Response profiles of enteric methane emissions and lactational performance during habituation to dietary coconut oil in dairy cows.

Dietary coconut oil (CNO) can reduce dry matter intake (DMI), enteric methane (eCH(4)) emissions, and milk fat yield of lactating cows. The goals of this research were to examine responses to different CNO concentrations during the habituation period (34-d) and to evaluate temporal patterns of DMI, eCH(4), and milk fat yield. Treatment diets contained (dry basis): 0.0% (CNO0), 1.3% (CNO1.3), 2.7% (CNO2.7), 3.3% (CNO3.3), or 4.0% CNO (CNO4). In experiment 1, 12 primi- or small secundiparous cows were housed in individual, environmentally controlled rooms and fed CNO0, CNO1.3, CNO2.7, or CNO4. Measurements included DMI, eCH(4), and milk yield and composition. Due to a precipitous drop in DMI (26%), cows fed CNO4 were replaced with cows fed CNO3.3 following d 10. Dietary CNO of 2.7% or more reduced eCH(4) emissions. Reduction was greater with increased CNO and during the first than the second half of the day. Simultaneously, decline in DMI of cows fed CNO2.7, CNO3.3, or CNO4 was increasingly precipitous with increased CNO concentration. Total-tract neutral detergent fiber (NDF) digestibility during wk 5 was reduced in cows fed CNO2.7 or CNO3.3, which in part explained concomitantly reduced eCH(4)/DMI. In addition, milk fat yield was depressed at an increasing rate in cows fed CNO2.7, CNO3.3, and CNO4. In experiment 2, DMI was measured individually in 12 multiparous cows during habituation to CNO0, CNO1.3, CNO2.7, or CNO3.3 for 21 d before relocation to individual, environmentally controlled rooms. Dietary CNO2.7 or CNO3.3 reduced DMI by d 4 and total-tract NDF digestibility during wk 5. Relocation to individual rooms was associated with a 15% reduction in DMI, which was not affected by treatment. Results showed that 2.7% or more dietary CNO reduced eCH(4) and DMI, caused milk fat depression, and decreased NDF digestibility.

Enteric methane emissions and lactational performance of Holstein cows fed different concentrations of coconut oil.

To determine if dietary medium-chain fatty acids (FA; C(8) to C(14)) may mitigate enteric methane emissions, 24 cows were blocked by body size (n=2) and randomly assigned to 1 sequence of dietary treatments. Diets were fed for 35 d each in 2 consecutive periods. Diets differed in concentrations of coconut oil (CNO; ~75% medium-chain FA): 0.0 (control) or 1.3, 2.7, or 3.3% CNO, dry matter basis. The control diet contained 50% forage (74% from corn silage), 16.5% crude protein (60% from rumen-degradable protein), 34% neutral detergent fiber (NDF; 71% from forage), and 28% starch, dry matter basis. Data and sample collections were from d 29 to 35 in environmentally controlled rooms to measure methane (CH(4)) production. Methane emitted was computed from the difference in concentrations of inlet and outlet air and flux as measured 8 times per day. Control cows emitted 464 g of CH(4)/d, consumed 22.9 kg of DM/d, and produced 34.8 kg of solids-corrected milk/d and 1.3 kg of milk fat/d. Treatment with 1.3, 2.7, or 3.3% dietary CNO reduced CH(4) (449, 291, and 253 g/d, respectively), but concomitantly depressed dry matter intake (21.4, 17.9, and 16.2 kg/d, respectively), solids-corrected milk yield (36.3, 28.4, and 26.8 kg/d, respectively), and milk fat yield (1.4, 0.9, and 0.9 kg/d, respectively). The amount of NDF digested in the total tract decreased with increased dietary CNO concentrations; thus, CH(4) emitted per unit of NDF digested rose from 118 to 128, 153, and 166 g/kg across CNO treatments. Dietary CNO did not significantly affect apparent digestibility of CP but increased apparent starch digestibility from 92 to 95%. No FA C(10) or shorter were detected in feces, and apparent digestibility decreased with increasing FA chain length. Coconut oil concentrations of 2.7 or 3.3% decreased yields of milk FA C(14). The highest milk fat concentration (3.69%; 1.3% CNO) was due to the greatest yields of C(12) to C(16) milk FA. Milk FA concentrations of C(18:2 trans-10,cis-12) were related to increased dietary CNO concentrations and presumably to depressed ruminal NDF digestion. Moderate dietary CNO concentrations (e.g., 1.3%) may benefit lactational performance; however, CNO concentrations greater than or equal to 2.7% depressed dry matter intake, milk yield, milk fat yield, and NDF utilization. If mitigation of enteric CH(4) emissions is due to decreased digestion of dietary NDF, then this will lessen a major advantage of ruminants compared with nonruminants in food-production systems. Thus, CNO has limited use for enteric CH(4) mitigation in lactating dairy cows.

Effect of an acidifying diet combined with zeolite and slight protein reduction on air emissions from laying hens of different ages.

The objectives of the study were to evaluate the effectiveness of a reduced-emission (RE) diet containing 6.9% of a CaSO(4)-zeolite mixture and slightly reduced CP to 21-, 38-, and 59-wk-old Hy-Line W-36 hens (trials 1, 2, and 3, respectively) on egg production and emissions of NH(3), H(2)S, NO, NO(2), CO(2), CH(4), and non-CH(4) total hydrocarbons as compared with feeding a commercial (CM) diet. At each age, 640 hens were allocated, randomly to 8 environmental chambers for a 3-wk period. On an analyzed basis, the CM diet contained 18.0, 17.0, and 16.2% CP and 0.25, 0.18, and 0.20% S in trials 1, 2, and 3, and the RE diet contained 17.0, 15.5, and 15.6% CP and 0.99, 1.20, and 1.10% S in trials 1, 2, and 3. Diets were formulated to contain similar Ca and P contents. Average daily egg weight (56.3 g), average daily egg production (81%), average daily feed intake (92.4 g), and BW change (23.5 g), across ages, were unaffected by diet (P > 0.05) over the study period. Age effects were observed for all performance variables and NH(3) emissions (P < 0.05). In trials 1, 2, and 3, daily NH(3) emissions from hens fed the RE diets (185.5, 312.2, and 333.5 mg/bird) were less than emissions from hens fed the CM diet (255.1, 560.6, and 616.3 mg/bird; P < 0.01). Daily emissions of H(2)S across trials from hens fed the RE diet were 4.08 mg/bird compared with 1.32 mg/bird from hens fed the CM diet (P < 0.01). Diet (P < 0.05) and age (P < 0.05) affected emissions of CO(2) and CH(4). A diet effect (P < 0.01) on NO emissions was observed. No diet or age effects (P > 0.05) were observed for NO(2) or non-CH(4) total hydrocarbons. Results demonstrated that diet and layer age influence air emissions from poultry operations.

Nutrient digestibility and mass balance in laying hens fed a commercial or acidifying diet.

The objectives of the current study were to evaluate the effect of an acidifying diet (gypsum) combined with zeolite and slightly reduced crude protein (R) vs. a control diet (C) on nutrient retention in laying hens and compare 3 approaches to estimating nutrient excretion from hens: 1) mass balance calculation (feed nutrients - egg nutrient), 2) use of an indigestible marker with analyzed feed and excreta nutrient content, and 3) an environmental chamber that allowed for capturing all excreted and volatilized nutrients. Hens (n = 640) were allocated randomly to 8 environmental chambers for 3-wk periods. Excreta samples were collected at the end of each trial to estimate apparent retention of N, S, P, and Ca. No diet effects on apparent retention of N were observed (53.44%, P > 0.05). Apparent retention of S, P, and Ca decreased in hens fed R diet (18.7, - 11.4, and 22.6%, respectively) compared with hens fed the C diet (40.7, 0.3, and 28.6%, respectively; P < 0.05). Total N excretion from hens fed the C and R diet was not different (1.16 g/hen/d); however, mass of chamber N remaining in excreta following the 3-wk period was less from hens fed the C diet (1.27 kg) than from hens fed the R diet (1.43 kg). Gaseous emissions of NH(3) over the 3-wk period from hens fed the C diet (0.74 kg per chamber) were greater than emissions from hens fed the R diet (0.45 kg). The 3-wk S excretion mass (estimated using the calculation, indigestible marker, and environmental chamber methods, respectively) was greater from hens fed the R diet (1.85, 1.54, and 1.27 kg, respectively) compared with hens fed the C diet (0.24, 0.20, and 0.14 kg, respectively). The 3-wk P excretion was similar between diets (0.68 kg). Results demonstrate that feeding the acidified diet resulted in decreased N emissions, but because of the acidulant fed, greatly increased S excretion and emissions.

Nitrogen excretion and ammonia emissions from pigs fed modified diets.

Two swine feeding trials were conducted (initial body weight = 47 +/- 2 and 41 +/- 3 kg for Trials 1 and 2, respectively) to evaluate reduced crude protein (CP) and yucca (Yucca schidigera Roezl ex Ortgies) extract-supplemented diets on NH3 emissions. In Trial 1, nine pigs were offered a corn-soybean meal diet (C, 174 g kg(-1) CP), a Lys-supplemented diet (L, 170 g kg(-1) CP), or a 145 g kg(-1) CP diet supplemented with Lys, Met, Thr, and Trp (LMTT). In Trial 2, nine pigs were fed diet L supplemented with 0, 62.5, or 125 mg of yucca extract per kg diet. Each feeding period consisted of a 4-d dietary adjustment followed by 72 h of continuous NH3 measurement. Urine and fecal samples were collected each period. Feeding the LMTT diet reduced (P < 0.05) average daily gain (ADG) and feed efficiency (G:F) compared to diet L. Fecal N concentration decreased with a reduction in dietary CP, but urinary ammonium increased from pigs fed diet LMTT (2.0 g kg(-1), wet basis) compared to those fed diet C (1.1 g kg(-1)) or L (1.0 g kg(-1)). When pigs were fed reduced CP diets NH3 emission rates decreased (2.46, 2.16, and 1.05 mg min(-1) for diets C, L, and LMTT). Yucca had no effect on feed intake, ADG, or G:F. Ammonium and N concentrations of manure and NH3 emission rates did not differ with yucca content. Caution must be executed to maintain animal performance when strategies are implemented to reduce NH3 emissions.

Blood-to-brain glucose transport and cerebral glucose metabolism are not reduced in poorly controlled type 1 diabetes.

To test the hypothesis that blood-to-brain glucose transport is reduced in poorly controlled type 1 diabetes, we studied seven patients with a mean (+/- SD) HbA1c level of 10.1 +/- 1.2% and nine nondiabetic subjects during hyperinsulinemic, mildly hypoglycemic (approximately 3.6 mmol/l, approximately 65 mg/dl) glucose clamps. Blood-to-brain glucose transport and cerebral glucose metabolism were calculated from rate constants derived from blood and brain time-activity curves--the latter determined by positron emission tomography (PET)--after intravenous injection of [1-(11)C]glucose using a model that includes a fourth rate constant to account for regional egress of 11C metabolites. Cerebral blood flow and cerebral blood volume were determined with intravenous H2(15)O and inhaled C(15)O, respectively, also by PET. At plateau plasma glucose concentrations of 3.6 +/- 0.0 and 3.7 +/- 0.1 mmol/l, rates of blood-to-brain glucose transport were similar in the two groups (23.7 +/- 2.2 and 21.6 +/- 2.9 micromol x 100 g(-1) x min(-1), P = 0.569, in the control subjects and the patients, respectively). There were also no differences in the rates of cerebral glucose metabolism (16.8 +/- 0.8 and 16.3 +/- 1.2 micromol x 100 g(-1) x min(-1), P = 0.693, respectively). Plasma epinephrine (1,380 +/- 340 vs. 450 +/- 170 pmol/l, P = 0.0440) and glucagon (26 +/- 5 vs. 12 +/- 1 pmol/l, P = 0.0300) responses to mild hypoglycemia were reduced in the patients with type 1 diabetes. We conclude that neither blood-to-brain glucose transport nor cerebral glucose metabolism is measurably reduced in people with poorly controlled type 1 diabetes.

Blood-to-brain glucose transport, cerebral glucose metabolism, and cerebral blood flow are not increased after hypoglycemia.

Recent antecedent hypoglycemia has been found to shift glycemic thresholds for autonomic (including adrenomedullary epinephrine), symptomatic, and other responses to subsequent hypoglycemia to lower plasma glucose concentrations. This change in threshold is the basis of the clinical syndromes of hypoglycemia unawareness and, in part, defective glucose counterregulation and the unifying concept of hypoglycemia-associated autonomic failure in type 1 diabetes. We tested in healthy young adults the hypothesis that recent antecedent hypoglycemia increases blood-to-brain glucose transport, a plausible mechanism of this phenomenon. Eight subjects were studied after euglycemia, and nine were studied after approximately 24 h of interprandial hypoglycemia ( approximately 55 mg/dl, approximately 3.0 mmol/l). The latter were shown to have reduced plasma epinephrine (P = 0.009), neurogenic symptoms (P = 0.009), and other responses to subsequent hypoglycemia. Global bihemispheric blood-to-brain glucose transport and cerebral glucose metabolism were calculated from rate constants derived from blood and brain time-activity curves-the latter determined by positron emission tomography (PET)-after intravenous injection of [1-(11)C]glucose at clamped plasma glucose concentrations of 65 mg/dl (3.6 mmol/l). For these calculations, a model was used that includes a fourth rate constant to account for egress of [(11)C] metabolites. Cerebral blood flow was measured with intravenous [(15)O]water using PET. After euglycemia and after hypoglycemia, rates of blood-to-brain glucose transport (24.6 +/- 2.3 and 22.4 +/- 2.4 micromol. 100 g(-1). min(-1), respectively), cerebral glucose metabolism (16.8 +/- 0.9 and 15.9 +/- 0.9 micromol. 100 g(-1). min(-1), respectively) and cerebral blood flow (56.8 +/- 3.9 and 53.3 +/- 4.4 ml. 100 g(-1). min(-1), respectively) were virtually identical. These data do not support the hypothesis that recent antecedent hypoglycemia increases blood-to-brain glucose transport during subsequent hypoglycemia. They do not exclude regional increments in blood-to-brain glucose transport. Alternatively, the fundamental alteration might lie beyond the blood-brain barrier.

Scintigraphic detection of coronary artery thrombi in patients with acute myocardial infarction.

To determine whether coronary thrombi can be detected scintigraphically after acute myocardial infarction, 24 patients were studied with a new method employing indium-111-labeled platelets and technetium-99m-labeled red blood cells. Nine patients with suspected infarction were evaluated initially within 9 hours of the onset of symptoms and again 18 to 24 hours after onset. Eight patients with neurologic symptoms but without overt cardiac disease and seven patients with angina but without infarction served as unmatched control subjects. Foci of net indium accumulation were detected after image processing that incorporated subtraction of blood pool activity. Carotid and pulmonary artery reference regions, in which blood pool activity is high and active platelet deposition unlikely, were used to correct digitized cardiac scintigrams for indium-111 platelet activity in the blood pool. In patients with infarction, distinct foci of net indium accumulation were present in regions corresponding to the coronary artery supplying ischemic zones. This occurred in seven of eight patients at the time of the earliest evaluation (5.6 +/- 3.3 hours [mean +/- SD] after the onset of symptoms) and in eight of nine patients at the time of subsequent imaging (23.6 +/- 1.9 hours after onset). Only 1 of the 15 control patients exhibited a cardiac focus of net indium accumulation. The percent of indium excess (100 [total indium-111 activity-blood pool indium-111 activity]/blood pool indium-111 activity) within the cardiac region measured (+/- SD) 16.8 +/- 11.6% in all patients with myocardial infarction (19.1 +/- 11.2% in those with visually identified foci) compared with 0.4 +/- 4.3% in control patients (p less than 0.001). This method permits early detection and sequential assessment of coronary artery thrombi. It should permit improved characterization of the role of platelets in the pathogenesis of acute manifestations of coronary vascular disease and improved evaluation of interventions designed to prevent or lyse coronary thrombi.

Carbon flux assessment in cow-calf grazing systems.

Greenhouse gas (GHG) fluxes and soil organic carbon (SOC) accumulation in grassland ecosystems are intimately linked to grazing management. This study assessed the carbon equivalent flux (Ceq) from 1) an irrigated, heavily stocked, low-density grazing system, 2) a nonirrigated, lightly stocked, high-density grazing system, and 3) a grazing-exclusion pasture site on the basis of the GHG emissions from pasture soils and enteric methane emissions from cows grazing different pasture treatments. Soil organic carbon and total soil nitrogen stocks were measured but not included in Ceq determination because of study duration and time needed to observe a change in soil composition. Light- and heavy-stocking systems had 36% and 43% greater Ceq than nongrazed pasture sites, respectively ( < 0.01). The largest contributor to increased Ceq from grazing systems was enteric CH emissions, which represented 15% and 32% of the overall emissions for lightly and heavily stocked grazing systems, respectively. Across years, grazing systems also had increased nitrous oxide (N2O; < 0.01) and CH emissions from pasture soils ( < 0.01) compared with nongrazed pasture sites but, overall, minimally contributed to total emissions. Results indicate no clear difference in Ceqflux between the grazing systems studied when SOC change is not incorporated ( = 0.11). A greater stocking rate potentially increased total SOC stock ( = 0.02), the addition of SOC deeper into the soil horizon ( = 0.01), and soil OM content to 30 cm ( < 0.01). The incorporation of long-term annual carbon sequestration into the determination of Ceq could change results and possibly differentiate the grazing systems studied.

Pasture-derived greenhouse gas emissions in cow-calf production systems.

There is a lack of information regarding carbon dioxide (CO), methane (CH), and nitrous oxide (NO) emissions from pasture soils and the effects of grazing. The objective of this study was to quantify greenhouse gas (GHG) fluxes from pasture soils grazed with cow-calf pairs managed with different stocking rates and densities. The central hypothesis was that irrigated low-density stocking systems (SysB) would result in greater GHG emissions from pasture soils than nonirrigated high-density stocking systems (SysA) and grazing-exclusion (GRE) pasture sites. The nonirrigated high-density stocking systems consisted of 120 cow-calf pairs rotating on a total of 120 ha (stocking rate 1 cow/ha, stocking density 112,000 kg BW/ha, rest period of 60 to 90 d). The irrigated low-density stocking systems consisted of 64 cow-calf pairs rotating on a total of 26 ha of pasture (stocking rate 2.5 cows/ha, stocking density 32,700 kg BW/ha, rest period of 18 to 30 d). Both systems consisted of mixed cool-season grass-legume pastures. Static chambers were randomly placed for collection of CO, CH, and NO samples. Soil temperature (ST), ambient temperature (temperature inside the chamber; AT), and soil water content (WC) were monitored and considered explanatory variables for GHG emissions. GHG fluxes were monitored for 3 yr (2011 to 2013) at the beginning (P1) and at the end (P2) of the grazing season, always postgrazing. Paddock was the experimental unit (3 pseudoreplicates per treatment), and chambers (30 chambers per paddock) were considered multiple measurements of each experimental unit. A completely randomized design considered the term year × period as a repeated measure and chamber nested within paddock and treatment as the random term. Generally, SysB had greater CO emissions than SysA and GRE pasture sites across years and periods ( < 0.01). Soil temperature, AT, and WC had effects on CO emissions. Methane and NO emissions were observed from pasture sites of the 3 systems, but the effect of grazing was not constantly significant for CH and NO emissions. In addition, ST, AT, and WC did not conclusively explain CH and NO emissions. No clear trade-offs between GHG were observed; generally, GHG emissions increased from 2011 to 2013, which was likely associated with weather conditions, such as higher daily temperature and precipitation events. The central hypothesis that SysB would result in greater GHG emissions from pasture soils than SysA and GRE was not confirmed.

Enteric methane from lactating beef cows managed with high- and low-input grazing systems.

The objective of this study was to compare methane (CH) emissions from lactating beef cows grazed with different combinations of stocking rate and density. We hypothesized that a low stocking rate coupled with high-stocking-density grazing management would result in poorer forage quality, thereby increasing enteric CH emissions. System A (SysA) consisted of 120 cow-calf pairs rotating on a total of 120 ha divided into 2-ha pastures (stocking rate 1 cow/ha, stocking density 112,000 kg BW/ha, rest period of 60 to 90 d). System B (SysB) consisted of 16 groups of 4 cow-calf pairs each rotating on a 1.6-ha pasture (stocking rate 2.5 cows/ha, stocking density 32,000 kg BW/ha, rest period of 18 to 30 d). Enteric CH measurements were collected using a sulfur hexafluoride (SF) tracer gas method. Sampling occurred during 2012 and 2013 in 2 periods: the beginning (P1) and end of the grazing season (P2). Cannulated Angus cows were stratified by weight, age, and parity and were assigned to each treatment ( = 6) in a crossover design with a doubly repeated measures design, with period and day as repeated measures (α = 0.05). Dry matter intake was determined using chromic oxide (CrO) as a marker. Forage samples were collected ( = 3) for nutrient composition analyses and total forage mass determination. Forage botanical composition was determined using the dry-weight-rank method. Postgrazing herbage mass was greater for SysA during P2 in 2012 ( < 0.01) and 2013 ( = 0.01). Grasses were predominant and represented 67% to 96% of pastures; legumes contributed 3% to 21% of pastures across periods and treatments. The proportion of legumes tended to be higher in SysB pasture sites in P2 than in P1. There were no treatment effects on DMI. There was a period effect on DMI ( < 0.01); DMI of SysA and SysB cows increased from P1 to P2 (4 and 1.1 kg DMI/d increase, respectively). Cows ingested, on average, 2.6% (SysA) and 2.8% (SysB) of their BW. There was no year effect on CH emissions ( = 0.16). Daily enteric CH emissions did not vary with treatment and ranged from 195 to 249 g CH/d across treatment. Enteric CH emissions per unit GE intake varied with treatment during P1 (6.4% and 3.8% for SysA and SysB, respectively; < 0.01). Across treatments and periods, enteric CH emission per unit GE intake was 4.6%, which could be considered low for grazing lactating beef cows. It is likely that cows in the present study were selecting high-quality forage and produced comparatively lower CH emissions.

Cerebral blood volume measured with inhaled C15O and positron emission tomography.

Local cerebral blood volume (CBV) has been measured previously with inhaled 11CO and positron emission tomography (PET). The model used assumes that equilibrium in tracer concentration has occurred between arterial and systemic venous blood before the PET measurement is made. To verify that this model may be used with the much shorter half-lived C15O, we have simultaneously measured arterial and venous blood radioactivity following C15O inhalation. Equilibrium occurred 95 +/- 39 s after inhalation (n = 7). If the PET measurement is commenced prior to arteriovenous equilibrium, significant errors occur in calculated CBV. These data indicate that C15O may be used as a tracer for CBV measurement provided that emission data collection commences at approximately 120 s after inhalation. Strict quality control measures must be maintained to minimize the contamination of administered C15O with 15O-labeled CO2.

Cerebral blood flow and cerebral metabolic rate of oxygen requirements for cerebral function and viability in humans.

This study was undertaken to determine the minimum CBF and CMRO2 required by the human brain to maintain normal function and viability for more than a few hours. Positron emission tomography (PET) was used to perform regional measurements in 50 subjects with varying degrees of cerebral ischemia but no evidence of infarction. There were 24 normal subjects, 24 subjects with arteriographic evidence of vascular disease of the carotid system, and two subjects with reversible ischemic neurological deficits due to cerebral vasospasm. Minimum values found in the 48 subjects with normal neurological function were 19 ml/100 g-min for regional cerebral blood flow (rCBF) and 1.3 ml/100 g-min for regional cerebral metabolic rate of oxygen (rCMRO2). Minimum values for all 50 subjects with viable cerebral tissue were 15 ml/100 g-min for rCBF and 1.3 ml/100 g-min for rCMRO2. Comparison of these measurements with values from 20 areas of established cerebral infarction in 10 subjects demonstrated that 80% (16/20) of infarcted regions had rCMRO2 values below the lower normal limit of 1.3 ml/100 g-min. Measurements of rCBF, regional cerebral blood volume, and oxygen extraction fraction were less useful for distinguishing viable from infarcted tissue. These data indicate that quantitative regional measurements of rCMRO2 with PET accurately distinguish viable from nonviable cerebral tissue and may be useful in the prospective identification of patients with reversible ischemia.

Cerebral oxygen metabolism after aneurysmal subarachnoid hemorrhage.

Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1-4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.

Regional asymmetries of cerebral blood flow, blood volume, and oxygen utilization and extraction in normal subjects.

Positron emission tomography (PET) and 15O-labeled radiotracers were used to measure regional CBF, cerebral blood volume (CBV), CMRO2, and oxygen extraction in 32 right-handed subjects at rest. Mean left hemispheric CBF (46.2 +/- 6.8 ml/100 g/min) and CMRO2 (2.60 +/- 0.59 ml/100 g/min) were significantly lower than right hemispheric values (47.4 +/- 7.2 and 2.66 +/- 0.61 ml/100 g/min, respectively; p less than 0.0001 for both), whereas left and right hemispheric CBV and oxygen extraction were not significantly different. We further investigated these asymmetries by comparing left- and right-sided values for specific cortical and subcortical regions. We found that left-sided CBF and CMRO2 were significantly lower than right-sided values for sensorimotor, occipital, and superior temporal regions, whereas only left-sided CBF values were lower for anterior cingulum. CBV was asymmetric for the anterior cingulate and mid-frontal regions, and oxygen extraction was asymmetric for the sensorimotor area. No asymmetries were observed in inferior parietal cortex, thalamus, putamen, or pallidum. Knowledge of these normal physiological asymmetries is essential for proper interpretation of PET studies of physiology and pathology. Furthermore, the ability to detect asymmetries with PET may lead to a better understanding of the lateralization of specific functions in the human brain.

An absolute measurement of brain water content using magnetic resonance imaging in two focal cerebral ischemic rat models.

Magnetic resonance imaging (MRI) was utilized to obtain absolute estimates of regional brain water content (W), and results were compared with those obtained with conventional wet/dry measurements. In total, 31 male Long-Evans rats were studied and divided into two groups based on the surgical procedures used to induce cerebral focal ischemia: suture (n = 18) and three-vessel ligation (TVL: n = 13) groups. Both relative spin density and T1 were extracted from the acquired MR images. After correcting for radiofrequency field inhomogeneities, T2* signal decay, and temperature effects, in vivo regional brain water content, in absolute terms, was obtained by normalizing the measured relative brain spin density of animals to that of a water phantom. A highly linear relationship between MR-estimated brain water content based on the normalized spin density and wet/dry measurements was obtained with slopes of 0.989 and 0.986 for the suture (r = 0.79) and TVL (r = 0.83) groups, respectively. Except for the normal subcortex of the TVL group (P < 0.02) and the normal hemisphere of the suture group (P < 0.003), no significant differences were observed between MR-estimated and wet/dry measurements of brain water content. In addition, a highly linear relationship between MR-measured R1 (= 1/T1) and 1/W of wet/dry measurements was obtained. However, slopes of the linear regression lines in the two groups were significantly different (P < 0.02), indicating that different R1 values were associated with the same water content depending on the model. These results show that an absolute measurement of in vivo regional brain water content can be obtained with MRI and potentially serves as a noninvasive means to monitor different therapeutic interventions for the management of brain edema subsequent to stroke and head trauma.

Quantitative magnetic resonance imaging in experimental hypercapnia: improvement in the relation between changes in brain R2 and the oxygen saturation of venous blood after correction for changes in cerebral blood volume.

Acute hypercapnia simultaneously induces increases in regional cerebral blood volume (rCBV) and the oxygen saturation of cerebral venous blood (Yv). Changes in both physiologic parameters may influence the changes in R2 (deltaR2) that can be measured in the brain with gradient echo magnetic resonance imaging. The authors examined the effect of incorporating independent measurements of the change in rCBV (deltarCBV) on the fidelity of the relation between deltaR2 and deltaYv in the setting of experimental hypercapnia. A two-dimensional T2-weighted gradient echo sequence was used to measure deltaR2 in the brain parenchyma of anesthetized rats in response to hypercapnia with respect to the control state. In parallel, estimates of rCBV were obtained using a three-dimensional steady-state approach in conjunction with a paramagnetic contrast agent during both control and hypercapnic states so that a deltarCBV could be calculated. Regional CBV values of 2.96 +/- 0.82% and 5.74 +/- 1.21% were obtained during the control and hypercapnic states, respectively, and linear relations between rCBV and CO2 tension in both arterial (r = 0.80) and jugular venous (r = 0.76) blood samples were obtained. When correlating deltaR2 directly with deltaYv, no clear relation was apparent, but a strong linear relation (r = 0.76) was observed when correction for deltarCBV was incorporated into the data analysis. These results are consistent with the current understanding of the mechanisms of blood oxygen level-dependent (BOLD) contrast and underscore the potential importance of taking into account deltarCBV when quantitative estimates of deltaYv from the "BOLD effect" are intended.

Cerebral glucose transport and metabolism in preterm human infants.

Few data regarding early developmental changes in cerebral (blood-to-brain) glucose transport (CTXglc) and CMRglc are available for humans. We measured CBF, CTXglc, and CMRglc with positron emission tomography at 4 to 7 days of life in six preterm human infants whose estimated gestational age was 25 to 34 weeks. The Michaelis-Menten constants Kt and Tmax were estimated from CTXglc and the calculated cerebral capillary plasma glucose concentration. Mean CMRglc was 8.8 mumol 100 g-1 min-1. The CMRglc did not correlate with plasma glucose concentration (r = .315, P = .543), whereas CTXglc showed a significant correlation with plasma glucose concentration (r = .836, P = .038). Estimation of the Michaelis-Menten constants from the best fit to the measured data produced values of Kt = 6.0 mumol mL-1 and Tmax = 32.6 mumol 100 g-1 min-1. These values for Kt in the developing human brain are similar to those that have been reported for the mature brain of adolescent and adult humans and adult nonhuman primates, indicating the affinity of the glucose transport protein for D-glucose is similar. However, Tmax is approximately one third to one half of the comparable values for mature brain, indicating a reduced number of available luminal transporters.

Autoregulatory vasodilation of parenchymal vessels is impaired during cerebral vasospasm.

Impaired CBF autoregulation during vasospasm after aneurysmal subarachnoid hemorrhage (SAH) could reflect impaired capacity of distal vessels to dilate in response to reduced local perfusion pressure or simply indicate that the perfusion pressure distal to large arteries in spasm is so low that vessels are already maximally dilated. Autoregulatory vasodilation can be detected in vivo as an increase in the parenchymal cerebral blood volume (CBV). Regional CBV, CBF, and oxygen extraction fraction in regions with and without angiographic vasospasm obtained from 29 positron emission tomography studies performed after intracranial aneurysm rupture were compared with data from 19 normal volunteers and five patients with carotid artery occlusion. Regional CBF was reduced compared to normal in regions from SAH patients with and without vasospasm as well as with ipsilateral carotid occlusion (P < .0001). Regional oxygen extraction fraction was higher during vasospasm and distal to carotid occlusion than both normal and SAH without vasospasm (P < .0001). Regional CBV was reduced compared to normal in regions with and without spasm, whereas it was increased ipsilateral to carotid occlusion (P < .0001). These findings of reduced parenchymal CBV during vasospasm under similar conditions of tissue hypoxia that produce increased CBV in patients with carotid occlusion provide evidence that parenchymal vessels distal to arteries with angiographic spasm after SAH do not show normal autoregulatory vasodilation.

Experimental hypoxemic hypoxia: effects of variation in hematocrit on magnetic resonance T2*-weighted brain images.

T2*-weighted gradient echo magnetic resonance images of rat brain were obtained dynamically during acute hypoxemic hypoxia to investigate the relations between changes in cerebral blood oxygen saturation (deltaYb), blood hematocrit (Hct), and R2* (deltaR2*). Images from hypoxemic rats with normal Hct (42.8%+/-2.33%; n=12) were compared with those from hypoxemic rats with mild (33.4%+/-1.88%; n=8) or moderate (27.14%+/-2.7%; n=10) reduction of Hct. A linear relation between deltaYb and deltaR2* was obtained for all three groups. However, the slopes of the linear regressions were statistically different from one another (P < 0.001), with the slopes of the regression lines increasing inversely with Hct; that is, the slope for normal Hct is less than the slope for mildly reduced Hct, which is less than the slope for moderately reduced Hct. These data suggest that for any given reduction in the oxygen saturation of cerebral blood, the deltaR2* will be of a lesser magnitude when the hemoglobin concentration is reduced; the data are consistent with existing theoretical models of deoxyhemoglobin content-dependent effects in T2*-weighted magnetic resonance imaging.