Delay in development after open-heart surgery in infants has frequently been reported. Inadequate brain perfusion and oxygenation during deep hypothermic cardiopulmonary bypass (CPB) may play an important role. We investigated the effect of CPB on cerebral perfusion and oxygenation in 12 neonates and infants (age 0–11 months) undergoing open-heart surgery. Changes in cerebral blood volume (ΔCBV; in ml/100 g brain tissue) and oxidation level of the intracerebral mitochondrial enzyme cytochrome aa₃ (ΔCytaa₃; in µmol/l) were measured with near infrared spectroscopy. Nasopharyngeal temperature (T_nas) for assessment of changes in brain temperature, and mean arterial blood pressure (MAP) were monitored continuously. CBV lowered during cooling and increased during rewarming. These changes were only related with changes in Tnas (p < 0.001; 0.07 ml·100 g^-1/°C). No relation was found with changes in MAP or pump flow rate of the heart-lung machine. During steady-state hypothermic CPB, changes in CBV were only related to changes in MAP (p < 0.001). The individual regression lines between ΔCBV and MAP became steeper at lower absolute T_nas. Cytaa₃ showed an increase shortly after the initiation of CPB in 9 patients, with a sustained decrease to baseline values in 8 patients towards the end of the CPB period. Two patients who had a circulatory arrest during CPB had a sharp decrease in Δcytaa₃ after cessation of the heart-lung pump and showed no complete recovery of ΔCytaa₃ to baseline at the end of the CPB period. We conclude that changes in CBV during CPB are related to changes in T_nas. During deep hypothermic steady-state CPB, changes in CBV and MAP were related to each other, suggesting lack of cerebral autoregulation. The large decrease in Cytaa₃ in 2 patients with circulatory arrest suggests that this procedure compromises energy metabolism of the brain cell.

Objective: To study the effect of cardiac contraction on left coronary artery pressure-flow relations at different vascular volumes and to compare these relations in the beating heart with those in the heart arrested in systole and diastole. Methods: Maximally vasodilated, Tyrode perfused, rabbit hearts (n56) with an intra-ventricular balloon were used. The left coronary artery was separately perfused via a cannula in the left main coronary artery. The slopes and the intercepts of left coronary pressure-flow relations were determined in the beating and arrested heart at different chamber volumes. A 3-factor design with repeated measures was used to compare the effect of three factors: phase of contraction (systole and diastole), chamber volume (V and V , left ventricular end-diastolic pressure 1.4 and 20 mm Hg, 0 1 respectively) and the type of contraction (beating and arrested; a measure of capacitive effects). Results: The phase of contraction has a significant effect on the intercepts (.40 mmHg, p50.00032) but not on the slopes of the pressure-flow relations. Chamber volume had a small effect on the intercepts (,5 mm Hg, p50.037), but not on the slopes of the pressure-flow relations. The type of contraction has a significant effect on the slopes (|10%, p50.00021) but not on the intercepts of the pressure-flow relations. Conclusions: In the isolated Tyrode perfused rabbit heart left coronary pressure-flow relations are mainly determined by contraction, while left ventricular chamber volume and capacitive effects contribute little. © 1998 Elsevier Science B. V. All rights reserved.Keywords: Diastolic arrest; KCl; Barium contracture; Isolated heart; Left ventricular pressure; Rabbit Introduction ventricular pressure, as used by the waterfall model [10]and the intra myocardial pump model [11][12][13], play a Coronary arterial inflow is impeded in systole as a result minor role in our concept. of cardiac muscle contraction. Previously, we have hypothEarlier, we studied the effect of cardiac contraction on esized that this diminished flow is the result of the varying coronary arterial inflow in the maximally dilated [5] and mechanical properties of the cardiac muscle during the autoregulating bed [4], while keeping constant arterial and heart cycle [1-6]. In the ventricular cavity, contraction venous pressures. In these studies, variation of left venresults in a time varying pressure-chamber volume relatricular pressure by changing left ventricular chamber tion, i.e., the time varying elastance [7,8]. In the coronary volume had little effect on the impeding of coronary flow. vessels, we assume cardiac contraction to have the same These findings are in line with the varying elastance effect, resulting in a time varying pressure-vascular volconcept. However, only one single perfusion pressure was ume or pressure-vascular cross-sectional area relation [9].used. Coronary pressure-flow relations in diastole were The decrease in cross-sectional area of the coronary determined in several studies [14][15][16]. Howe...

Objective. To investigate whether or not postasphyctic cerebral hypoperfusion and decreased cerebral metabolism occur in the perinatally asphyxiated neonate, as has been reported in adults and newborn animals. Methods. Using near-infrared spectroscopy, we monitored changes in oxyhemoglobin (HbO2), deoxyhemoglobin (HbR), total hemoglobin (HbO2 + HbR, which represents changes in cerebral blood volume [CBV]), and cytochrome oxidase (Cytaa3, which indicates changes in oxidation level of this intracerebral mitochondrial enzyme). Thirty-one neonates (gestational age &gt;34 weeks), divided into three groups, were monitored between 2 and 12 hours or between 12 and 24 hours of life. Group I consisted of healthy newborns: N = 8 (2 to 12 hours) and N = 5 (12 to 24 hours). Patients in group II were moderately asphyxiated newborns but neurologically normal in the first 24 hours of life: N = 6 (2 to 12 hours) and N = 3 (12 to 24 hours). Group III consisted of severely asphyxiated newborns with an abnormal neurologic behavior within 24 hours after birth: N = 5 (2 to 12 hours) and N = 4 (12 to 24 hours). Results. From 2 to 12 h, CBV levels in groups I and II were stable. In group III CBV decreased in all infants. This decrease in CBV was associated with a drop in both HbO2 and HbR. Cytaa3 was stable in groups I and II, but showed a marked decrease in two of the five infants of group III. There was a positive relationship between CBV and mean arterial blood pressure in groups II and III. Between 12 and 24 hours, all groups showed stable CBV and Cytaa3 patterns. A positive relation existed now between transcutaneous Pco2 and CBV in groups II and III. Conclusions. CBV, HbO2 HbR, and Cytaa3 decreased in the first 12 hours of life in severely asphyxiated neonates who subsequently developed neurologic abnormalities. We therefore suggest that posthypoxic-ischemic reperfusion injury of the brain during early neonatal life occurs in neonates with severe birth asphyxia.

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