Rise In Cardiac Output Research Articles

Circulatory and metabolic responses to carbon monoxide hypoxia during beta-adrenergic blockade.

The role(s) of beta-adrenoceptors in whole body and hindlimb skeletal muscle cardiovascular and metabolic responses during carbon monoxide hypoxia (COH) was studied in anesthetized dogs. One group of animals was beta-blocked with propranolol (beta 1- and beta 2-blockade), a second was given ICI 118,551 (beta 2-blockade), and a third served as a time control. Immediately after a control-sampling period, COH was induced (about a 63% decrease in arterial O2 content), and additional measurements were then obtained at 30 and 60 min of hypoxia. Cardiac output values were not different between the three series at control; an increase (P less than 0.05) occurred in all groups during COH. This rise was greatest in the COH group; the values for the propranolol- and ICI 118,551-blocked groups were not different from each other during COH. Hindlimb blood flow rose (P less than 0.05) during COH only in the control group. Both whole body (30 min) and hindlimb (30 and 60 min) resistance values were greater during hypoxia in the beta-blocked groups (P less than 0.05) than in the control series. Furthermore, whole body oxygen uptake decreased (P less than 0.05) in both beta-blocked groups during COH. We conclude that approximately 35% of the rise in cardiac output occurring during COH depended on peripheral vasodilation mediated through beta 2-adrenoceptors.

Hemodynamic profiles at rest and during supine exercise after orthotopic cardiac transplantation

To characterize the spectrum of hemodynamic findings after orthotopic cardiac transplantation, 20 healthy heart transplant recipients with no evidence of cardiac dysfunction by noninvasive testing were studied for 1 to 51 months (mean 15) following surgery. After routine endomyocardial biopsy, right-sided heart pressures and thermodilution cardiac outputs were measured at rest (supine) and during symptom-limited, graded supine exercise. In addition, the effect of respiration on right atrial pressures and waveforms was determined at rest (supine, legs down), and after passive leg raising (volume loading). During exercise, striking increases of pulmonary artery, pulmonary artery wedge and right atrial pressures were seen. The mean pulmonary artery pressure rose 45% during the first stage of exercise (p < 0.001) and by peak exercise it had increased 87% above resting values. The pulmonary artery wedge pressure increased significantly with passive leg elevation (p < 0.001) and during the first stage of exercise rose 61% above baseline values. By peak exercise the mean pulmonary artery wedge pressure was more than double the resting value. Similarly, the right atrial mean pressure increased significantly (p < 0.001) with passive leg elevation and nearly tripled at peak exercise. All values promptly returned to near baseline after exercise. The cardiac output increased 98% during exercise. During early exercise, the rise in cardiac output was mediated primarily by an increase in stroke volume. At rest, there was an abnormal response in right atrial mean pressure during slow deep inspiration in 7 individuals with legs down and in 12 after passive leg elevation (volume loading), including 4 of 10 patients studied beyond 1 year. Abnormal resting and exercise hemodynamics are a common finding after orthotopic cardiac transplantation in the absence of apparent cardiac pathology.

Effects of Fenoterol on Oxygen Transport in Patients with Chronic Airflow Obstruction

A rise in cardiac output and a fall in arterial oxygen tension are well known side effects of bronchodilator drugs, particularly beta-adrenergic agonists. In recent years, fenoterol (Berotec), an effective beta-adrenergic agonist, has been used at increasing rates in asthmatic subjects, as well as in patients with chronic obstructive pulmonary disease (COPD). The effects of fenoterol on systemic hemodynamics or arterial oxygenation (or both) in patients with COPD have not been investigated; in these individuals, who often have increased sympathetic tone and hypoxemia even at rest, cardiovascular stimulation and a fall in arterial oxygen tension would be particularly undesirable side effects. In 14 patients with COPD (seven without a reversible component of airflow obstruction [group 1]; and seven with a reversible component of airflow obstruction [group 2]), we studied all of the important parameters of oxygen transport before and 60 minutes after administration of fenoterol. Studies were performed at rest and after exercise. At baseline, group 1 showed a faster heart rate, a lower cardiac output, a lower arterial oxygen flow, a wider arteriovenous oxygen content difference (C[a-v]O2), and a higher fraction of oxygen extracted by the tissues from a given arterial oxygen flow. In both groups, all measured parameters, including cardiac output and arterial oxygen pressure (PaO2) remained statistically unchanged one hour after administration of fenoterol; with exercise, the heart rate, blood pressure, minute ventilation, oxygen consumption, C(a-v)O2, and the percentage of oxygen extracted from arterial oxygen flow, as well as cardiac output and PaO2, increased in all instances; the exercise responses were not affected by the drug. These results suggest that at the time of its maximal effect on the airways (60 minutes), fenoterol has no untoward effect on the oxygen transport system, at rest or during exercise, in patients with COPD with or without a reversible component.

Pulmonary vasomotor responses to neural activation in man.

Passive adaptation to changes in flow is an established mechanism of regulation of pulmonary vasomotility. The role of the autonomic nervous system is not well defined in man. To separate the neural from the mechanical component (variation in flow) the venous return and the lung blood flow of six normal men (while undergoing haemodynamic diagnostic procedures) were impeded by a balloon tipped catheter placed in the inferior vena cava. Mental arithmetic and cold pressor tests were used as sympathetic activators. When the venous return was impeded cardiac output was reduced by a mean of 540 ml compared with baseline. During the arithmetic test the rise in cardiac output fell from 2140 ml when venous return was unimpeded to 890 ml when venous return was impeded. This stimulus changed from being a slight pulmonary vasodilator to being an unequivocal vasoconstrictor. Cold stimulation had little effect on cardiac output and caused an increase in pulmonary arteriolar resistance. This effect was more than doubled when flow through the lungs was impeded. These observations suggest that a neural regulation of the pulmonary circulation exists in man, which is disclosed (arithmetic test) or potentiated (cold pressor test) when the influence of mechanical factors is prevented or reduced.

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i.e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

Lung mechanics, gas exchange, pulmonary perfusion, and hemodynamics in a canine model of acute Pseudomonas pneumonia.

Acute bilateral hemorrhagic pneumonia was induced in 6 dogs (pneumonia group) by endotracheal inoculation with Pseudomonas aeruginosa. Measurements of lung mechanics, gas exchange, distribution of pulmonary blood flow, and hemodynamics were made prior to inoculation and 5 hr later when pneumonia was established. These findings were compared to the same measurements in 6 other dogs inoculated with a sterile broth (control group). While there were no significant changes in lung mechanics in the control group, pneumonia caused a significant and proportional reduction (42%) in total lung capacity (TLC) and functional residual capacity (FRC). Although tidal lung compliance was reduced in the pneumonia group, neither the specific compliance nor the deflation pressure-volume curve, with lung volume expressed as a percentage of observed TLC, changed significantly. Pneumonia caused marked hypoxemia with a mean increase in shunt and venous admixture of 35% and 52%, respectively, while the control group developed only minimal abnormalities in gas exchange. Perfusion of the consolidated lung region, determined by radioactive microspheres and expressed as a percentage of total pulmonary blood flow, showed a small but significant decrease from baseline (53 +/- 13%) to established pneumonia (44 +/- 14%), while no change in lobar perfusion was seen in the control group. Only the infected animals showed significant changes in hemodynamics with a rise in cardiac output and fall in mean systemic arterial pressure and vascular resistance. We conclude that acute experimental Pseudomonas pneumonia causes reduction of FRC by filling of alveoli with inflammatory exudate and further reduction of TLC by preventing these alveoli from inflating at higher lung volumes without evidence for a change in the elastic properties of the remaining inflated lung; marked hypoxemia caused by maintenance of perfusion of consolidated lung with reduced or absent ventilation; and a hyperdynamic septic hemodynamic state similar to that seen in humans.

6 Rheology of the sickle cell disorders

The sickling process causes secondary changes in cell shape, size, cation and water content, and membrane structure that contribute to the impairment of intrinsic cell deformability (Figure 2). This rheological defect is partially compensated by a low haematocrit, which moderates the rise in whole-blood viscosity, and by a rise in cardiac output which increases capillary flow velocity (Berger and King, 1982). A delicate balance exists between these mechanisms and any local disturbance of this balance by pathological changes in factors extrinsic to the sickle cell (Figure 2) can precipitate vaso-occlusion. There is still considerable controversy over the site (arteriolar, capillary, or venular) of vaso-occlusion, the type of sickle cell (reversibly sickled or irreversibly sickled) that is primarily involved, and the relative importance of extra-erythrocytic precipitating factors such as stasis, hypoxia, hyperosmolality, acidosis, alteration in temperature, acute-phase rise in plasma proteins and leukocytes, prothrombotic changes in coagulation factors and platelets, and adhesion of blood cells to vascular endothelium (Figure 2). A low-grade hypercoagulable state has been described in patients with SS (Leichtman and Brewer, 1978; Richardson et al, 1979) which may be related to the procoagulant effect of the shift of phosphatidyl serine to the outer lipid bilayer of the sickle cell (Chiu et al, 1981; Franck et al, 1985). Platelets appear to accumulate at sites of vaso-occlusion (Siegel et al, 1985) and their migration to the vessel wall may be enhanced by the presence of poorly deformable erythrocytes (Aarts et al, 1984). Endothelial cell damage in the arterial or venous circulation may also contribute (Klug et al, 1982). Thus vaso-occlusion appears to result from a complex interaction between blood cells, plasma proteins and endothelium and any one of several precipitating factors may disturb the fragile steady state and cause a painful crisis. The study of sickle cells by rheological methods has considerable potential for investigating the pathophysiology of vaso-occlusive episodes in the SCD and for monitoring, both in vitro and ex vivo, the efficacy of antisickling compounds. Because of the multiple intrinsic and extrinsic factors that contribute to the rheological defect, it is not yet known which of these should be the primary target for an antisickling agent. In-vitro rheological studies in which different metabolic stresses can be applied to intact sickle cells in the presence of a putative antisickling drug should help to answer this question.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrial natriuretic peptides in man.

Research on the physiological role of atrial peptides in man is limited, and the potential for these peptides, or more stable analogues, in therapeutics is uncertain. It is clear, however, that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are increased in volunteers taking a high sodium diet, and are elevated in patients with heart failure, chronic renal failure, and primary aldosteronism. There is suggestive evidence that IR-ANP levels are increased also in essential hypertension, although overlap with normotensives is considerable. Injection or infusion of atrial peptides into man results in a diuresis, an increased output of urine electrolytes, a fall in blood pressure and a rise in heart rate, suppression of aldosterone and sometimes of renin also, and stimulation of norepinephrine. In essential hypertensives, urinary effects may be greater than in normotensives. Heart failure patients show a rise in cardiac output and falls in both systemic and pulmonary arterial pressure. Over the next few years and especially if specific antagonists can be developed, the physiologic and pathophysiologic roles of atrial peptides in normal man and in clinical disorders should be clarified. It is possible that stable analogues of atrial peptides will find a place in the treatment of cardiac failure, renal failure, and perhaps hypertension.

Cardiovascular and metabolic responses to temperature in Coluber constrictor.

The cardiovascular adjustments associated with elevated metabolic demand caused by rising body temperature were investigated in Coluber constrictor. From 16 to 35 degrees C, O2 consumption increased roughly ninefold. Systemic blood flow, determined by the Fick method, increased approximately 4.5-fold and arteriovenous O2 difference increased approximately 2-fold. Heart rate steadily increased over the temperature range examined. At the cooler temperatures stroke volume also increased but, above approximately 25 degrees C, stroke volume declined with rising temperature. The changes in stroke volume may result from the direct effect of temperature on myocardial contractility. The thermal dependence of blood convection requirement in C. constrictor is similar to changes in air convection requirement determined in a previous study. Consequently the minute ventilation-to-perfusion ratio appears to be independent of temperature, at least from 20 to 35 degrees C. Systemic arterial blood pressure increases with rising body temperature due to the rise in cardiac output, whereas vascular resistance declines. Blood pressure in snakes disturbed by the investigator is roughly two times higher than in resting animals at all temperatures studied. This marked change in blood pressure suggests an "alarm reaction" mediated by the sympathetic nervous system.

Cardiac dynamics during supine exercise in cyclosporine-treated orthotopic heart transplant recipients: Assessment by radionuclide angiography

The mechanisms by which the denervated heart responds to supine exercise were assessed by equilibrium gated radionuclide angiography in 18 cardiac transplant recipients 1 to 25 months (mean 11) after surgery. Results were compared with those in 15 normal subjects. Exercise duration among transplant recipients did not differ significantly from that in normal subjects. The heart rate at rest in transplant patients was 30% higher than in normal volunteers. Heart rate increased only 3% between rest and the first stage of exercise in transplant recipients compared with a 37% increase in the normal group (p less than 0.001). Cardiac output at rest was similar in both groups although the rate of rise of cardiac output and peak cardiac output were significantly lower among the transplant recipients. In early exercise, the means by which cardiac output increased in the transplant patients differed significantly from normal. In the transplant recipients, the left ventricular end-diastolic volume index increased 14% compared with a decrease of 2% in normal subjects (p less than 0.001) during the first stage of exercise. At the same time, the end-systolic volume index increased 6% in the transplant group but decreased 11% in normal subjects (p less than 0.001). These changes resulted in an overall increase in stroke volume by 20% in the transplant group compared with only a slight increase (+3%) in normal subjects (p less than 0.001) during the first stage of exercise. Among transplant recipients, the stroke volume index plateaued after the first stage of exercise, which, in combination with the blunted chronotropic response, resulted in a peak cardiac index 25% lower than that in normal subjects (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Isometric Exercise: Cardiovascular Responses in Normal and Cardiac Populations

Isometric exercise produces a characteristic pressor increase in blood pressure which may be important in maintaining perfusion of muscle during sustained contraction. This response is mediated by combined central and peripheral afferent input to medullary cardiovascular centers. In normal individuals the increase in blood pressure is mediated by a rise in cardiac output with little or no change in systemic vascular resistance. However, the pressor response is also maintained during pharmacologic blockade or surgical denervation by increasing systemic vascular resistance. Left ventricular function is normally maintained or improves in normal subjects and cardiac patients with mild impairment of left ventricular contractility. Patients with poor left ventricular function may show deterioration during isometric exercise, although this pattern of response is difficult to predict from resting studies. Recent studies have shown that patients with uncomplicated myocardial infarction can perform submaximum isometric exercise such as carrying weights in the range of 30 to 50 lb without difficulty or adverse responses. In addition, many patients who show ischemic ST depression or angina during dynamic exercise may have a reduced ischemic response during isometric or combined isometric and dynamic exercise. Isometric exercises are frequently encountered in activities of daily living and many occupational tasks. Cardiac patients should be gradually exposed to submaximum isometric training in supervised cardiac rehabilitation programs. Specific job tasks that require isometric or combined isometric and dynamic activities may be evaluated by work simulation studies. This approach to cardiac rehabilitation may facilitate patients who wish to return to a job requiring frequent isometric muscle contraction. Finally, there is a need for additional research on the long-term effects of isometric exercise training on left ventricular hypertrophy and performance. The vigorous training regimens currently utilized by international class and professional athletes should stimulate longitudinal studies of physiologic and pathophysiologic outcomes of intense isometric exercise training programs.

Pulmonary vascular obstruction in severe ARDS: angiographic alterations after i.v. fibrinolytic therapy.

IV streptokinase was infused to test the potential reversibility of adult respiratory distress syndrome (ARDS) associated pulmonary vascular thrombosis in five patients suffering from severe ARDS with elevated mean pulmonary artery pressure, increased pulmonary vascular resistance, and angiographically documented pulmonary vascular thrombosis. At 48 hr there was clearance of obstructions in arteries larger than 1 mm in diameter in all patients, increased filling of the microvasculature and small arteries less than 1 mm in diameter in four patients, a fall in pulmonary vascular resistance in all patients, a rise in cardiac output in four patients, improved oxygenation (PAO2/FlO2) in three patients, and variable changes in shunt fraction and ventilator pressures. Expressed as a mean fraction of the preinfusion controls, the postinfusion physiologic values were pulmonary artery pressure = 0.89 mm Hg, pulmonary vascular resistance = 0.68 mm Hg X min/L, cardiac output = 1.36 L/min, central venous pressure = 0.77 cm H2O, pulmonary capillary wedge pressure = 0.92 mm Hg, PAO2/FlO2 = 1.08, and shunt fraction = 0.95. Follow-up angiography showed no evidence of reocclusion. Postmortem studies of the three nonsurvivors confirmed recanalization of thrombosed pulmonary arteries. One documented bleeding episode occurred. We conclude that fibrinolytic infusion can lyse thrombi and possibly improve hemodynamics and oxygenation in ARDS-associated pulmonary vascular thrombosis.

Acceptable hematocrit levels in surgical patients.

AbstractThe ready availability of blood and blood components has resulted in a liberal use of blood transfusions; however, the transfusion of blood is still associated with significant risks for the recipient. The appearance of the acquired immunodeficiency syndrome and the evidence that homologous blood can induce immunosuppression and thereby impair the host resistance of surgical patients has led to a reconsideration of the indications for blood transfusions. It has also fostered application of alternative methods with the aim of reducing the number of homologous blood transfusions. Based on the data available from studies on intentional perioperative hemodilution in patients undergoing elective surgery, and data from patients in intensive care, a hematocrit level of about 30% is acceptable for surgical patients, provided oxygen transport is not impaired by the reduced saturation of arterial blood or inadequate perfusion. The basic mechanism that compensates for the reduced oxygen capacity of the blood is a rise in cardiac output and stroke volume, both depending on adequate venous return and myocardial function. The hematocrit setpoint has to be determined for the individual patient with regard to the history of the underlying disease, circulating blood volume, and actual oxygen needs. By accepting a perioperative hematocrit level of 30% for patients without respiratory and cardiac disease or increased oxygen demand, respectively, the number of transfusions of homologous blood can be reduced and dangerous side effects can be avoided.

Electrocardiographically discrete right and left ventricular QRS complexes: A case report

A patient with congestive cardiomyopathy manifested a right ventricular QRS followed after 80 msec. by a left ventricular QRS in response to a single atrial depolarization. The ventricular sequence was reversible when the left ventricle was paced directly. Virtually the entire ipsilateral ventricular ejection period occurred during diastolic filling of the contralateral ventricle. Triggered left ventricular pacing, using the right ventricular electrogram as trigger, shortened the QRSRV-QRSLV interval and resulted in a reduction of left ventricular filling pressure and a significant rise in cardiac output. These findings indicated an independent contribution of this unique form of interventricular conduction disturbance to deterioration in hemodynamic performance.

Present state of intentional hemodilution.

Preoperative intentional hemodilution is induced by isovolemic exchange of whole blood with colloid solutions in order to gain autologous blood while maintaining normovolemia. The basic mechanism that compensates for the fall of oxygen capacity of the diluted blood is the rise in cardiac output, and organ blood flow, factors that result from the improved fluidity of blood at lower hematocrits. Normal tissues maintain adequate oxygenation during hemodilution through the enhanced redistribution of blood. In ischemic tissues this effect is enhanced, and causes an increase in the oxygenation of ischemic tissues. Limited preoperative and intraoperative hemodilution are alternatives to donor blood transfusion in patients undergoing elective surgery. In shock patients the hemodilution achieved with red cell free primary volume substitutes is an effective treatment for shock-induced microcirculatory disorders; furthermore, intentional hemodilution is the most effectual hemorheological therapy for the treatment of ischemic disease.

Nitroprusside vs. a Nitroprusside-Trimethaphan Mixture for Induced Hypotension

Changes in hemodynamic variables and whole blood cyanide and plasma thiocyanate concentrations associated with the infusion of sodium nitroprusside were compared with those during administration of a mixture of sodium nitroprusside (25 mg) and trimethaphan camsylate (250 mg) in a solution of 5% dextrose in water in twenty subjects who required deliberate hypotension for major orthopedic procedures. Subjects were randomly assigned to receive nitroprusside alone (group 1; n = 10) or the nitroprusside-trimethaphan mixture (group 2; n = 10). All subjects received a similar anesthetic technique, consisting of 5 mg/kg thiopental, 1 mg/kg succinylcholine, 1% halothane, 0.2 mg/kg metocurine, and 60% nitrous oxide in oxygen. Mean arterial pressure decreased and was maintained at 55 mm Hg for 258 ± 4 and 266 ± 8 minutes in groups 1 and 2. Arterial hypotension was associated with a rise in cardiac output and heart rate in group 1 but not in group 2. Subjects in group 2 required less nitroprusside than did those in group 1 (1.39 ± 0.3 and 5.82 ± 0.63 µg/kg/min) because of the synergistic or additive action of the combination. After 4 hours of hypotension, the whole blood cyanide level rose from 3.5 ± 1.1 to 96.6 ± 14.0 µg/dl (1.35 ± 0.27 to 37.2 ± 5.4 µmol/L) in group 1 and from 3.7 ± 1.1 to 22.7 ± 4.2 µg/dl (1.42 ± 0.4 to 8.7 ± 1.6 µmol/L) in group 2. Plasma thiocyanate levels rose 2 hours after nitroprusside termination. Significant changes in pH and base deficit occurred late in the course of hypotension in group 1 only; there was a correlation (r = 0.896) between peak blood cyanide levels and decreases in base excess. A rebound increase in mean arterial pressure after termination of hypotension occurred only in group 1. Mean blood pressure increased an average of 13.5 (range 6 to 27) and 21.5 (range 8 to 32) mm Hg over the prehypotension and awake levels. Blood pressure was maximally increased 15 minutes after the end of the infusion and was associated with an increase in systemic vascular resistance; cardiac output did not change. One subject developed ST segment depression and required reinstitution of nitroprusside infusion. There were no adverse effects during or after cessation of the drug mixture. Clinical Pharmacology and Therapeutics (1985) 37, 264–270; doi:10.1038/clpt.1985.38

Effects of Secretin Infusion on Myocardial Performance and Metabolism in the Dog

The effects of pharmacological doses of secretin were studied in closed-chest, pentobarbital anesthetized dogs. Infusion of secretin 16 clinical units (CU)/kg-h caused a rise in cardiac output (p less than 0.01), peak first derivative of the left ventricular pressure (p less than 0.01), and heart rate (p less than 0.01) and a fall in systemic arteriolar resistance (p less than 0.01) and left ventricular end-diastolic pressure (p less than 0.01). Stroke volume did not change significantly. Myocardial blood flow and oxygen consumption were unchanged. Secretin caused reductions in arterial lactate (p less than 0.01) and glucose (p less than 0.05) concentrations, and arterial concentrations of free fatty acids and insulin were unaltered. There was no change in myocardial uptake of lactate, glucose, or FFA. Secretin 64 CU/kg-h infused in two dogs caused further changes of the hemodynamic variables. Thus, secretin enhances left ventricular function in intact anesthetized dog by combined vasodilating, inotropic, and chronotropic effects, without changing myocardial oxygen or substrate uptake.

A structurally novel stimulator of guanylate cyclase with long-lasting hypotensive activity in the dog

Studies were undertaken to characterize the activity of diphenyliodonium hexafluorophosphate (DIFP) as a structurally novel stimulator of soluble guanylate cyclase from rat lung and make comparisons to the activity of sodium nitroprusside (SNP). In addition, the effectsof these two compounds on several cardiovascular parameters in anesthetized dogs were determined. DIFP stipulated guanylate cyclase activity within the same concentration range (10–300 μM) as SNP, causing a maximal 2-3-fold activation. The activities of both SNP and DIFP were dependent on the presence of dithiothreitol and inhibited by methylene blue. In anesthetized dogs, DIFP (i.v.) elicited a dose-related, long-lasting fall (> 3 h) in mean arterial pressure (MAP) which was accompanied by a reduction in total peripheral resistance and a transient rise in cardiac output. These effects on MAP were similar to those of SNP except they were of a much longer duration. In addition, both SNP and DIFP produced slight bradycardia and reduced negative dP/dt. The e results suggest that DIFP and SNP, while structurally dissimilar, activate guanylate cyclase by a related mechanism which may be involved in vascular relaxation leading to reduced blood pressure.

Baseline hemodynamic state and response to hemodilution in patients with acute cerebral ischemia.

Hemodynamic data were obtained in 9 patients (mean age 65 yrs) with carotid territory cerebral infarct within the preceding 24 hours (mean 14 +/- 8) as part of a pilot study testing the feasibility and safety of hypervolemic hemodilution. Pulmonary arterial catheters (PACs) were placed without complication in all patients, and after baseline measurements were obtained, up to 1500 cc of 6% hetastarch in 0.9% sodium chloride was administered the first day and up to 1000 cc per day the second and third days. Pulmonary wedge pressure (PWP) rose from 6.3 +/- 3.5 to 14.4 +/- 3.4 mm Hg (p less than 0.001) without development of congestive heart failure in any patient. This was accompanied by a drop in hematocrit (Hct) from 40.3 +/- 3.4 to 32.9 +/- 2.0 (p less than 0.001) and rise in cardiac output (CO) from 4.3 +/- 1.0 to 5.3 +/- 0.6 (p less than 0.05). Phlebotomy of 250 cc was performed in 2 patients and 500 cc in one in order to reduce Hct to desired levels. The volume of fluid needed to raise PWP to 15 was unpredictable (2361 +/- 1106 cc) and therefore PACs were necessary to monitor the rate and volume of fluid administration. The data show that PWP is sufficiently low and Hct sufficiently high following stroke in most patients that hemodilution by volume expansion with phlebotomy added if necessary can be undertaken safely with appropriate monitoring of hemodynamic function, and that this therapy results in optimal reduction of Hct and increased CO without risk of hypotension.

Myocardial blood flow during cardiac tamponade in dogs with coronary occlusion: Effects of isoproterenol

To determine the effects of cardiac tamponade in dogs with ligation of the left anterior descending coronary artery, fluid was introduced into the pericardial space to raise right and left atrial and pericardial pressures, first to 7 to 9 mm Hg and then to 11 to 12 mm Hg. Normal and ischemic myocardial blood flow fell approximately 20% to 25% during mild tamponade (1.27 ± 0.16 to 1.00 ± 0.06 ml/min/gm and 0.52 ± 0.12 to 0.39 ± 0.08 ml/min/gm, respectively) and by 50% during moderate tamponade (0.66 ± 0.08 and 0.23 ± 0.05 ml/min/gm, respectively). The inner/outer left ventricular wall blood flow ratio decreased modestly from 1.16 to 1.08 ( p < 0.025) in normal areas but increased from 0.53 to 0.61 ( p < 0.05) in the ischemic regions, suggesting possible epicardial vessel compression. Isoproterenol resulted in prompt decreases in pericardial and filling pressures, 16% increase in aortic pressure, and 200% rise in cardiac output. Normal myocardial blood flow more than doubled (1.55 ± 0.12 ml/min/gm, p < 0.001). Although average ischemic blood flow rose slightly to 0.42 ± 0.10 ml/min/gm, the increase was not significant. Furthermore, changes in ischemic blood flow were heterogeneous with frank decrease in one dog. Therefore, although isoproterenol has salutary hemodynamic effects, its unpredictable action on myocardial blood flow should cause one to use it cautiously in those with tamponade who are believed to have coronary occlusive disease.