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PubMed2000

Effects on dogs of surface-induced hypothermia and rewarming on the right heart function and pulmonary circulation.

Hypothermia is commonly found in accidents on land and at sea, yet its pulmonary circulatory effects have not been studied before. To study the effects of hypothermia on the right heart function and pulmonary circulation, cardiac catheterization was carried out on nine anaesthetized beagle dogs. The dogs were cooled between ice bags until the temperature in the pulmonary artery was 25 degrees C and then rewarmed using a heating box especially constructed for this purpose. Heart rate decreased significantly (P < 0.01) during cooling. Cardiac output also diminished mainly because of decreased heart rate. Total pulmonary resistance increased in the cold (P < 0.05) and returned to the initial level during rewarming. The peak rate of increase in pressure (dP/dtmax) of the right ventricular pressure curve did not show any significant change. Retardation in relaxation in hypothermia was indicated by an increase (P < 0.01) in the peak negative dP/dt of the right ventricular pressure curve. According to our results, the contraction rate did not change, but the relaxation rate decreased significantly during cooling. No signs of heart failure were observed and all parameters returned to normal during rewarming. In conclusion, right ventricular function was not compromised even during deep hypothermia.

Animals↗
PubMed1991

The role of nitric oxide as an endogenous regulator of platelet and neutrophil activation within the pulmonary circulation of the rabbit.

1. Intravenous (i.v.) administration of adenosine diphosphate (ADP), platelet activating factor (PAF) and thrombin induced a dose-related accumulation of 111indium-labelled platelets within the thoracic region of anaesthetized rabbits. 2. I.v. administration of the inhibitor of NO biosynthesis, L-NG-nitro arginine methyl ester (L-NAME; 10 mg kg-1) significantly potentiated the peak platelet accumulation induced by ADP, PAF and thrombin. Additionally L-NAME prolonged the disaggregation of platelets in comparison to D-NAME (10 mg kg-1). Such changes were reversible by the administration of L-arginine (900 mg kg-1). 3. I.v. administration of PAF induced a small accumulation of 111indium-labelled neutrophils within the pulmonary circulation which could be greatly potentiated by pretreatment of the animals with L-NAME. In contrast, thrombin administration did not cause significant accumulation of 11indium-labelled erythrocytes in the pulmonary circulation of anaesthetized rabbits. 4. Intracarotid (i.c.) administration of thrombin induced a marked accumulation of radiolabelled platelets within the cranial vasculature which was not potentiated by the prior administration of L-NAME (at either 10 mg kg-1 or 100 mg kg-1). 5. These results suggest that endogenous NO may regulate platelet and polymorphonuclear leukocyte activation within the pulmonary but not the cerebral circulation of rabbits.

Adenosine Diphosphate↗
PubMed1992

Pressure-flow relationships of the pulmonary circulation during endotoxin infusion in intact dogs.

BACKGROUND AND METHODS: We aimed to characterize the effects of an endotoxin insult (Escherichia coli 0127:B8) on the relationships between pulmonary vascular pressure and flow in intact dogs. To achieve this goal, multipoint plots of total pressure gradient, arterial pressure gradient, and venous pressure gradient vs. flow were generated by graded inflation of a right atrial balloon, which was used to vary flow. The partitioning of the total pressure decrease across the pulmonary vasculature (total pressure gradient = pulmonary arterial pressure-pulmonary artery occlusion pressure [PAOP]) into gradients across pulmonary arterial (arterial pressure gradient = pulmonary arterial pressure--effective capillary pressure) and pulmonary venous (venous pressure gradient = effective capillary pressure--PAOP) regions was assessed by a waveform mathematical analysis of the pulmonary arterial pressure profile during arterial occlusion, with computation of both PAOP and effective pulmonary capillary pressures. Slopes and extrapolated pressure intercepts from linear regression fits to the pulmonary vascular pressure/flow plots were determined in seven dogs after a 2-hr endotoxic infusion interval and were compared with the corresponding values that characterized a similar group of sham-operated dogs. RESULTS: Under normal conditions, the extrapolated pressure intercept for pulmonary arterial pressure gradient was virtually 0 mm Hg; for total pulmonary arterial pressure gradient and pulmonary venous pressure gradient, the mean extrapolated pressure intercepts were substantially positive: 2.4 +/- 0.2 and 2.1 +/- 0.3 mm Hg, respectively. Endotoxin infusion at 0.25 micrograms/kg/min significantly increased the pressure intercepts from 2.4 to 8.7 and from 2.1 to 8.3 mm Hg of total pressure gradient and venous pressure gradient vs. flow, respectively. This infusion produced a minor, nonsignificant change in the intercept of arterial pressure gradient vs. flow, whereas it increased its slope significantly (p less than .05) from 0.036 to 0.081 mm Hg/mL/min/kg. CONCLUSIONS: These data suggest that endotoxin's effects on vascular resistance are exerted at two different loci such that these effects are additive. These endotoxin-induced effects consisted of increased vascular resistance of the arterial segment and appearance of a Starling resistor at the venous side of the pulmonary circulation, which acted as the relevant back-pressure to flow.

Animals↗
PubMed1991

Disappearance of molsidomine effects on pulmonary circulation of patients with chronic obstructive pulmonary disease after a three week treatment.

The effect of oral molsidomine (M) on the pulmonary artery hypertension of patients with chronic obstructive pulmonary disease (COPD) was investigated during an acute study (4 mg once) and after a 3 week-treatment (3 times 4 mg a day), on a double-blind basis in 16 patients, 8 receiving a placebo, and 8 molsidomine. Ventilatory and cardiocirculatory indices were obtained at rest and during exercise. When acutely given, molsidomine reduces the mean pulmonary arterial pressure (PAP), the pulmonary vascular resistance (PVR) and the arterial O2 partial pressure (PaO2), increasing heart rate (HR) as well as the alveo-arterial O2 partial pressure difference (P(A-a)O2). During exercise, pulmonary arterial pressure and pulmonary vascular resistance decrease while heart rate increases without modification of arterial blood gases. After a 3-week treatment, molsidomine no more improves any index but significantly reduces cardiac output during exercise and consequently the O2 delivery to the tissues. The same feature has already been observed for other nitrates. It thus seems inappropriate to prescribe nitrates or nitrate-like drugs to chronic obstructive pulmonary disease patients with a view to lower their pulmonary hypertension.

Blood Gas Analysis↗
PubMed1993

Protective effects of E5, an antiendotoxin monoclonal antibody, in the ovine pulmonary circulation.

The cross-protective effects of a murine immunoglobulin M monoclonal antilipid A antibody (E5 MAb) were tested by challenging awake sheep with mixtures of in vitro incubated E5 MAb (0.02 mg/kg) with lipopolysaccharide (LPS, 0.02 micrograms/kg) derived from Escherichia coli O111:B4, E. coli O55:B5, or Serratia marcescens. Intravenous infusion of these LPS preparations without antibody into awake sheep produced a similar pattern of fever, leukopenia, plasma thromboxane B2 (TxB2) release, and acute pulmonary vasoconstriction with pulmonary hypertension. The addition of MAb E5 to LPS from E. coli O111:B4 reduced these responses to the LPS in a fashion comparable to that achieved with an MAb specific to the E. coli O111:B4 O-side chain. Incubation of LPS derived from E. coli O55:B5 with the E5 MAb only slightly diminished acute pulmonary hypertension, the delayed temperature increase, and the degree of leukopenia (all P = NS) but reduced the mean peak TxB2 at 60 min (P < 0.05) compared with a control infusion of E. coli O55:B5 LPS. We were unable to demonstrate any protective effects on the pulmonary circulation from incubating E5 with LPS derived from S. marcescens. Preincubation of B55 MAb (a murine immunoglobulin M MAb directed against a human milk fat globulin), the control antibody, with LPS from E. coli 0111:B4 decreased the mean peak TxB2 but had no effect on the other parameters. We conclude that incubating E5 with LPS protects the pulmonary circulation of sheep from challenge with LPS derived from the parent E. coli strain. There were trends toward protection by E5 against LPS from 055:B5 E. coli, but these did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Squamous cells in the maternal pulmonary circulation.

Identification of squamous cells in the maternal pulmonary arterial circulation, either at autopsy or in blood aspirated from a pulmonary artery catheter, is currently regarded as pathognomonic for amniotic fluid embolism. Sixteen pregnant women underwent pulmonary arterial catheterization for a variety of medical indications. Examination of the buffy coat fraction of the distal lumen aspirate resulted in the identification of squamous cells in all cases. Squamous cells were similarly identified in control specimens from 17 nonpregnant patients; however, the difference in cell count between the pregnant and nonpregnant patients was significant. Such cells presumably reflect, in part, bloodstream contamination from sites of venous access. Reliable differentiation of adult from fetal squamous cells is not possible; however, the significant increase in cell count documented in pregnant patients suggests a possible fetal origin for some squamous cells detected during pregnancy. The detection of squamous cells in the pulmonary arterial circulation of pregnant women is not pathognomonic for amniotic fluid embolism. In a critically ill obstetric patient, such a finding should not deter the clinician from a thorough search for other causes of hemodynamic instability.

Cell Count↗
PubMed2000

Prolonged infusions of estradiol dilate the ovine fetal pulmonary circulation.

Factors mediating both the rapid and sustained fall in pulmonary vascular resistance (PVR) at birth are incompletely understood. Acute or prolonged estrogen treatment causes vasodilation of several vascular beds in adults. Although fetal estrogen levels rise in late gestation, their effects in the fetal pulmonary circulation have not been studied. To determine whether estrogens can cause pulmonary vasodilation in the fetus, we infused 17beta-estradiol (E2) into the left pulmonary artery (LPA) of chronically catheterized fetal lambs, measured pulmonary artery pressure and LPA blood flow, and calculated PVR. Brief E2 administration (1-, 10-, and 100-microg doses) did not change baseline pulmonary hemodynamics and failed to enhance endothelium-dependent vasodilation as assessed by the dilator response to acetylcholine. However, prolonged E2 infusion (2- 8 d) caused a 2.6-fold increase in pulmonary blood flow (73+/-6 versus 188+/-44 mL/min, baseline versus E2 treatment, p<0.05), and the response was sustained for at least several hours. Treatment with the nitric oxide synthase inhibitor nitro-L-arginine (L-NA) reversed the E2-induced fall in PVR (0.15+/-0.05 versus 0.51+/-0.15 mm Hg/mL/min; before versus after L-NA, p<0.05). Endothelial nitric oxide synthase expression and endothelin-1 content were not different in E2-responders and controls, suggesting that altered expression of these mediators did not account for the increased flow. We conclude that prolonged E2 infusion causes an unusual pattern of vasodilation in the ovine fetal lung. On the basis of these observations of exogenous E2 treatment, we speculate that endogenous E2 enhances pulmonary vasodilation at birth.

Animals↗
PubMed1990

Pulmonary vascular cine MR imaging: a noninvasive approach to dynamic imaging of the pulmonary circulation.

Cine gradient-recalled magnetic resonance (MR) imaging, which has flow sensitivity and high temporal resolution, may potentially yield both morphologic and dynamic flow-related information in the pulmonary vasculature. The authors used this modality to evaluate pulmonary vessels in 12 healthy subjects and in 14 patients with a variety of cardiopulmonary disorders. Normal pulmonary arteries and veins were characterized by distinctive signal intensity and diameter variations as well as motion of the vessels during the cardiac cycle. Patients with pulmonary arterial hypertension demonstrated loss of the normal pulsatile systolic increase and diastolic decline in velocity-related signal intensity and in diameter of the proximal pulmonary arteries. Disorders of pulmonary venous signal and diameter profiles during the cardiac cycle, which show a characteristic biphasic pattern in healthy subjects, were identified in five patients with mitral valvular disease. These initial results indicate that cine MR imaging techniques hold promise in the evaluation of pathophysiologic conditions in the pulmonary circulation.

Adult↗
PubMed1994

Perioperative management of pulmonary circulation in children with congenital cardiac defects.

Congenital cardiac defects and the clinical symptoms they exhibit are affected intimately by the relation they have with pulmonary circulation. Cardiac lesions that increase pulmonary blood flow often occur clinically with signs and symptoms of congestive heart failure, including hepatomegaly, tachycardia, diaphoresis, and feeding difficulties. However, in the neonatal period, pulmonary vascular resistance often remains elevated, decreasing the pulmonary blood flow and, therefore, severity of symptoms. Cardiac lesions that reduce pulmonary blood flow often manifest early in life with clinical signs and symptoms of cyanosis, tachypnea, and acidosis. Finally, cardiac lesions that result in isolated pulmonary blood flow manifest immediately in the neonatal period, with profound cyanosis and acidosis. In all three groups of cardiac anomalies, critical care nurses play a key role in the control of pulmonary vascular resistance and blood flow by collaborating in therapies designed to increase, decrease, or promote mixing to reduce morbidity and mortality.

Critical Care↗
PubMed1977

Pulmonary circulation--vertebral venous interconnections in the chickens.

Injections of India ink colored blood, latex, and plastic followed by study of corrosion casts and dissections were used to determine the interconnections of the vertebral venous system and pulmonary circulation in the chicken. Multiple, minute connections are found to the intercostal veins, small mesenteric veins and others connected to the vertebral venous system. Thus, blood can flow in quantities between the vertebral venous system and the pulmonary circulation depending upon pressure gradients.

Animals↗
PubMed1992

Hemodynamic effects of exogenous nitric oxide in ovine transitional pulmonary circulation.

To determine the hemodynamic effects of exogenous nitric oxide (NO) on the immature pulmonary circulation, we studied the response to NO inhalation in 19 mechanically ventilated late-gestation ovine fetuses in three separate protocols. In protocol 1, we examined the relative effects of 1) mechanical ventilation while maintaining fetal arterial O2 tension (PaO2) constant [fractional inspired O2 concentration (FIO2) less than 0.10)], 2) NO inhalation [5-20 parts per million (ppm)] at fetal PaO2, and 3) high FIO2 (1.00) (n = 7). NO increased left pulmonary artery blood flow (Qlpa) in a dose-dependent fashion, from 254 +/- 62 (baseline) to 398 +/- 49 ml/min with 20 ppm NO (P less than 0.001). The response of Qlpa to a FIO2 equal to 1.00 was not different from NO alone. Systemic arterial pressure was not affected by NO. In protocol 2 we studied the effects of prolonged NO inhalation (2 h, 20 ppm) during mechanical ventilation with low FIO2 (n = 4). NO increased Qlpa from 267 +/- 92 to 468 +/- 75 ml/min at 10 min of NO inhalation (P less than 0.001). The increase in Qlpa was sustained during the entire 2-h study period. In protocol 3 we measured left ventricular output (LVO), systemic vascular resistance (SVR), and ductus arteriosus shunting using radiolabeled microspheres (n = 8) during baseline mechanical ventilation and 20 ppm NO inhalation. LVO and SVR were not significantly different in the two study periods; however, the percentage of LVO that reached the lungs (predominantly left-to-right shunting across the ductus arteriosus) increased from 18 +/- 5 to 43 +/- 4% during NO inhalation.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1998

Role of EDRF in pulmonary circulation during sustained hypoxia.

The pulmonary artery pressure (PAP) response to hypoxia is characterized by an initial vasoconstriction followed by vasodilation. Pulmonary vessels can release endothelium-derived relaxing factor (EDRF), which is considered to be nitric oxide (NO), but the role of EDRF in the regulation of normal and hypoxic pulmonary vascular tone is still uncertain. We designed this study to address the in vivo role of EDRF in vasodilation during sustained hypoxia. We studied the effects of an EDRF-synthesis inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), on the pulmonary vascular response to sustained hypoxia (10% O2, 20 min) in normoxic (N) and chronically hypoxic (CH) rats. Biphasic PAP response was observed in N rats, whereas PAP was unchanged in CH rats during sustained hypoxic exposure. The L-NAME-induced PAP increase during normoxia was greater in CH than in N rats, suggesting that basal EDRF plays an important role in attenuating the severity of pulmonary hypertension in CH rats. Administration of L-NAME increased the initial increment in PAP by acute hypoxia and shifted the PAP response upward throughout sustained hypoxia, while still showing the biphasic pattern, in N rats. In contrast, PAP increased acutely and remained elevated with little recovery in the late phase in CH rats. The inducible NO synthase messenger RNA (mRNA) expression and protein showed greater increases in the lungs of CH than in N rats. These results suggest that EDRF release during sustained hypoxia may partly contribute to the roll-off in PAP response during sustained hypoxia in N rats, and that augmented EDRF may prevent a further increase in PAP during chronic hypoxia.

Alkalosis↗