ventricular tachycardia (VT) with a mean left ventricular ejection fraction (EF) of 39 +/- 14% were enrolled in a prospective single-blind, placebo-controlled study. Hemodynamic measurements were performed at rest and during supine bicycle exercise on placebo and moricizine therapy (10 mg/kg/day). Although 16 of 19 patients experienced no rest or exercise deterioration in hemodynamic parameters during drug dosing, three patients had acute deterioration of pulmonary capillary wedge pressure and cardiac index (CI) on moricizine. During follow-up of 6 +/- 3 months, two subgroups were identified: 10 of 19 patients had effective long-term reduction in VT, whereas 9 of 19 patients had poor control of ventricular arrhythmia or congestive heart failure and were discontinued from the trial. Baseline EF and hemodynamic parameters at rest were similar in both patient subgroups. However, protocol dropouts had a hemodynamic response to exercise on moricizine that was significantly depressed as compared to patients with a favorable antiarrhythmic outcome (p less than 0.02). The following hemodynamic profile characterizes patients unlikely to have an antiarrhythmic response to moricizine: an increase in CI of less than 1.0 L/min/m2 and no increase in left ventricular stroke work index during supine exercise.

Exercise Test↗

Comparison of late clinical status between patients with different hemodynamic findings after repair of tetralogy of Fallot.

Long-term results and postoperative hemodynamic findings were reviewed in 144 cases of tetralogy of Fallot. A correlation was found between the late clinical status of patients and the postoperative hemodynamic findings. The mortality in our series of patients followed for 10 years was 6.25%. Each of the deaths occurred in the group with unsatisfactory postoperative hemodynamic findings. An ideal late clinical result can be anticipated in most patients with excellent or satisfactory postoperative hemodynamic findings. The greater the deviation from normal hemodynamic findings, the worse the prognosis. From the excellent group to the unsatisfactory group, the incidence of late ideal result decreased from 95% to 61.1%, while the incidence of poor result increased from 0% to 27.8%. Among various factors in patients in the unsatisfactory hemodynamic group, right ventricular outflow tract obstruction seems to have the worst late result. A large right ventricular-pulmonary artery pressure gradient was noted in three of four who died suddenly. The late result of patients with a small shunt (pulmonary blood flow/systemic blood flow less than 2) seems acceptable; the decision to reoperate in these patients should be made very cautiously.

Child↗

Hemodynamics versus biopsy findings during cardiac transplant rejection.

Before the use of cyclosporine as the major component for immunosuppression after cardiac transplantation, rejection was accompanied by catastrophic hemodynamic decompensation. However, the hemodynamic changes that occur during rejection after cardiac transplantation in patients treated with cyclosporine have not been clearly described. Between July 1986 and October 1989, 89 adults underwent orthotopic heart transplantation at the University of Michigan Medical Center. All patients received triple-drug therapy immunosuppression consisting of steroids, cyclosporine, and azathioprine. Cardiac hemodynamics were measured and correlated with the histologic assessment of rejection. There have been ten deaths among these 89 patients for an overall survival of 89%. There were no deaths from rejection. One hundred fifty-three of the biopsy specimens were read as grade 0, 31 were grade 1, 75 were grade 2, 103 were grade 3, and 9 patients had grade 4 biopsy specimens. No hemodynamic differences were noted in patients with increasing grade of rejection. Five patients (5/9, 55%) with severe rejection (grade 4) had symptoms of congestive heart failure at the time of biopsy. These symptomatic grade 4 patients differed from asymptomatic grade 4 patients only in cardiac output (2.9 versus 5.2 L/min). Overall hemodynamic decompensation was not evident as rejection grade increased. Routine serial endomyocardial biopsies remain the procedure of choice in the diagnosis of rejection in the asymptomatic patient after cardiac transplantation as hemodynamics do not predict degree of rejection.

Adult↗

Beneficial hemodynamic effects of two weeks' milrinone treatment in conscious rats with heart failure.

Milrinone is a phosphodiesterase inhibitor which combines vasodilating effects with inotropic effects. Hemodynamic improvement after acute administration and increased survival with chronic milrinone therapy in rats with heart failure have been reported before, and suggest long-term hemodynamic improvement. However, no detailed hemodynamic studies are available on prolonged milrinone therapy in rats with heart failure. Therefore, the hemodynamic effects of 2 weeks' milrinone therapy were now investigated in conscious rats with heart failure due to myocardial infarction. The effects were compared to hemodynamic changes after acute administration. Acute milrinone increased the baseline cardiac output in infarcted rats by increasing heart rate rather than stroke volume. However, the maximal cardiac output achieved when the heart was stimulated through a volume load was improved due to increased stroke volume as well as increased heart rate. The increase in maximally stimulated cardiac output after acute milrinone was found to be related to infarct size. Two weeks' milrinone therapy in chronically infarcted rats dose dependently restored the hemodynamic changes which were caused by infarction. In contrast to acute administration, two weeks' milrinone restored cardiac function without an increase in heart rate. The effects were achieved at a rate of administration which presumably has no acute inotropic effects. The data indicate that acute milrinone in infarcted rats has vasodilating effects. Positive inotropic effects, possibly masked by concomitant venodilatation at baseline conditions, became overt after stimulation by volume loading. Long-term milrinone dose dependently restored cardiac function in infarcted rats without effects on heart rate or mean arterial pressure, suggesting that different mechanisms may be involved.

Animals↗

Nitrotyrosine attenuates the hemodynamic effects of adrenoceptor agonists in vivo: relevance to the pathophysiology of peroxynitrite.

Peroxynitrite, which attenuates catecholamine-mediated hemodynamic responses in vivo, nitrates free tyrosine residues to form the specific product, 3-nitro-L-tyrosine. The chemical structure of 3-nitro-L-tyrosine is similar to that of the endogenous catecholamines. Therefore, 3-nitro-L-tyrosine may interfere with catecholamine hemodynamic function in vivo. The hemodynamic responses produced by norepinephrine (1-4 micrograms/kg, i.v., n = 6), epinephrine (0.5-4 micrograms/kg, i.v., n = 7), phenylephrine (1-8 micrograms/kg, i.v., n = 5), and isoproterenol (100-400 ng/kg, i.v., n = 5) were attenuated, while the hemodynamic responses produced by arginine vasopressin (50-250 ng/kg; i.v., n = 5) were unaffected following the administration of 3-nitro-L-tyrosine (2.5 mumol/kg, i.v.) in pentobarbital-anesthetized rats. These results demonstrate substantial and selective attenuation of the hemodynamic effects produced by alpha- and beta-adrenoceptor agonists, raising the possibility that 3-nitro-L-tyrosine may play a role in the hemodynamic dysfunction associated with inflammatory conditions in which the formation of peroxynitrite is favored.

Adrenergic Agonists↗

Hemodynamic effects of endotoxin and platelet activating factor in cirrhotic rats.

Acute infections may influence the hemodynamic alterations of liver disease. Therefore, the hemodynamic effects of endotoxin (LPS E. coli 0111:B4) in conscious, normal, and cirrhotic rats were compared. Endotoxin decreased cardiac index in cirrhotic but not in normal rats. Although the effect of endotoxin on portal tributary blood flow was minor in all animals, a reduction in portal pressure was found in cirrhotic rats. Because the most marked hemodynamic effects were observed in cirrhotic rats, the second part of our study investigated whether platelet activating factor played a role in endotoxin-induced hemodynamic alterations in the cirrhotic model. Platelet activating factor reduced cardiac index and kidney blood flow but did not influence portal tributary blood flow. Two antagonists to platelet activating factor reduced the adverse renal blood flow lowering effects of endotoxin in cirrhotic rats. Thus, it is suggested that the hemodynamic changes observed in cirrhosis may be aggravated during acute infections. Under this condition, antagonists to platelet activating factor may be of benefit in the prevention of hemodynamic complications induced by endotoxin.

Animals↗

Differentiated hemodynamic responses to central versus peripheral administration of corticotropin-releasing factor in conscious rats.

Corticotropin-releasing factor (CRF) modifies cardiovascular function and hemodynamic status after administration into the central nervous system and into the peripheral circulation. The mechanisms by which CRF alters arterial pressure and heart rate have been examined in detail whereas little information exists regarding the processes mediating CRF-induced changes in regional blood flow. Therefore, studies were performed in conscious, unrestrained Sprague-Dawley rats to examine potential mechanisms underlying the regional hemodynamic effects of intracerebroventricular versus intravenous administration of CRF. Intracerebroventricular administration of CRF increased arterial pressure, heart rate, and mesenteric vascular resistance while decreasing iliac vascular resistance. Intravenous pretreatment with the CRF receptor antagonist, alpha-helical CRF9-41, did not alter the cardiovascular and hemodynamic responses to central administration of CRF. In contrast, prior ganglionic blockade prevented CRF-induced responses except for the reduction in iliac vascular resistance. Intravenous administration of CRF reduced arterial pressure and mesenteric vascular resistance, elevated heart rate, and transiently increased iliac vascular resistance. Intravenous pretreatment with alpha-helical CRF9-41 completely abolished the cardiovascular and hemodynamic responses to peripheral administration of CRF. Ganglionic blockade prior to intravenous administration of CRF augmented the reductions in arterial blood pressure and mesenteric vascular resistance, prevented the increase in heart rate, and unmasked a decrease in iliac vascular resistance. The divergent actions and mechanisms of action of CRF on regional hemodynamics when administered peripherally, as opposed to centrally, indicate that this peptide produces different hemodynamic effects that are specific to its site of action.

Animals↗

Hemodynamic effects of oral sotalol during both sinus rhythm and atrial fibrillation.

OBJECTIVES: This study investigated the hemodynamic effects of oral sotalol during both sinus rhythm and paroxysmal atrial fibrillation. BACKGROUND: The hemodynamic effects of most antiarrhythmic drugs have been characterized in subjects during sinus rhythm. However, there are no data concerning these effects on the paroxysmal tachyarrhythmias. METHODS: In 17 patients with paroxysmal atrial fibrillation and without heart failure (aged 62 +/- 11 years, ejection fraction 51 +/- 4%), an electrophysiologic-hemodynamic study was performed twice. In the first study, hemodynamic variables were evaluated both during sinus rhythm and after the induction of atrial fibrillation. Sotalol (160 or 240 mg/day) was administered for 6 to 7 days and the study was then repeated with the same methods. RESULTS: The drug significantly diminished heart rate during both sinus rhythm and atrial fibrillation. During sinus rhythm, sotalol did not change systemic pressures and significantly increased left and right ventricular end-diastolic, left and right atrial and pulmonary pressures. Cardiac index decreased, whereas stroke volume was unchanged after the drug. Ejection fraction and left ventricular end-diastolic and end-systolic volumes evaluated by echocardiography were unchanged after sotalol. During atrial fibrillation, the drug had less evident effects on cardiac function. Left ventricular end-diastolic, left atrial and pulmonary pressures did not increase significantly. CONCLUSIONS: The hemodynamic changes induced by oral sotalol appear to be mainly related to an involvement of ventricular distensibility; this effect is less evident during atrial fibrillation than during sinus rhythm. In patients with paroxysmal atrial fibrillation without heart failure treated with oral sotalol, a recurrence of the tachyarrhythmia is hemodynamically well tolerated.

Administration, Oral↗

Rapid hemodynamic improvement after reperfusion during right ventricular infarction.

OBJECTIVES: This study sought to determine the effects of reperfusion on hemodynamic status and hospital course in patients with right ventricular infarction. BACKGROUND: In contrast to the relatively low risk associated with acute inferior myocardial infarction, right ventricular infarction is associated with higher in-hospital morbidity and mortality. However, the potential benefits of reperfusion in patients with right ventricular infarction are unknown. Consequently, this study evaluated the potential benefits of primary angioplasty in patients with right ventricular infarction. METHODS: Of 141 consecutive patients admitted to the hospital for inferior myocardial infarction, 27 were identified as having right ventricular involvement by electrocardiographic and hemodynamic criteria. Seventeen patients achieved patency of the infarct-related right coronary artery by primary coronary angioplasty within 24 h of hospital admission, but 10 patients did not. All patients had invasive hemodynamic monitoring at the time of hospital admission, and subsequent serial hemodynamic status and clinical events were recorded. RESULTS: Patients with successful reperfusion demonstrated improved right atrial pressure, pulmonary capillary wedge pressure and right atrial/pulmonary capillary wedge pressure ratio as early as 8 h after reperfusion, whereas patients without reperfusion had no hemodynamic improvement over 24 h. Right atrial pressure demonstrated the greatest 8-h improvement after successful reperfusion (15.4 +/- 0.8 to 8.4 +/- 0.8 mm Hg [mean +/- SD], p < 0.05) but was unchanged without reperfusion (13.7 +/- 0.9 to 13.9 +/- 0.8 mm Hg, p = NS). Additionally, persistently elevated right atrial pressure was associated with increased mortality. CONCLUSIONS: Reperfusion in the setting of right ventricular infarction leads to rapid hemodynamic improvement and may result in improved survival.

Aged↗