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Biomedical subjects

E M Nemoto

Publications and source records attributed to E M Nemoto.

At least 19 recordsLinked to original sources
PubMed2006

Dynamics of cerebral venous and intracranial pressures.

Traumatic brain injury and stroke are both characterized by an ischemic core surrounded by a penumbra of low to hyperemic flows. The underperfused ischemic core is the focus of edema development, but the source of the edema fluid is not known. We hypothesized that flow of edema fluid into the tissue is derived from cerebral venous circulation pressure, which always exceeds intracranial pressure (ICP). As a first step toward testing this hypothesis, the aim of the current study was to determine whether cerebral venous pressure in the normal brain is always equal to or higher than ICP. In studies on 2 pigs, cerebral cortical venous, intracranial (subarachnoid), sagittal sinus, and central venous pressures were monitored with manipulation of ICP by raising and lowering a reservoir above and below the external auditory meatus zero point. The results show that cerebral venous pressure is always higher than or equal to ICP at pressures of up to 60 mmHg. On the basis of these observations, we hypothesize that increased cerebral venous pressure initiated after traumatic brain injury and stroke drives edema fluid into the tissue, which thereby increases ICP and a further increase in cerebral venous pressure in a vicious cycle of brain edema.

Animals↗
PubMed2004

Increased hepatic platelet activating factor (PAF) and PAF receptors in carbon tetrachloride induced liver cirrhosis.

BACKGROUND AND AIMS: The liver is a major site for the synthesis and actions of platelet activating factor (PAF), a potent hepatic vasoconstrictor and systemic vasodilator. As PAF is implicated in portal hypertension and hyperdynamic circulation associated with liver cirrhosis, we characterised changes in the hepatic PAF system in experimental cirrhosis. METHODS: In rats made cirrhotic by carbon tetrachloride (CCl(4)) administration for eight weeks, we determined hepatic levels of PAF and its cognate receptor, and the effects of PAF and PAF antagonist (BN52021) on portal and arterial pressure. RESULTS: Compared with control rats, cirrhotic rats had higher hepatic PAF levels, higher apparent hepatic efflux of PAF, and higher PAF levels in arterial blood (p<0.01, p<0.01, p<0.05, respectively). Relative to controls, cirrhotic livers had elevated hepatic PAF receptors (by mRNA and protein levels and [(3)H]PAF binding), higher (p<0.01) baseline hepatic portal pressure, and an augmented (p = 0.03) portal pressure response to PAF infusion (1 microg/kg). Portal infusion of BN52021 (5 mg/kg) showed that elevated endogenous PAF was responsible for 23% of the cirrhotic portal pressure increase but made no contribution to systemic hypotension. Finally, increased PAF receptor density was observed in the contractile perisinusoidal stellate cells isolated from cirrhotic livers relative to those from control livers. CONCLUSIONS: In cirrhosis, increased hepatic release of PAF elevates systemic PAF; in combination with upregulated hepatic PAF receptors in stellate cells, this contributes to portal hypertension.

Animals↗
PubMed2001

Regional low-flow perfusion provides somatic circulatory support during neonatal aortic arch surgery.

BACKGROUND: Regional low-flow perfusion has been shown to provide cerebral circulatory support during neonatal aortic arch operations. However, its ability to provide somatic circulatory support remains unknown. METHODS: Fifteen neonates undergoing arch reconstruction with regional perfusion were studied. Three techniques were used to assess somatic perfusion: abdominal aortic blood pressure, quadriceps blood flow (near-infrared spectroscopy), and gastric tonometry. RESULTS: Twelve patients required operation for hypoplastic left heart syndrome, and 3 required arch reconstruction with a biventricular repair. There was one death (7%). Abdominal aortic blood pressure was higher (12+/-3 mm Hg versus 0+/-0 mm Hg), and quadriceps blood volumes (5+/-24 versus -17+/-26) and oxygen saturations (57+/-25 versus 33+/-12) were greater during regional perfusion than during deep hypothermic circulatory arrest (p < 0.05). During rewarming, the arterial-gastric mucosal carbon dioxide tension difference was lower after circulatory arrest than after regional perfusion (-3.3+/-0.3 mm Hg versus 7.8+/-7.6 mm Hg, p < 0.05). CONCLUSIONS: Regional low-flow perfusion provides somatic circulatory support during neonatal arch surgical procedures. Support of the subdiaphragmatic viscera should improve the ability of neonates to survive the postoperative period.

Aorta, Abdominal↗
PubMed2001

Endotoxin treatment causes an upregulation of the endothelin system in the liver: amelioration of increased portal resistance by endothelin receptor antagonism.

BACKGROUND: Mechanisms underlying hepatic microcirculatory failure during endotoxemia are incompletely understood. Because endothelin-1 (ET-1) has been implicated in endotoxin-induced liver injury, we investigated the hepatic ET-1 system in endotoxin-treated rats. METHODS: Rats were treated with endotoxin (Escherichia coli lipopolysaccharide; 3 mg/kg, i.p.), and various determinations were made 24 h later. RESULTS: Endotoxin treatment caused 11.2 +/- 1.6% weight loss, a decrease in mean arterial pressure (MAP; 96 +/- 5 mmHg vs 108 +/- 3 mmHg; P < 0.05) and an increase in portal pressure (11.6 +/- 1.3 mmHg vs 7.4 +/- 1 mmHg; P < 0.02). No significant changes in the serum levels of liver enzymes or hepatocellular necrosis were observed. Endotoxin caused increases in hepatic ET-1 (from 345 +/- 31 to 565 +/- 38 pg/g; P < 0.01), ET-1 receptor density (from 179 +/- 16 to 340 +/- 26 fmol/mg; P < 0.02), and mRNA expression of preproendothelin-1, and ET(A) and ET(B) receptors. While the serum nitric oxide (nitrite +/- nitrate) concentration was increased in endotoxin-treated rats, that of ET-1 remained unchanged. A mixed ET(A)/ET(B) receptor antagonist, TAK-044 (10 mg/kg, i.v.), reduced the weight loss from 11.2 +/- 1.6% to 5.9 +/- 2.9% (P < 0.05) and the portal pressure from 11.6 +/- 1.3 mmHg to 8.6 +/- 0.7 mmHg (P < 0.05) in endotoxin-treated rats. The mixed ET(A)/ET(B) receptor antagonist also caused an increase in serum ET-1 concentration, but did not affect serum nitric oxide and MAP in endotoxin-treated rats. CONCLUSIONS: These results suggest that the upregulated hepatic ET-1 system is an important mechanism of increased portal resistance and related complications of endotoxemia.

Animals↗
PubMed2001

Hypothermic cardiopulmonary bypass alters oxygen/glucose uptake in the pediatric brain.

OBJECTIVES: Neurologic morbidity related to cardiac surgery has been recognized as a major morbidity. A variety of causes related to cardiopulmonary bypass, including microemboli, nonpulsatile flow, hemodilution, and inflammatory mediation, have been proposed. Because oxygen and glucose are the predominant metabolic substrates for the brain, we sought to examine the uptake of these substrates by the pediatric brain during hypothermic cardiopulmonary bypass. METHODS: Eleven children (median age 5 months, range 1 day-17 years) undergoing a variety of cardiac surgical procedures with the use of hypothermic cardiopulmonary bypass were studied. Cerebral arteriovenous differences for oxygen, glucose, and lactate were obtained before, during, and after bypass. On the basis of the predictable stoichiometric relationship for the oxidation of glucose, the relationship of substrate uptake was expressed as the oxygen/glucose index.Oxygen/glucose index (%) = (arteriovenous oxygen difference [micromol/mL]/arteriovenous glucose difference [micromol/mL] x 6) x 100 RESULTS: All children survived with no obvious neurologic sequelae. During cooling on cardiopulmonary bypass, the oxygen/glucose indexes fell significantly from prebypass values (53% +/- 19% at 28 degrees C and 54% +/- 25% at 24 degrees C vs 117% +/- 70%; P <.05, analysis of variance). This decline resulted from decreased oxygen uptake with stable glucose uptake (P <.05). Although oxygen and glucose uptake both increased with rewarming, the net effect was only a slight increase in oxygen/glucose index (62% +/- 16%). Postbypass oxygen/glucose index exceeded prebypass values (149% +/- 83%). CONCLUSIONS: Hypothermic cardiopulmonary bypass alters the relationship between oxygen and glucose uptake in the pediatric brain. The relationship of these findings to bypass-related neurologic morbidity remains to be explored.

Adolescent↗
PubMed2001

Association of intraluminal thrombus in abdominal aortic aneurysm with local hypoxia and wall weakening.

PURPOSE: Our previous computer models suggested that intraluminal thrombus (ILT) within an abdominal aortic aneurysm (AAA) attenuates oxygen diffusion to the AAA wall, possibly causing localized hypoxia and contributing to wall weakening. The purpose of this work was to investigate this possibility. METHODS: In one arm of this study, patients with AAA were placed in one of two groups: (1) those with an ILT of 4-mm or greater thickness on the anterior surface or (2) those with little (< 4 mm) or no ILT at this site. During surgical resection but before aortic cross-clamping, a needle-type polarographic partial pressure of oxygen (PO2) electrode was inserted into the wall of the exposed AAA, and the PO2 was measured. The probe was advanced, and measurements were made midway through the thrombus and in the lumen. Mural and mid-ILT PO2 measurements were normalized by the intraluminal PO2 measurement to account for patient variability. In the second arm of this study, two AAA wall specimens were obtained from two different sites of the same aneurysm at the time of surgical resection: group I specimens had thick adherent ILT, and group II specimens had thinner or no adherent ILT. Nonaneurysmal tissue was also obtained from the infrarenal aorta of organ donors. Specimens were subjected to histologic, immunohistochemical, and tensile strength analyses to provide data on degree of inflammation (% area inflammatory cells), neovascularization (number of capillaries per high-power field), and tensile strength (peak attainable load). Additional specimens were subjected to Western blotting and immunohistochemistry for qualitative evaluation of expression of the cellular hypoxia marker oxygen-regulated protein. RESULTS: The PO2 measured within the AAA wall in group I (n = 4) and group II (n = 7) patients was 18% +/- 9% luminal value versus 60% +/- 6% (mean +/- SEM; P <.01). The normalized PO2 within the ILT of group I patients was 39% +/- 10% (P =.08 with respect to the group I wall value). Group I tissue specimens showed greater inflammation (P <.05) compared with both group II specimens and nonaneurysmal tissue: 2.9% +/- 0.6% area (n = 7) versus 1.7% +/- 0.3% area (n = 7) versus 0.2% +/- 0.1% area (n = 3), respectively. We found similar differences for neovascularization (number of vessels/high-power field), but only group I versus control was significantly different (P <.05): 16.9 +/- 1.6 (n = 7) vs 13.0 +/- 2.3 (n = 7) vs 8.7 +/- 2.0 (n = 3), respectively. Both Western blotting and immunohistochemistry results suggest that oxygen-regulated protein is more abundantly expressed in group I versus group II specimens. Tensile strength of group I specimens was significantly less (P <.05) than that for group II specimens: 138 +/- 19 N/cm2 (n = 7) versus 216 +/- 34 N/cm2 (n = 7), respectively. CONCLUSION: Our results suggest that localized hypoxia occurs in regions of thicker ILT in AAA. This may lead to increased, localized mural neovascularization and inflammation, as well as regional wall weakening. We conclude that ILT may play an important role in the pathology and natural history of AAA.

Aged↗
PubMed2001

Cerebrovascular reserve in patients with carotid occlusive disease assessed by stable xenon-enhanced ct cerebral blood flow and transcranial Doppler.

BACKGROUND AND PURPOSE: Cerebrovascular reserve (CVR) by both transcranial Doppler ultrasonography (TCD) and quantitative cerebral blood flow (CBF) can identify subgroups of patients at increased risk for stroke. A direct comparison of CVR measurements obtained with both technologies in patients with cerebrovascular occlusive disease is lacking. METHODS: CVRs before and after acetazolamide administration (1 g IV) were measured by TCD insonation of the middle cerebral artery (MCA) and CBF obtained with stable xenon CT (Xe/CT) in 38 patients with carotid occlusive disease. Sensitivity/specificity calculations were based on 2 Xe/CT MCA values: an average over 4 levels and the level with the lowest percent change in CBF. Compromised CVR was defined as no reactivity or a decrease in reactivity. RESULTS: Using the analysis of the systolic TCD, we found that velocity changes compared with the average Xe/CT MCA CVR showed a sensitivity of 33%, specificity of 90.6%, positive predictive value of 54.5%, and negative predictive value of 80%. The sensitivity of TCD compared with the lowest Xe/CT CBF CVR was 35.5%, specificity and positive predictive values were 100%, and negative predictive value was 66.7%. The index of validity was between 72% and 76%. CONCLUSIONS: TCD is much less sensitive than Xe/CT CBF in identifying patients with compromised CVR. This may be a result of the inability of TCD to identify patients with compromised reserves when their MCA blood flow comes from collateral sources. The lack of correlation between TCD and Xe/CT CBF for identifying patients with compromised CVR should be considered when stroke risk assessments are made by TCD.

Acetazolamide↗
PubMed2000

Regional low-flow perfusion provides cerebral circulatory support during neonatal aortic arch reconstruction.

OBJECTIVE: Because of concerns regarding the effects of deep hypothermia and circulatory arrest on the neonatal brain, we have developed a technique of regional low-flow perfusion that provides cerebral circulatory support during neonatal aortic arch reconstruction. METHODS: We studied the effects of regional low-flow perfusion on cerebral oxygen saturation and blood volume as measured by near-infrared spectroscopy in 6 neonates who underwent aortic arch reconstruction and compared these effects with 6 children who underwent cardiac repair with deep hypothermia and circulatory arrest. RESULTS: All the children survived with no observed neurologic sequelae. Near-infrared spectroscopy documented significant decreases in both cerebral blood volume and oxygen saturations in children who underwent repair with deep hypothermia and circulatory arrest as compared with children with regional low-flow perfusion. Reacquisition of baseline cerebral blood volume and cerebral oxygen saturations were accomplished with a regional low-flow perfusion rate of 20 mL x kg(-1) x min(-1). CONCLUSIONS: Regional low-flow perfusion is a safe and simple bypass management technique that provides cerebral circulatory support during neonatal aortic arch reconstruction. The reduction of deep hypothermia and circulatory arrest time required may reduce the risk of cognitive and psychomotor deficits.

Aorta, Thoracic↗
PubMed2000

Clinical experience with cerebral oximetry in stroke and cardiac arrest.

OBJECTIVE: To address the ability and reliability of the INVOS 3100A (Somanetics, Troy, MI) cerebral oximeter to detect cerebral desaturation in patients and the interpretation of cerebral oximetry measurements using the INVOS 3100A in stroke and cardiac arrest. DESIGN: Case reports of two patients. SETTING: Neurologic Intensive Care Unit of a University Hospital. PATIENTS: Two patients suffering occlusive strokes of the middle cerebral artery. One later suffered a cardiac arrest. RESULTS: The first case, a patient who suffered cardiac arrest while undergoing continuous cerebral oximetry, clearly demonstrated the ability of the INVOS 3100A to detect rapid tissue vascular oxyhemoglobin desaturation in the brain during circulatory arrest. In the second case, oximetry readings were obtained in a patient with a right internal carotid artery occlusion and an infarct in the middle cerebral artery territory. The circulation of the anterior cerebral artery (ACA) territory was intact. Stable xenon-computed tomography of local cerebral blood flow showed no perfusion in the infarct, and oximetry readings were between 60 and 65. In the border zone between the middle cerebral artery and the ACA, readings of 35 to 40 were obtained, and over the ACA territory, the readings were in the 60s. CONCLUSIONS: Oximetry by near infrared spectroscopy reflects the balance between regional oxygen supply and demand. In dead or infarcted nonmetabolizing brain, saturation may be near normal because of sequestered cerebral venous blood in capillaries and venous capacitance vessels and contribution from overlying tissue. In regionally or globally ischemic, but metabolizing brain, saturation decreases because oxygen supply is insufficient to meet metabolic demand. These observations are supported by previously reported "normal" readings in unperfused or dead brains.

Aged↗
PubMed2000

Comparison of two commercially available near-infrared spectroscopy instruments for cerebral oximetry. Technical note.

Two near-infrared spectroscopy (NIRS) devices were compared with regard to their responses to changes in cerebral hemoglobin oxygenation induced by hypoxia and hypercapnia in five healthy volunteers. Sensors belonging to each NIRS device were placed on opposite sides of the volunteer's forehead. The INVOS-3100A device, approved by the United States Food and Drug Administration, records the percentage of oxyhemoglobin (HbO2) saturation and the investigational NIRO500 device records absolute changes in HbO2, deoxyhemoglobin, and total hemoglobin in micromolar concentrations referenced to an arbitrary baseline. The volunteers breathed separate mixtures of 7% CO2 in O2 and 10% O2 for 5 minutes in random order. Arterial blood pressure, end-tidal CO2 (ETCO2), arterial O2 saturation, and electrocardiographic data were continuously monitored. Hypercapnia increased (p < 0.01) ETCO2 from 42+/-2 to 56+/-3 mm Hg (mean +/- standard deviation), resulting in a 7.3+/-0.2% increase (p < 0.005) in cerebral HbO2 saturation detected by the INVOS3100A device and an 11.6+/-3 microM increase (p < 0.0008) in HbO2 detected by the NIRO500. Hypoxia decreased (p < 0.01) arterial HbO2 saturation from 98+/-1 to 87+/-3%, causing a 5.1+/-1.2% decrease (p < 0.01) in the percentage of HbO2 saturation detected by the INVOS3100A device and a 9.7+/-6.3 microM decrease in HbO2 detected by the NIRO500. The responses of the NIRO500 and the INVOS3100A instruments to changes in cerebral oxygenation resulting from hypercapnia and hypoxia were generally similar; however, responses tended to be greater when recorded by the NIRO500 device, perhaps because, unlike the INVOS3100A device, the NIRO500 does not correct for skin and bone contamination.

Blood Gas Monitoring, Transcutaneous↗
PubMed1999

Near-infrared spectroscopy monitored cerebral venous thrombolysis.

BACKGROUND: Cerebral venous thrombosis is a clinical entity which is readily diagnosed with the advent of modern imaging techniques. Anticoagulation is now a standard therapy, but more recent treatment strategies have included endovascular thrombolysis. While the endpoint of this intervention both clinically and radiographically has not been defined, noninvasive monitoring techniques may add further objective measures of treatment response. CLINICAL PRESENTATION: We present a patient with a four day history of worsening headache and papilledema on exam. Superior sagittal, straight, and bilateral transverse sinus thromboses were identified on computed tomography and angiography. INTERVENTION: Emergent endovascular thrombolysis by a transvenous approach re-established venous patency and resulted in immediate resolution of the patient's symptoms. Cerebral oximetry by near-infrared spectroscopy was utilized during the procedure, and changes in chromophore concentrations correlated directly with angiographic and clinical resolution of the thrombosis. CONCLUSION: Near-infrared spectroscopy can provide continuous feedback during thrombolytic therapy in cerebral venous thrombosis and may help define endpoints of such intervention.

Adult↗