Sexually selected dichromatism in the hihi Notiomystis cincta: multiple colours for multiple receivers.

Why do some bird species show dramatic sexual dichromatism in their plumage? Sexual selection is the most common answer to this question. However, other competing explanations mean it is unwise to assume that all sexual dichromatism has evolved by this mechanism. Even if sexual selection is involved, further work is necessary to determine whether dichromatism results from competition amongst rival males, or by female choice for attractive traits, or both. Here, we test whether sexually dichromatic hihi (Notiomystis cincta) plumage is currently under sexual selection, with detailed behavioural and genetic analyses of a free-living island population. Bateman gradients measured for males and females reveal the potential for sexual selection, whilst selection gradients, relating reproductive success to specific colourful traits, show that there is stabilizing selection on white ear tuft length in males. By correlating colourful male plumage with different components of reproductive success, we show that properties of yellow plumage are most likely a product of male-male competition, whilst properties of the black and white plumage are an outcome of both male-male competition and female choice. Male plumage therefore potentially signals to multiple receivers (rival males and potential mates), and this may explain the multicoloured appearance of one of the most strikingly dichromatic species in New Zealand.

Successful treatment of life-threatening acute chest syndrome of sickle cell disease with venovenous extracorporeal membrane oxygenation.

PURPOSE: We describe a pediatric patient with sickle cell disease and life-threatening acute chest syndrome who was successfully treated with venovenous extracorporeal membrane oxygenation (ECMO). PATIENT AND METHODS: An 8-year-old boy with sickle cell disease presented with vaso-occlusive crisis, which progressed to fulminant acute chest syndrome requiring a partial exchange transfusion and mechanical ventilation. Despite very high ventilator settings and significant barotrauma, hypoxia persisted and circulatory failure occurred. He was then successfully treated with venovenous ECMO for 11 days. One month after decannulation he had a seizure associated with abnormalities on magnetic resonance images (MRIs). His disease has been managed with a chronic transfusion program since then. Follow-up after 5 years reveals normal pulmonary function tests, a normal magnetic resonance angiogram (MRA), and above-average cognitive skills. CONCLUSION: This is the first report of a pediatric patient with acute chest syndrome successfully managed with venovenous ECMO. His course was complicated by a seizure associated with MRI abnormalities, although the outcome has been excellent. This case suggests that treatment with venovenous ECMO should be strongly considered for sickle cell patients with life-threatening acute chest syndrome, despite maximal conventional support.

Impairment of cerebral autoregulation during venovenous extracorporeal membrane oxygenation in the newborn lamb.

OBJECTIVE: To study the effects of venovenous extracorporeal membrane oxygenation (ECMO) on cerebral autoregulation in the newborn lamb. DESIGN: Animal studies, using newborn lambs, with comparison of two randomized treatment groups. SUBJECTS: Newborn lambs of mixed breed, 1 to 7 days of age, were randomized into two study groups: control animals, with jugular vein ligation but no ECMO (n = 6), and ECMO animals placed on venovenous ECMO (n = 6). SETTING: Laboratory animal facilities of the Department of Anesthesiology and Critical Care Medicine at The Johns Hopkins Medical Institutions, Baltimore, MD. INTERVENTIONS: Animals were anesthetized with pentobarbital, intubated, and ventilated, and monitoring catheters were inserted. Control animals had their right jugular vein ligated, and a cerebral autoregulation curve was performed after 1 hr of stabilization. ECMO animals were placed on venovenous ECMO and after 1 hr of stabilization, they had a cerebral autoregulation curve performed. Cerebral autoregulation was examined by increasing intracranial pressure, thereby decreasing cerebral perfusion pressure. Intracranial pressure was increased by infusion of artificial cerebrospinal fluid into the lateral ventricle of the brain. MEASUREMENTS AND MAIN RESULTS: Four ranges of cerebral perfusion pressure were evaluated: a) baseline (1 hr after initiation of bypass in venovenous ECMO or completion of surgery in controls); b) cerebral perfusion pressure of 55 to 40 mm Hg; c) cerebral perfusion pressure of 39 to 25 mm Hg; and d) cerebral perfusion pressure of < 25 mm Hg. Cerebral blood flow (radiolabeled microspheres), cerebral oxygen consumption, fractional oxygen extraction, and oxygen transport values were calculated at each study period. In ECMO animals, cerebral blood flow (cerebral hemispheres) decreased from a baseline measurement of 46 +/- 9 (SD) mL/100 g/ min to 29 +/- 12 mL/100 g/min at a cerebral perfusion pressure of < 25 mm Hg. In the control group, cerebral blood flow was unchanged from baseline at any range of cerebral perfusion pressure. Cerebral oxygen consumption was unchanged from baseline as cerebral perfusion pressure decreased in either group. When cerebral oxygen consumption was compared between the two groups, it was lower in the ECMO group at baseline and at a cerebral perfusion pressure of < 25 mm Hg. At a cerebral perfusion pressure of < 25 mm Hg, cerebral blood flow, cerebral oxygen delivery, and metabolic rate were lower in the ECMO group than in the control group, and fractional oxygen extraction and cerebral vascular resistance were higher, indicating that autoregulation was impaired. There was no difference between blood flow in the right and left cerebral hemispheres when autoregulation was impaired in the ECMO animals. CONCLUSIONS: These findings indicate that cerebral autoregulation was altered in animals on venovenous ECMO, with cerebral blood flow decreasing at a cerebral perfusion pressure of < 25 mm Hg, compared with control animals which showed no changes at the same cerebral perfusion pressure. This disruption of cerebral autoregulation decreased cerebral oxygen metabolism despite an increased oxygen extraction in ECMO animals.

Predictors of acute respiratory failure after bone marrow transplantation in children.

OBJECTIVE: To determine factors associated with acute respiratory failure after bone marrow transplantation which can be identified before the onset of lung disease. DESIGN: Population-based, retrospective study. SETTING: A referral-based pediatric intensive care unit and bone marrow transplant center. PATIENTS: Thirty-nine patients with lung disease (abnormal chest radiograph or a need for supplemental oxygen) were identified from a group of 318 pediatric bone marrow transplant patients from 1978 to 1988. Thirty-four of 39 patients with complete data were further classified into patients with mild lung disease (recovery without needing endotracheal intubation, n = 16) and patients with acute respiratory failure (requirement for endotracheal intubation, n = 18). INTERVENTIONS: Regression analyses were performed to define risk factors for development of respiratory failure (multivariate logistic regression) and for a shortened interval between the identification of lung disease and respiratory failure (Cox proportional hazards analysis). MEASUREMENTS AND MAIN RESULTS: Ninety-three percent (15/16) of patients with mild lung disease survived. Conversely, only 9% (2/23) of patients with respiratory failure survived. Predictors of respiratory failure included graft vs. host disease (odds ratio 28.3, 95% confidence interval 1.9-421, p = .015), a prelung disease (baseline) circulating creatinine concentration of > 1.5 mg/dL (> 132.6 mumol/L) (odds ratio 28.4, 95% confidence interval 1.4-577, p = .029), and male gender (odds ratio 14.6, 95% confidence interval 1-210, p = .049). Predictors of a shortened time to onset of respiratory failure included baseline serum creatinine value of > 1.5 mg/dL (> 132.6 mumol/L) (hazard ratio 6.2, 95% confidence interval 1.5-26.5, p = .013) and baseline total bilirubin concentration > 1.4 mg/dL (> 23.9 mumol/L) (hazard ratio 4.5, 95% confidence interval 0.98-20.7, p = .053). The median time to onset of respiratory failure was 4 days in patients with baseline creatinine values > or = 1.5 mg/dL (> 132.6 mumol/L) and 5 days in patients with baseline bilirubin concentrations > or = 1.4 mg/dL (> 23.9 mumol/L) vs. > 26 days in patients with creatinine < 1.5 mg/dL (< 132.6 mumol/L) and > 29 days in patients with bilirubin < 1.4 mg/dL (< 23.9 mumol/L) (Kaplan-Meier analysis). CONCLUSIONS: Renal and liver dysfunction preceded clinical evidence of lung disease in bone marrow transplant patients who developed respiratory failure. Lung disease leading to respiratory failure and adult respiratory distress syndrome appears to develop as one component of the multiple organ failure syndrome in pediatric bone marrow transplant patients.

Impaired cerebral autoregulation in the newborn lamb during recovery from severe, prolonged hypoxia, combined with carotid artery and jugular vein ligation.

OBJECTIVE: To study the effect of severe prolonged hypoxia combined with ligation of the carotid artery and jugular vein (simulating pre-extracorporeal membrane oxygenation [ECMO] events) on cerebral autoregulation in the newborn lamb. DESIGN: Animal studies, using the newborn lamb, with comparison of two randomized treatment groups. SUBJECTS: Newborn lambs of mixed breed, 1 to 7 days of age, were used for the study. Two groups of animals were studied: a normoxic control group (n = 7) and a hypoxic group (n = 8). SETTING: Work was conducted in the research laboratories of the Department of Anesthesiology, Critical Care Medicine at The Johns Hopkins Medical Institutions, Baltimore, MD. INTERVENTIONS: Animals were anesthetized (pentobarbital), intubated, and mechanically ventilated. We examined the effect of prolonged severe hypoxia combined with carotid artery and jugular vein ligation on cerebral autoregulation during recovery from this insult. Control animals were maintained in a normoxic state (3 hrs) without carotid artery or jugular vein ligation. Hypoxic animals with carotid artery and jugular vein ligation were exposed to a 2-hr period of hypoxia (arterial oxygen saturation 44 +/- 14%; PaO2 30 +/- 3 torr [4 +/- 0.4 kPa]) followed by a 1-hr normoxic recovery period. Cerebral autoregulation was evaluated at the end of the 1-hr recovery period in hypoxic animals, and after 3 hrs of normoxia in control animals. Cerebral perfusion pressure was decreased by increasing intracranial pressure, with infusion of artificial cerebrospinal fluid into an intracranial pressure catheter in the lateral ventricle of the brain. MEASUREMENTS: Studies were taken at four ranges of cerebral perfusion pressure: > 55 mm Hg; 55 to 40 mm Hg; 39 to 26 mm Hg; and < or = 25 mm Hg. Cerebral blood flow was measured using the radiolabeled microsphere technique. Cerebral oxygen consumption, fractional oxygen extraction, and oxygen transport values were calculated at each study period. MAIN RESULTS: Two hours of severe hypoxia increased cerebral blood flow by 110%, whereas cerebral oxygen consumption was unchanged. In hypoxic animals, cerebral autoregulation was altered, with both cerebral blood flow and cerebral oxygen consumption decreasing at a cerebral perfusion pressure of 39 to 26 mm Hg compared with unchanged cerebral blood flow or cerebral oxygen consumption at a cerebral perfusion pressure of < or = 25 mm Hg in control animals. At the point of loss of autoregulation, significant right-to-left hemispheric cerebral blood flow changes occurred in hypoxic animals. In hypoxic animals, cerebellar cerebral blood flow changes were similar to those changes in the total cerebrum, while brain stem and caudate decreased cerebral blood flow only at a cerebral perfusion pressure of < or = 25 mm Hg. CONCLUSIONS: These findings indicate that cerebral autoregulation is disrupted during the recovery phase from an insult caused by prolonged, severe hypoxia with carotid artery and jugular vein ligation. This insult results in significant differences in right and left hemispheric cerebral blood flow rates when cerebral autoregulation is lost. If these results can be extrapolated to the human state, they may help to explain the role of pre-ECMO hypoxia combined with vessel ligation as a risk factor in cerebral injury in ECMO patients.

The cerebrovascular response to prolonged hypoxia with carotid artery and jugular vein ligation in the newborn lamb.

This study was designed to evaluate the effect of ligation of the carotid artery and/or jugular vein, after exposure to prolonged (4 hours) hypoxia, and the effect of acute normalization of PaO2 after prolonged hypoxia with vessel ligation, on the cerebral circulation. Twelve 1- to 7-day-old lambs were anesthetized with pentobarbital. Catheters were placed in the femoral artery and vein, left ventricle, lingual artery, and sagittal sinus. Cerebral blood flow (CBF) was determined using the radiolabeled microsphere technique. After baseline studies, the animals were made hypoxic with a nitrogen/air mixture, to lower PaO2 to 36 +/- 5 mm Hg for 4 hours, followed by 1 hour of normoxia. After four hours of hypoxia, studies were performed. The animals were divided into two groups to evaluate carotid artery and jugular vein ligation separately. In group I, the carotid artery was ligated first, with studies performed after 5 minutes; this was followed by ligation of the jugular vein, with studies after 5 minutes. In group II, the jugular vein was ligated first, with studies after 5 minutes; this was followed by ligation of the carotid artery, with studies after 5 minutes. With regard to physiological variables, there were no differences between the groups. CBF increased 106% (P < .001 compared with the baseline value) after 4 hours of hypoxia, maintaining cerebral oxygen consumption (CMRO2) and oxygen transport (OT) constant in both groups. Ligation of either the carotid artery or jugular vein after 4 hours of hypoxia, did not alter CBF responses to hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular response to carbon dioxide in lambs receiving extracorporeal membrane oxygenation.

OBJECTIVE: To determine if the institution of extracorporeal membrane oxygenation (ECMO) alters the cerebrovascular response to changes in PaCO2. DESIGN: Prospective, randomized, controlled animal trial. SUBJECTS: Anesthetized 1- to 7-day-old lambs of mixed breed (n = 16). SETTING: University research laboratory. INTERVENTIONS: The experimental group was placed on ECMO. Both experimental and control groups (n = 8) were exposed to three concentrations of PaCO2 (hypocarbia, normocarbia, and hypercarbia) by varying mechanical ventilation and by adding carbon dioxide to the ventilator gases. MEASUREMENTS AND MAIN RESULTS: Cerebral blood flow was measured by the radiolabeled microsphere method. Arterial blood gases and sagittal sinus blood gases were drawn at the time of cerebral blood flow measurement so that cerebral metabolism, cerebral oxygen transport, and extraction could be calculated. In the control group, as PaCO2 increased from 34 +/- 2 (SD) to 53 +/- 4 torr (4.5 +/- 0.3 to 7.1 +/- 0.5 kPa), cerebral blood flow increased from 53 +/- 12 to 147 +/- 50 mL/min/100 g. This increase in cerebral blood flow was not different from that of the ECMO group, where PaCO2 increased from 33 +/- 2 to 56 +/- 3 torr (4.4 +/- 0.3 to 7.5 +/- 0.4 kPa) and cerebral blood flow increased from 48 +/- 17 to 106 +/- 38 mL/min/100 g. As PaCO2 decreased from 34 +/- 2 to 19 +/- 2 torr (4.5 +/- 0.27 to 2.5 +/- 0.27 kPa), cerebral blood flow decreased from 53 +/- 12 to 43 +/- 8 mL/min/100 g in the control group. This decrease was not different from that of the ECMO group, where cerebral blood flow decreased from 48 +/- 17 to 39 +/- 10 mL/min/100 g as PaCO2 decreased from 33 +/- 2 to 22 +/- 3 torr (4.4 +/- 0.3 to 2.9 +/- 0.4 kPa). When regional cerebral blood flow was analyzed, no regional differences in the cerebrovascular responses to PaCO2 between ECMO and control groups were found. The cerebral metabolic rate was not different between ECMO and control groups at any level of PaCO2, nor was the cerebral metabolic rate affected by changes in PaCO2. Oxygen extraction increased with hypocarbia and decreased with hypercarbia in a similar fashion in both ECMO and control groups. CONCLUSION: The cerebrovascular response to changes in PaCO2 was unaffected by ECMO.

Effect of extracorporeal membrane oxygenation on platelets in newborns.

OBJECTIVES: To examine the effect of extracorporeal membrane oxygenation (ECMO) therapy on platelet function and number and to determine the in vivo survival of transfused platelets during ECMO. DESIGN: Prospective study of all neonates treated with ECMO during a 6-month period. SETTING: Neonatal intensive care unit in a tertiary referral center. PATIENTS: Ten infants, < 1 wk of age, with respiratory failure requiring ECMO. INTERVENTIONS: None. MEASUREMENTS: Platelet counts were measured at timed intervals to determine the effect of ECMO on platelet counts. The change in platelet counts after transfusion was also measured. Whole blood platelet aggregation studies were performed to determine the effect of ECMO on platelet function. MAIN RESULTS: A mean decrease of 26% from the baseline platelet count was found 15 mins after the initiation of ECMO, with an additional mean decrease of 16% by the end of 1 hr (p < .05). Fifteen minutes after platelet transfusions, a 17% mean increase in platelet counts was measured (p < .05). One hour after platelet transfusion, the platelet count had decreased to pretransfusion values. Platelet aggregation studies 15 mins after starting ECMO showed a 46% mean decrease in the response to collagen from baseline (p > .05), and a significantly (p < .05) reduced response to ristocetin and to adenosine 5'-diphosphate. Platelet adenosine triphosphate release was also significantly reduced. Single-unit platelet transfusions failed to correct platelet aggregation abnormalities. Resolution of platelet aggregation abnormalities and normalization of platelet counts occurred 8 hrs off ECMO. CONCLUSIONS: The results of these studies show that qualitative and quantitative platelet changes occur while a neonate is receiving ECMO. The survival rate of transfused platelets is reduced, and the acquired platelet dysfunction is not reversed by the transfusion of platelets with normal function while the patient is receiving ECMO.

Impairment of cerebral autoregulation during extracorporeal membrane oxygenation in newborn lambs.

This study was designed to evaluate the effect of normothermic partial bypass, or venoarterial extracorporeal membrane oxygenation (ECMO), on cerebral autoregulation. Fourteen newborn lambs, 1-7 d of age, were randomized into two groups: control (ligation of right carotid artery and jugular vein without ECMO; n = 7) and ECMO (ligation with placement on routine venoarterial ECMO at 120-150 mL/kg/min; n = 7). After 1 h of ECMO or stabilization in controls, cerebral autoregulation was evaluated by lowering cerebral perfusion pressure (CPP) by increasing intracranial pressure through infusion of artificial cerebrospinal fluid into the lateral ventricle. Four ranges of CPP were evaluated: 1) baseline, 2) 55-40, 3) 39-25, and 4) < 25 mm Hg. In ECMO animals, cerebral blood flow (CBF) decreased from baseline (39 +/- 7 mL/100 g/min) to 23 +/- 7 and 12 +/- 2 at CPP of 39-25 and < 25 mm Hg. In the control group, CBF was unchanged from baseline (48 +/- 11 mL/100 g/min) until CPP was < 25 mm Hg, at which time it decreased to 27 +/- 16 mL/100 g/min. Cerebral oxygen consumption decreased from baseline (4.2 +/- 1.1 mL/100 g/min) to 4.0 +/- 0.7 and 3.2 +/- 1.3 mL/100 g/min at CPP of 39-25 and < 25 mm Hg, respectively, in the ECMO group. In the control group, cerebral oxygen consumption was unchanged from baseline (4.2 +/- 1.1 mL/100 g/min) until CPP was reduced to < 25 mm Hg (3.2 +/- 1.3 mL/100 g/min). When CBF autoregulation was altered, i.e. when total CBF decreased, right-left hemispheric CBF differences were noted in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial venous system in newborns treated with extracorporeal membrane oxygenation: Doppler US evaluation after ligation of the right jugular vein.

There is little information regarding alterations in cerebral venous flow related to ligation of the right jugular vein in newborns treated with extracorporeal membrane oxygenation (ECMO). The authors performed duplex and color Doppler sonographic evaluations of the intracranial venous system in 23 consecutive newborns during ECMO. The superior sagittal sinus (SSS) was visualized in every newborn, and the left transverse sinus was seen in 14 newborns (61%). The relative contribution of a jugular bulb catheter was evaluated in 16 newborns by measuring average blood flow velocities in the SSS with the catheter open (baseline) and with the catheter temporarily occluded. Occlusion of the catheter resulted in significantly reduced SSS blood flow velocities (P = .01). Persistent reductions in SSS flow velocity were associated with a significantly higher risk of cerebrovascular injury (P = .002). These results show that alterations in cerebral venous drainage are not uncommon in newborns treated with venoarterial ECMO and suggest a possible association between abnormal venous drainage and cerebrovascular injury in these newborns.

Intracranial blood flow: quantification with duplex Doppler and color Doppler flow US.

The authors compared changes in cerebral blood flow (CBF), determined by means of injection of radiolabeled microspheres, with Doppler blood flow measurements obtained simultaneously in the middle (n = 9) and anterior cerebral arteries (n = 3) in 12 newborn lambs. Doppler estimates of blood flow and mean blood flow velocity correlated well with changes in CBF. However, with changes in mean blood flow velocity, the degree of change in CBF tended to be underestimated. The resistive index correlated well with perfusion pressure but correlated weakly with cerebrovascular resistance and poorly with changes in CBF. Doppler blood flow estimates and mean blood flow velocities correlate well with changes in CBF and allow significant improvement in accuracy over instantaneous velocity or pulsatility measurements alone. Determination of absolute blood flow remains difficult due to systolic and diastolic differences in vessel diameter and intrinsic error in true diameter measurement with currently available color flow technology.

Effect of extracorporeal membrane oxygenation on cerebral blood flow and cerebral oxygen metabolism in newborn sheep.

Extracorporeal membrane oxygenation (ECMO) supplies respiratory support to term or near-term infants with respiratory failure. Although infants requiring this therapy may have already sustained significant hypoxia and/or ischemia predisposing them to neurologic injury, the high incidence of neuroimaging abnormalities in the ECMO population raises concerns about the additional neurologic risk associated with the ECMO procedure itself. Our study was undertaken to evaluate the effects of ECMO on the normal neonatal cerebral circulation. Thirteen newborn lambs (1-7 d of age) were placed on normothermic venoarterial ECMO using a silicone membrane oxygenator and roller occlusion pump. Regional brain blood flows, cerebral oxygen consumption, fractional oxygen extraction, and oxygen transport were determined 30 and 120 min after initiation of ECMO. Neither cerebral blood flow (baseline, 60.2 +/- 23.6; 30 min, 56.1 +/- 18.1; 120 min 56.1 +/- 12.9 mL/100 g/min) nor oxygen metabolism (cerebral oxygen consumption: baseline, 4.48 +/- 1.48; 30 min, 3.86 +/- 1.53; 120 min, 4.10 +/- 1.32 mL/100 g/min and oxygen extraction: baseline, 0.52 +/- 0.09; 30 min, 0.47 +/- 0.14; 120 min, 0.46 +/- 0.14 mL/100 g/min) changed after the initiation of ECMO. Regional and left/right blood flow differences were not noted. These findings suggest that in healthy newborn lambs, initiation of ECMO does not alter cerebral blood flow or oxygen metabolism.