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Isoproterenol, dobutamine, dopamine, and nitroprusside are four vasoactive drugs used to decrease pulmonary arterial pressure and increase cardiac output in newborns, infants, and children with sepsis. Thromboxane A2 likely produces some of the hemodynamic changes in sepsis, and U46619, a thromboxane A2 mimetic, produces similar changes in lambs. We studied the hemodynamic effects of these four vasoactive drugs in 10 spontaneously breathing newborn lambs during an infusion of U46619. After baseline hemodynamic measurements, U46619 (1-2 micrograms/kg/min) was infused to increase pulmonary arterial pressure and to decrease cardiac output. Then, either isoproterenol (0.05-1.0 micrograms/kg/min), dobutamine (5-20 micrograms/kg/min), dopamine (3-30 micrograms/kg/min), or nitroprusside (0.5-10.0 micrograms/kg/min) was infused. Every 10 min, measurements were repeated and the dose increased. U46619 significantly increased pulmonary arterial pressure by 182% and decreased cardiac output by 25% (p less than 0.05). Isoproterenol decreased pulmonary arterial pressure by 30% (p less than 0.05) and increased cardiac output by 25% (p less than 0.05) at low doses, and increased cardiac output by 115% at the maximum dose (p less than 0.05). Dobutamine decreased pulmonary arterial pressure by 11% (p less than 0.05) at low doses, and increased cardiac output by 28% (p less than 0.05) at low doses, and increased cardiac output by 71% at the maximum dose (p less than 0.05). Dopamine did not decrease pulmonary arterial pressure or increase cardiac output. Nitroprusside decreased pulmonary arterial pressure by 11% at the maximum dose (p less than 0.05). Isoproterenol and dobutamine may be more useful than dopamine and nitroprusside in the management of pulmonary hypertension and decreased cardiac output during sepsis.

The effects of surfactant (S) replacement therapy for hyaliane membrane disease (HMD) on cardiac output and patent ductus arteriosus (PDA) volumetric shunting is unknown. Also natural surfactant has been implicated in intraventricular hemorrhage in the preterm secondary to decreased cardiac output without altering ventilatory parameters

Unanesthetized newborn pigs were studied to evaluate the immediate (10 min) and delayed (45 min) effects of increased ventilation pressure coupled with cyclooxygenase inhibition. Cardiac output and cerebral blood flow were measured at a low (5 cm H2O) and high (30 cm H2O) mean airway pressure (Paw) before and 45 min after 5 mg/kg of indomethacin. In a second group, these parameters were also measured 10 min after indomethacin was given during ventilation at a Paw of 30 cm H2O. Before treatment with indomethacin, increasing Paw decreased cardiac output without affecting cerebral blood flow. Baseline (Paw = 5 cm H2O) cerebral blood flow decreased 40% 45 min after indomethacin treatment. Adding the stress of a ventilation-induced drop in cardiac output did not further depress cerebral blood flow. When indomethacin was administered during high Paw, cerebral blood flow decreased markedly within 10 min. Cerebral oxygen consumption was maintained by increasing oxygen extraction. Therefore, indomethacin decreases cerebral blood flow at a high Paw. The fall in cerebral blood flow decreases brain oxygen delivery. However, cerebral oxygen consumption is maintained by an increase in oxygen extraction

Decreased cardiac output (CO) and systemic oxygen transport (SOT) in polycythemia (P) are attributed to increased blood viscosity and regarded as potentially harmful. Since P is common in cyanotic heart disease, we studied its effects on CO, SOT and left ventricular coronary blood flow (CBF) and oxygen transport (LVOT) in dogs with acute isovolumlc P. Hematocrit increase to 65-70% caused falls in CO and SOT; despite P, CO rose with hypoxemia or adenosine infusion. P markedly decreased CBF and cardiac work; slightly decreased LVOT, myocardial oxygen consumption and coronary sinus oxygen saturation; and increased coronary vascular resistance(Rc). Cardiac stress (pacing, aortic stenosis, arteriovenous fistula), hypoxemia and adenosine infusion lowered Rc. Changes in LVOT were more closely related to changes in pressure work and myocardial oxygen consumption than to hematocrit. With maximal coronary vasodilatation, Rc doubled when hematocrit rose from 45% to 65%. Our results Indicate that autoregulation is more important than viscosity in regulating CO, CBF, SOT and LVOT in P. With maximal coronary vasodilatation, however, increased blood viscosity in P reduces LVOT and suggests that with maximal stress there could be ischemlc myocardial damage.

While P commonly occurs in patients with H most hemodynamic studies of P have been done with normoxia. This study examined the combined effects of P and H. In 11 splenectomized, anesthetized dogs hematocrit was increased=42.6±1.2 to 65.5±0.6 (SEM)% by isovolumic exchanges with fresh canine packed RBC's. studies were done during normoxia (N) (PaO2 113.8±4.2 mmHg) and H (PaO2 40.5±1.6). P alone increased pulmonary vascular resistance (PVR) 112±5.4% (p

Shifts in the number and maturity of blood neutrophils serve as important diagnostic aids. Mature neutrophils (PMN) circulate in two pools, marginating and circulating but it is not known if immature neutrophils (bands) do and if they are regulated by the same physiologic controls. The kinetics of circulating PMN and bands was studied in six week old pigs who were anesthetized with halothane, intubated and ventilated. During 5hr of observation, the number (mean ± SEM; x109/L) of PMN (5.3 ± 0.4) and bands (0.7 ± 0.1) remained constant. Ten min after PMN demargination was induced by adrenalin (5ml/10,000 IV), PMN increased by 2 fold while the number of bands did not change. When pigs were cooled to 29°C over 60 min, PMN fell from 5.3 ± 0.7 to 3.4 ± 0.6. This was due to increased margination secondary to decreased cardiac output and bradycardia. In contrast, circulating bands did not fall over the 5hr of observation. When endotoxin (E. coli 0111: B4) was given to hypothermic pigs (29°C), the number of circulating PMN did not increase over preinjection values while bands increased from 0.7 ± 0.2 to 4.9 ± 1.6. Our findings suggest that physiologic controls affecting PMNs and bands may differ. Bands may not circulate in the same blood pools as PMN do. The number of bands may help identify different causes of leukocytosis. In conditions causing increased PMN margination, for example bradycardia and hypotension, bacterial infections may be associated with an increase in circulating bands.