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Biomedical subjects

F van Bel

Publications and source records attributed to F van Bel.

At least 37 records · Page 2Linked to original sources

Haemodynamic consequences of phototherapy in term infants.

UNLABELLED: The effect of blue-light phototherapy on cardiac output and brain and kidney perfusion was studied in 12 term infants with pulsed Doppler ultrasound. Mean (+/-SD) gestational age and birth weight were 39.0 (+/-1.6) weeks and 3438 (+/-533) g respectively. Mean (+/-SD) age of the infants at which phototherapy was initiated was 3.5 (+/-0.8) days. Left ventricular output (LVO), mean left pulmonary artery blood flow (LPA), mean blood flow velocities of the internal carotid (CBFV) and renal (RBFV) arteries were studied in all infants prior to the onset of phototherapy, 30 min, 2 h, and 12 h after initiation of phototherapy, and before and 12-24 h after discontinuation of phototherapy. LVO decreased immediately after the onset of phototherapy. However, after 12 h, LVO returned to pre-phototherapy values. LPA increased significantly after 12 h of exposure. LPA returned to pre-phototherapy values after discontinuation of phototherapy. CBFV increased, whereas RBFV decreased significantly after 2 h of exposure. After discontinuation of phototherapy CBFV as well as RBFV values returned to pre-phototherapy values. CONCLUSION: Phototherapy does affect cardiac output and organ blood flow velocity in term infants. After termination of phototherapy the effect of phototherapy disappears.

Blood Flow Velocity↗

Electrocortical brain activity during hypoxia and hypotension in anesthetized newborn lambs.

Blood gas and blood pressure disturbances do influence cerebral blood flow in newborns. To what extent cerebral blood flow changes affect electrocortical brain activity remains uncertain. We studied the effect of severe hypoxia and hemorrhagic hypotension on carotid artery blood flow and electrocortical brain activity in newborn anesthetized lambs. During hypoxia carotid artery blood flow increased significantly, whereas electrocortical brain activity remained unchanged. The hemorrhagic hypotension study showed that the lower limit of the autoregulatory ability of the cerebral vascular bed was 60 mmHg. Electrocortical brain activity however remained stable until mean aortic pressure had dropped below 30 mmHg, carotid artery blood flow below 10.6 ml/kg/min, and cerebral oxygen delivery below 1.4 ml/kg/min.

Anesthesia↗

Doppler sonographic study of the effect of indomethacin on cardiac and pulmonary hemodynamics of the preterm infant.

OBJECTIVE: Indomethacin (INDO) causes an increase in systemic vascular resistance and decrease in perfusion of important organ systems in preterm infants treated for patent ductus arteriosus (PDA). Information on the effect of INDO on cardiac and pulmonary hemodynamics of these babies is scarce. METHODS: The left ventricular output (LVO), resistance in the ascending aorta (R(Ao)), determined mean cerebral blood velocity (cerebral-mv), ductal-peak and mean blood velocity (ductal-pv and -mv) and pulmonary artery peak and mean blood velocity (pulmonary pv and -mv) were measured, before, and up to 12 h after 0.1 mg/kg of INDO in 20 preterm infants with PDA using Doppler echocardiography. RESULTS: LVO was abnormally high (mean+/-S.E.M.: 354+/-50 ml/min/kg) before INDO treatment, and an important left-to-right shunt through the ductus was detectable in all infants. At 1 h after INDO treatment, R(Ao) had significantly increased with a significant decrease in LVO and cerebral-mv. Ductal patency and pulmonary vascular resistance seemed not to be affected at this early stage, as indicated by unchanged ductal and pulmonary arterial blood velocities. At 4 h post-INDO, ductal-pv and -mv, and to a lesser extent pulmonary-pv and -mv, were transiently lower as compared to pre-INDO, 1 and 12 h post-INDO values. This coincided with a transient absence of clinical signs of PDA at 4 h post-INDO in a substantial number of infants. R(Ao) steadily decreased and LVO steadily increased, whereas cerebral-mv normalized from 4 h post-INDO onward. CONCLUSIONS: no important action of INDO was detected on pulmonary arterial blood velocity or pulmonary function.

Carotid Artery, Internal↗

Effect of exchange transfusion on brain perfusion and electrocortical brain activity in newborn lambs.

Changes in brain perfusion (using ultrasonic-determined changes in carotid artery blood flow: Qcar) and electrocortical brain activity (ECBA, obtained by a Lectromed cerebral function monitor) were studied during exchange transfusion using the push-pull method in the newborn lamb. Changes in mean arterial blood pressure (MABP), Qcar, heart rate (HR), and ECBA were observed during all exchange transfusions: MABP, Qcar, and ECBA decreased during the withdrawal period and increased during the infusion period, whereas HR showed the opposite phenomenon. Changes in ECBA appeared to be primarily associated with changes in brain perfusion (p < 0.05). These changes in brain perfusion were, however, caused by changes in MABP (p < 0.0001). We concluded that exchange transfusions caused moderate changes in brain perfusion, however changes in ECBA appeared to be very small, and have probably no clinical importance.

Animals↗

Effect of deferoxamine and allopurinol on non-protein-bound iron concentrations in plasma and cortical brain tissue of newborn lambs following hypoxia-ischemia.

Reduction of non-protein-bound iron (NPBI) using iron chelators may attenuate hypoxia-ischemia-induced reperfusion injury of the brain. This study investigated whether administration of low-dose deferoxamine and allopurinol, both having NPBI-chelating properties, reduced hypoxia-ischemia-induced NPBI formation in plasma effluent from the brain and in cerebral cortical tissue. Twenty-one newborn lambs underwent severe hypoxia-ischemia. Upon reperfusion and reoxygenation the lambs received either a placebo (n = 7), or deferoxamine 2.5 mg/kg (n = 7) or allopurinol 20 mg/kg (n = 7). The post-hypoxic-ischemic NPBI levels in plasma were significantly lower after deferoxamine but not after allopurinol as compared to placebo-treated lambs. Cortical NPBI levels in both deferoxamine and allopurinol-treated lambs were significantly lower than NPBI levels in placebo-treated lambs. We conclude that deferoxamine effectively lowers NPBI in plasma effluent from the brain, and that both, deferoxamine and allopurinol, lower NPBI in cortical brain tissue.

Allopurinol↗

[Nitric oxide inhalation in newborn infants with pulmonary hypertension].

Nitric oxide (NO) is an important endogenous vasodilator. NO, produced in the endothelial cell, causes vasodilation by relaxation of the vascular smooth muscle cell. Inhalation of NO plays a role in the treatment of persistent pulmonary hypertension of the newborn, a syndrome with considerable morbidity and mortality. NO inhalation specifically leads to pulmonary vasodilation without systemic hypotension, since NO binds avidly to haemoglobin. Neonates with pulmonary hypertension associated with lung hypoplasia, meconium aspiration syndrome, infantile inspiratory distress syndrome due to surfactant deficiency, and sepsis have been treated with inhaled NO. Literature data on NO inhalation and experience in our units with NO inhalation show an improvement in arterial oxygen tension and a decreased need for extracorporeal membrane oxygenation, but no reduction in mortality. NO toxicity as a result of NO inhalation in the newborn has not been reported yet.

Administration, Inhalation↗

The effect of phototherapy on cerebral blood flow velocity in preterm infants.

Cerebral blood flow velocity was studied with two-dimensional/pulsed Doppler ultrasound before, during and after discontinuation of phototherapy in 22 preterm infants (gestational age < or =32 weeks), who were treated for a minimum of 12h with blue-light phototherapy for non-haemolytic hyperbilirubinaemia. Before the cerebral blood flow velocity measurements, patency of the ductus arteriosus was diagnosed by Doppler echocardiography. All infants had normal brain ultrasound scans. Mean cerebral blood flow velocity increased significantly after initiation of phototherapy in all infants. Only in "healthy" (non-ventilated) infants did cerebral blood flow velocity return to pre-phototherapy values (baseline) after discontinuation of phototherapy, whereas in "unhealthy" (ventilated) infants cerebral blood flow velocity did not return to baseline. In 10 infants the ductus arteriosus reopened during phototherapy. In those infants, mean cerebral blood flow velocity returned to pre-phototherapy values after 2 h of phototherapy prior to its discontinuation.

Blood Flow Velocity↗

The effect of phototherapy on renal blood flow velocity in preterm infants.

Mean renal blood flow velocity (RBFV) was studied with two-dimensional/ pulsed Doppler ultrasound and relative renal vascular resistance (RVR) was calculated before, during, and after phototherapy treatment in 30 preterm infants (gestational age < or = 32 weeks) who were treated for a minimum of 12 h with phototherapy for nonhemolytic hyperbilirubinemia. RBFV decreased, whereas RVR increased significantly after the initiation of phototherapy. In 'healthy' (nonventilated) infants RBFV and RVR returned to baseline values after discontinuation of phototherapy. Whereas in 'unhealthy' (ventilated) infants, RBFV and RVR did not return to baseline values after discontinuation of phototherapy. In 16 infants (> 50% of the cases) the ductus arteriosus reopened during phototherapy.

Blood Flow Velocity↗

The effect of antioxidative combination therapy on post hypoxic-ischemic perfusion, metabolism, and electrical activity of the newborn brain.

Reoxygenation and reperfusion after severe hypoxia and ischemia (HI) contribute substantially to birth asphyxia-related brain injury. Excess production of free radicals via metabolization of arachidonic acid, xanthine oxidase, and non-protein-bound iron play an important role. Cerebral reperfusion injury is characterized by a decrease in perfusion, oxygen consumption, and electrical activity of the brain. Reduction of free radical production may attenuate these features. We therefore induced severe HI in 35 newborn lambs, and upon reperfusion the lambs received a placebo [control (CONT), n = 7], the cyclooxygenase inhibitor indomethacin (INDO, 0.3 mg/kg/i.v., n = 7), the xanthine oxidase inhibitor allopurinol (ALLO, 20 mg/kg/i.v., n = 7), the iron chelator deferoxamine (DFO, 2.5 mg/kg/i.v., n = 7), or a combination of these drugs (COMB, n = 7). In each group changes (%) from pre-HI values were investigated for brain perfusion [measured by carotid artery flow (Qcar, mL/min)], (relative) cerebral O2 metabolism (CMR(O2)), and electrocortical brain activity (ECBA, microV) at 15, 60, 120, and 180 min post-HI. Qcar decreased significantly at 120 and 180 min post-HI in CONT (p < 0.05), but not in INDO, ALLO, DFO, and COMB groups. CMR(O2) decreased significantly in CONT at 60 min post-HI (p < 0.05), remained stable in DFO and INDO, and was significantly higher in ALLO and COMB (p < 0.05) at 120 and 180 min post-HI. ECBA was significantly lower in CONT during the whole post-HI period (p < 0.05), ECBA in INDO and COMB were significantly decreased at 60 and 120 min post-HI (p < 0.05), but recovered afterward, whereas DFO and ALLO remained stable during the post-HI period. In conclusion preservation of Qcar and CMR(O2), and recovery of ECBA occurred after treatment with INDO, ALLO, and DFO; combination of these drugs did not have an additional positive effect.

Allopurinol↗

Oxidative stress during post-hypoxic-ischemic reperfusion in the newborn lamb: the effect of nitric oxide synthesis inhibition.

Post-hypoxic-ischemic (HI) reperfusion induces endothelium and neurons to produce excessive amounts of nitric oxide and superoxide, leading to peroxynitrite formation, release of protein-bound metal ions (i.e. iron), and cytotoxic oxidants. We produced severe HI in 18 newborn lambs and serially determined plasma prooxidants (non-protein-bound iron), lipid peroxidation (malondialdehyde), and antioxidative capacity [ratio of ascorbic acid/dehydroascorbic acid (AA/DHA), alpha-tocopherol, sulfhydryl groups, allantoin/uric acid ratio, and vitamin A] in blood effluent from the brain before and at 15, 60, 120, and 180 min after HI. The lambs were divided in three groups: six received a placebo (CONT), six received low dose (10 mg/kg/i.v.) N omega-nitro-L-arginine (NLA-10) to block nitric oxide production, and six received high dose NLA (40 mg/kg/i.v.; NLA-40), immediately after completion of HI. Non-protein-bound iron increased in all groups after HI but was significantly lower in both NLA groups at 180 min post-HI (p < 0.05), the AA/DHA ratio showed a consistent decrease in CONT (at 60 min post-HI, p < 0.05), but remained stable in NLA lambs. alpha-Tocopherol decreased steadily in the CONT, but not in the NLA lambs [180 post-H: 1.9 +/- 0.9 versus 4.2 +/- 0.7 microM (NLA-40), p < 0.05). Malondialdehyde was significantly higher in CONT lambs 120 min post-H compared with NLA groups [0.61 +/- 017 versus 0.44 +/- 0.05 microM (NLA-40), p < 0.05]. Vitamin A and sulfhydryl groups did not differ among groups. We conclude that post-H inhibition of nitric oxide synthesis diminishes non-protein-bound iron increment and preserves antioxidant capacity.

Animals↗

Perinatal regulation of the cerebral circulation: role of nitric oxide and prostaglandins.

Nitric oxide (NO) influences cerebral vascular tone both in the normal fetus and in the hypoxemic fetus, but during postnatal life this regulating role of NO seems less prominent. It is therefore possible that under conditions when arterial oxygen content is at postnatal levels NO exerts no action on smooth muscle. We therefore examined the impact of NO on cerebral blood flow and vascular resistance in five near-term lamb fetuses during intrauterine ventilation and oxygenation. Four additional fetuses were pretreated with indomethacin to investigate a possible additional regulatory role of prostaglandins on cerebral vascular resistance. Cerebral blood flow (Qbrain) was measured using radionuclide-labeled microspheres. A tracheal tube was inserted to ventilate the fetus. After recovery, Qbrain and resistance in the cerebral vascular bed (Rcer) were measured during the following subsequent conditions: before and after increasing fetal arterial O2 content by ventilation with air, after inhibition of NO production with N(omega)-nitro-L-arginine during and after cessation of ventilation, and finally after infusion of L-arginine to increase nitric oxide production. Ventilation decreased Qbrain (95 +/- 18 to 47 +/- 15 mL/100 g/min) and increased Rcer. N(omega)-Nitro-L-arginine did not alter Qbrain (52 +/- 13 mL/100 g/min) or Rcer during ventilation and oxygenation, indicating no modulating role of NO during higher arterial oxygen content. On cessation of ventilation, PO2 returned to fetal levels and Qbrain increased significantly, but did not return to baseline fetal values (83 +/- 7 mL/min). Infusion of L-arginine increased Qbrain to baseline fetal levels (116 +/- 30 mL/min). However, indomethacin pretreatment prevented the rise in cerebral blood flow after cessation of ventilation and after additional L-arginine infusion (Qbrain 53 +/- 20 and 52 +/- 4 mL/100 g/min. respectively). These studies indicate that, during postnatal levels of arterial oxygen content, NO does not exert an action on smooth muscle cells of the cerebral resistance vessels as it does at lower arterial (fetal) oxygen content. They further show that prostaglandins are important in facilitating the full expression of NO-induced vasodilation.

Animals↗

Inhalation of nitric oxide: effect on cerebral hemodynamics and activity, and antioxidant status in the newborn lamb.

Ventilation with nitric oxide (NO) is increasingly being used to treat pulmonary hypertension in the newborn. In the brain, NO has vasoactive properties and is involved in neurotransmission. However, the effect of inhaled NO on the cerebral blood flow (CBF) and on the cerebral activity is not known. Furthermore, there is little information on the influence of this free radical gas on the redox status in pulmonary vessels. We therefore investigated the effect of inhaled NO (2-60 ppm) on CBF, cerebral activity and redox status in blood effluent from the pulmonary circulation in 6 ventilated newborn lambs before and during group B streptococci (GBS)-induced pulmonary hypertension. Blood pressure in the pulmonary artery (P(ap)) and aorta (Pao), carotid artery blood flow (Qcar) to assess changes in CBF, and electrocortical activity were measured. Blood gases, indices of free radical status and methemoglobin were determined in blood samples obtained from the left ventricle. Inhalation of NO, before and during GBS-induced pulmonary hypertension, decreased P(ap) and PCO2 and increased PO2. Multiple linear regression revealed that Qcar was positively related to PCO2, but not to inhaled NO or PO2 before or during GBS conditions. Electrocortical activity and indices of antioxidative capacity and lipid peroxidation did not change significantly. Methemoglobin was not detected. In conclusion, inhalation of NO (up to 60 ppm) lowered P(ap) without directly affecting CBF, electrocortical activity, and redox status in the pulmonary vessels. CBF, however, can indirectly be influenced by NO-mediated changes in PCO2.

Administration, Inhalation↗

Biochemical lung maturity, static respiratory compliance, and pulmonary gas transfer in intubated preterm infants with and without respiratory distress syndrome.

We investigated the relationship between tests of biochemical lung maturity [lecithin/sphingomyelin ratio (L/S ratio)], static compliance of the respiratory system (Crs), and estimates of pulmonary gas transfer [venous admixture and arterial/alveolar (a/A) ratio] in a group of intubated preterm infants with and without respiratory distress syndrome (RDS). Thirty infants were studied once (n = 26) or twice (n = 4). The L/S ratio was obtained by means of high-performance thin-layer chromatography and determination of the phosphorus content. Crs was obtained by the multiple occlusion technique. Transcutaneous blood gases and the percentage of oxygen in the inspired gas were recorded and estimates of pulmonary gas transfer were calculated using algorithms. L/S ratio and Crs correlated well (r = 0.73), indicating a higher compliance in biochemically more mature lungs. Both the a/A ratio and venous admixture correlated significantly with the L/S ratio and Crs (P < 0.001). Crs, L/S ratio, and a/A ratio decreased with increasing severity of radiological RDS, and the percentage venous admixture increased (P < 0.001). Sequential measurements in four infants during the acute phase and after RDS resolved indicated that clinical improvement coincided with improvements in biochemical lung maturity, Crs, and estimates of pulmonary gas transfer.

Chromatography, High Pressure Liquid↗

Interaction between afterload and contractility in the newborn heart: evidence of homeometric autoregulation in the intact circulation.

OBJECTIVES: We undertook the present study to determine whether afterload and contractility interact in the hearts of newborn lambs. We specifically investigated whether stepwise increases in afterload increase contractility. BACKGROUND: Several studies in the isolated and intact adult dog heart have shown that afterload and contractility are not independent determinants of cardiac performance; rather, they interact. Afterload and contractility are unlikely to interact in the newborn heart because the factors that may mediate the interaction in the adult are missing in the newborn. METHODS: We measured contractility at different steady state levels of afterload in seven newborn lambs under complete anesthesia. Contractility was measured by three different indexes: end-systolic pressure-volume relations (slope and volume position); preload-corrected first derivative of left ventricular pressure (dP/dtmax); and preload-corrected stroke work. Left ventricular pressure and volume were measured with a micromanometer and conductance catheter, respectively. Preload and afterload were manipulated by inflating or deflating a balloon catheter in the inferior vena cava and descending thoracic aorta, respectively. Data are expressed as mean value +/- 1 SD. RESULTS: Stepwise increases in afterload increased contractility, independent of which of the three indexes was used. The slope of the end-systolic pressure-volume relation increased from a mean baseline value of 4.44 +/- 2.43 to 6.69 +/- 2.89 kPa/ml at the highest level of afterload. Concomitantly, volume at 14 kPa of the end-systolic pressure-volume relation decreased from 3.34 +/- 1.52 ml at baseline to 1.12 +/- 0.83 ml at the highest afterload. The other two indexes showed qualitatively similar changes. Beats selected from unloading interventions on the basis of the same end-diastolic volume for each level of afterload showed no difference in stroke volume. CONCLUSIONS: This study in newborn lambs demonstrates that stepwise increases in afterload increase contractility considerably and that this enables the heart to maintain stroke volume at different levels of afterload. This forms direct evidence for the existence of homeometric autoregulation in the intact newborn heart.

Analysis of Variance↗

Respiratory illness in families of preterm infants with chronic lung disease.

AIMS--To examine the relation, based on two types of questionnaires, between (1) chronic lung disease of the newborn (CLDN) and lower respiratory illness (LRI) in siblings, and between (2) CLDN and asthma, chronic obstruction pulmonary disease (COPD), or allergy in parents and grandparents. METHODS--Data from 209 children born before 32 weeks of gestation were randomly taken from the records of three neonatal units. Taking into account age and gender, the excess of LRI was calculated for each family compared with the average of all families. Subsequently whether CLDN was associated with an excess of LRI in the family was tested. RESULTS--Thirty one (14.8%) children were diagnosed as having CLDN. The family probability index for LRI did not differ between children with or without CLDN. The prevalence of COPD, asthma, and allergy in parents of children with CLDN was similar to that of children without CLDN. The prevalence of LRI was 18.1% in study children, 29.6% in children with CLDN, and 16.9% in children without CLDN (P < 0.01). These prevalences were higher compared with that of a group of term siblings (9.3%) (P = 0.05). CONCLUSIONS--These findings suggest that CLDN in preterm children is not related to a genetic or familial predisposition towards asthma, COPD, or allergy.

Asthma↗

Acute effects of indomethacin on cerebral hemodynamics and oxygenation.

Although an indomethacin-induced decrease of brain perfusion in preterm infants has been well established, the acute effects of this vasoactive drug on cerebral hemodynamics and oxygenation are not well documented. Using near infrared spectroscopy we monitored in 6 very preterm infants changes in cerebral blood volume (delta CBV) and cytochrome oxidase concentration (delta Cytaa3), used as relative measures of changes in brain perfusion and as an indicator for cellular oxygenation of brain tissue, during and up to 1 h after indomethacin infusion. delta CBV showed a quick blood-pressure-related increase as compared to baseline (preindomethacin values) during indomethacin infusion (averaged maximal increase 13%), followed by a sharp decrease below baseline values (averaged maximal decrease 24%). There was a sustained recovery to baseline during the registration period. delta Cytaa3 showed a small, early increase in 4 of 6 babies, followed by a substantial decrease below baseline in 5 babies. delta Cytaa3 showed only a partial recovery in those 5 babies during the study period. We conclude that a therapeutic dose of indomethacin may cause substantial swings in brain perfusion and a marked and rather longstanding decrease in Cytaa3, suggesting a decrease in cellular oxygenation of brain tissue. Awareness of these effects may be important in sick preterm babies during periods of pulmonary and cardiac instability.

Blood Gas Monitoring, Transcutaneous↗

Role of nitric oxide in the regulation of the cerebral circulation in the lamb fetus during normoxemia and hypoxemia.

The influence of nitric oxide (NO) blockade on resting tone and on hypoxia-induced vasodilatation of the cerebral vascular bed was examined in chronically instrumented lamb fetuses. Total (Qbrain-tot) and regional brain blood flow were measured using radioactive microspheres. NO blockade was achieved by N omega-nitro-L-arginine (NNLA) infusion into the carotid artery via a lingual artery. Fetal cerebral blood flow and cerebral vascular resistance (Rcer) were determined during normoxemia and hypoxemia and before and during infusion of L-arginine. During normoxemia, the brain blood flow decreased, and the resistance increased significantly after NNLA infusion (Qbrain-tot from 129 +/- 25 to 89 +/- 26 ml/100 g/min, p < 0.05; Rcer from 0.46 +/- 0.03 to 0.80 +/- 0.09 mm Hg/ml/100 g/min, p < 0.05). During hypoxemia before NNLA infusion, Qbrain-tot increased (from 129 +/- 25 to 187 +/- 56 ml/100 g/min, p < 0.05), and Rcer decreased (from 0.46 +/- 0.03 to 0.39 +/- 0.07 mm Hg/ml/100 g/min, p < 0.05). This vasodilatory response was largely blocked after NNLA (Qbrain-tot 143 +/- 45 ml/100 g/min; Rcer 0.58 +/- 0.07 mm Hg/ml/100 g/min). The response to hypoxemia was restored after infusion of L-arginine (Qbrain-tot 180 +/- 47 ml/100 g/min). The resting tone of the cerebral vascular bed of the lamb fetus is under NO control, and NO mediates the cerebral vasodilatory response to hypoxia in the lamb fetus.

Animals↗

Cerebral blood volume changes during exchange transfusions in infants born at or near term.

We investigated the effects on cerebral hemodynamics of blood pressure changes during exchange transfusions in infants born at or near term, using near infrared spectroscopy in eight stable infants (mean gestational age, 36.2 +/- 1.3 weeks) who underwent a total of 21 exchange transfusions for erythroblastosis fetalis (rhesus hemolytic disease). Changes in mean arterial blood pressure derived from an indwelling umbilical arterial catheter, transcutaneous arterial oxygen and carbon dioxide tension, as well as changes in cerebral oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (HbR), and total hemoglobin (Hbtot = HbO2 + HbR), were recorded continuously from 15 minutes before until the completion of the exchange transfusion. Relative change(s) in cerebral blood volume (dCBV) were calculated as follows: dCBV = change in Hbtot x 0.89/Venous hemoglobin. Changes in mean arterial blood pressure and dCBV were observed during all exchange transfusions; a decrease was found during the withdrawal period and an increase during the infusion period. The mean response of dCBV to a change in mean arterial blood pressure was 0.011 ml.100 gm-1.mm Hg. Multivariate analysis showed that dCBV were primarily associated with changes in mean arterial blood pressure, followed by changes in arterial oxygen tension and in exchange cycle duration. We conclude that in stable term and near-term infants, hemorrhagically induced blood pressure changes provoke dCBV.

Blood Pressure↗