Biomedical subjects

Shosuke Takahashi

Publications and source records attributed to Shosuke Takahashi.

At least 19 recordsLinked to original sources

PubMed2006

Rapid and random turnover of mitochondrial DNA in rat hepatocytes of primary culture.

It is known that mitochondrial DNA (mtDNA) replication is independent of the cell cycle. Even in post-mitotic cells in which nuclear DNA replication has ceased, mtDNA is believed to still be replicating. Here, we investigated the turnover rate of mtDNA in primary rat hepatocytes, which are quiescent cells. Southwestern blot analysis using 5-bromo-2'-deoxyuridine (BrdU) was employed to estimate the activity of full-length mtDNA replication and to determine efficient doses of replication inhibitors. Southern blot analysis showed that a two-day treatment with 20mM 2',3'-dideoxycytidine and 0.2mug/ml ethidium bromide caused a 37% reduction in the amount of mtDNA, indicating that the hepatocytes had a considerably high rate of turnover of mtDNA. Further, pulse-chase analysis using Southwestern analysis showed that the amount of newly synthesized mtDNA labeled with BrdU declined to 60% of the basal level within two days. Because the rate of reduction of the new mtDNA was very similar to the overall turnover rate described above, it appears that degrading mtDNA molecules were randomly chosen. Thus, we demonstrated that there is highly active and random turnover of mtDNA in hepatocytes.

Animals↗

PubMed2006

[Dexmedetomidine].

Dexmedetomidine, a potent and highly selective alpha2-agonist, provides a unique "conscious sedation" (patients appear to be asleep, but are readily roused), analgesia, without respiratory depression. In order to provide a comfortable sedation to the ICU patients, careful evaluation of sedation and analgesia level, and the consistent treatment by medical teams are necessary. We may expect the usefulness of dexmedetomidine in the settings other than the ICU, from its pharmacological properties. Clinical applications of dexmedetomidine for several procedures such as awake craniotomy, fiberoptic tracheal intubation, or MRI examination have been reported, suggesting its usefulness and problems. The major problem with dexmedetomidine is its hemodynamic effects. Because this drug often causes hypotension, hypertension and bradycardia, it should be used under the control by skilled medical teams.

Adrenergic alpha-Agonists↗

PubMed2005

Noninvasive assessment of left ventricular pressure-area relationship using transesophageal echocardiography and tonometry during cardiac and abdominal aortic surgery.

PURPOSE: The purpose of this study was to noninvasively evaluate intraoperative left ventricular (LV) performance by an online pressure-area relationship using transesophageal echocardiography (TEE) and tonometry. METHODS: In study 1, LV pressure with a micromanometer catheter, LV cross-sectional area with TEE, direct radial pressure, and tonometric arterial pressure were simultaneously recorded in 5 patients (10 measurements) undergoing cardiac surgery. End-systolic elastance (E'es) was determined from pressure-area loops during inferior vena caval (IVC) occlusion. In study 2, in 16 patients undergoing repair of abdominal aortic aneurysm, LV performance (E'es; effective arterial load, E'a, and LV end-diastolic area, LV-EDA) was examined by noninvasive assessment of pressure-area loops using TEE and tonometry at aortic cross-clamping and unclamping. RESULTS: E'es by tonometric arterial pressure closely correlated with E'es by LV pressure (r = 0.92) in study 1. E'es at aortic clamping were not significantly different from those at unclamping. The clamping increased LV-EDA and E'a by approximately 13% and 44%, and the unclamping significantly decreased by 9% and 22%, respectively. CONCLUSION: Our results demonstrated that online tonometric arterial pressure and LV area measured by automated border detection (ABD) of TEE might be used to calculate E'es to estimate LV contractility and allow the estimation of LV performance during aortic clamping and unclamping.

Aged↗

PubMed2005

Influence of diabetes mellitus, hypercholesterolemia, and their combination on EDHF-mediated responses in mice.

The endothelium synthesizes and releases several vasodilator substances, including vasodilator prostaglandins, NO, and EDHF. NO-mediated relaxations are reduced by various risk factors, such as diabetes mellitus and hypercholesterolemia. However, it remains to be elucidated whether EDHF-mediated relaxations also are reduced by those factors and their combination. In this study, we addressed this point in mice. We used small mesenteric arteries from control, diabetic (streptozotocin-induced), apolipoprotein-E-deficient (ApoE-/-), and diabetic ApoE-/- mice. In control mice, endothelium-dependent relaxations to acetylcholine were largely mediated by EDHF. This EDHF-mediated component was slightly reduced in diabetic mice, preserved in ApoE-/- mice, and markedly reduced in diabetic ApoE-/- mice with an increase in NO-mediated component and a negative contribution of indomethacin-sensitive endothelium-derived contracting factor (EDCF). Endothelium-independent relaxations to sodium nitroprusside or NS1619, a direct opener of calcium-activated K channels, were attenuated in ApoE-/- and diabetic ApoE-/- mice. Endothelium-dependent hyperpolarizations were significantly reduced in diabetic mice, preserved in ApoE-/- mice, and again markedly reduced in diabetic ApoE-/- mice. These results indicate that hypercholesterolemia alone minimally affects the EDHF-mediated relaxations, and diabetes mellitus significantly attenuated the responses, whereas their combination markedly attenuates the responses with a compensatory involvement of NO and a negative contribution of EDCF.

Acetylcholine↗

PubMed2004

Inactivation of protease-activated receptor-1 by proteolytic removal of the ligand region in vascular endothelial cells.

Proteolysis plays an important role in inactivating protease-activated receptor-1 (PAR1). We aimed to determine the cleavage site(s) responsive for the proteolytic inactivation of PAR1 in human umbilical vein endothelial cells. Fura-2 fluorometry revealed that the preceding stimulation with trypsin abolished the subsequent [Ca(2+)](i) response to thrombin, while the responses to PAR1-activating peptides remained intact. On the other hand, thrombin had no effect on the subsequent response to trypsin. The immunostaining with antibodies against the residues 35-46 (SPAN12) and 51-64 (WEDE15) revealed the broad boundaries of cleavage. Trypsin removed both epitopes from the cell surface within 3 min, while thrombin removed the epitope of SPAN12. The longer incubation with thrombin removed the epitope of WEDE15. However, PAR1-activating peptides thereafter induced an attenuated but significant elevation of [Ca(2+)](i). Not only the receptor internalization as observed with a confocal microscope, but also an additional cleavage was thus suggested to contribute to the thrombin-induced removal of the epitope of WEDE15. The analyses of the PAR1 mutants identified three cleavage sites for trypsin; residues 41-42, 70-71 and 82-83. The cleavage at the latter two sites was suggested to dominate that at the former, and thus remove the ligand region (residues 42-47). The inactivation of PAR1 due to proteolytic removal of the ligand region may contribute not only to the inactivation of PAR1 by proteases such as trypsin, but also to the termination of the intracellular signaling initiated by thrombin in the vascular endothelial cells.

Calcium Signaling↗

PubMed2004

Transduction of the N-terminal fragments of MYPT1 enhances myofilament Ca2+ sensitivity in an intact coronary artery.

OBJECTIVE: The region of the 110 kDa regulatory subunit (MYPT1) of smooth muscle myosin phosphatase involved in the regulation of contraction was determined under physiological conditions. METHODS AND RESULTS: Using HIV Tat protein-mediated protein transduction, the N-terminal fragments of MYPT1 were introduced to the intact porcine coronary arterial strips. Pre-incubation with 3 micromol/L TAT-MYPT1(1-374), a construct containing the Tat peptide and the residues 1 to 374 of MYPT1, for 15 minutes augmented (2.4-fold) the subsequent contraction induced by adding 1.25 mmol/L of extracellular Ca2+ under 118 mmol/L K+ depolarization, with no augmentation of the [Ca2+]i elevation. The deletion of the Tat peptide, MYPT1(1-374), abolished the augmenting effect. TAT-MYPT1(1-296) demonstrated a weaker but significant augmentation (1.7-fold). However, TAT-MYPT1(1-171), TAT-MYPT1(39-374), TAT-MYPT1(39-296), and TAT-MYPT1(297-374) had no augmenting activity. The myosin light chain phosphorylation level as a function of extracellular Ca2+ concentrations was shifted to the left in the strips pretreated with TAT-MYPT1(1-374) compared with the control. CONCLUSIONS: Region 1 to 296 was the minimal region involved in the enhancement of contraction, and region 297 to 374 played a supplemental role. These results suggested that the interaction mainly between catalytic subunit and MYPT1 play a critical role in the regulation of the endogenous myosin phosphatase in intact smooth muscle.

Actin Cytoskeleton↗

PubMed2004

Changes in body temperature during profound hypothermic cardiopulmonary bypass in adult patients undergoing aortic arch reconstruction.

PURPOSE: Our aim was to characterize changes in body temperatures during profound hypothermic cardiopulmonary bypass (CPB) conducted with the sternum opened. METHODS: In ten adult patients who underwent profound hypothermic (< 20 degrees C) CPB for aortic arch reconstruction, pulmonary arterial temperature (PAT), nasopharyngeal temperature (NPT), forehead deep-tissue temperature (FHT), and urinary bladder temperature (UBT) were recorded every 1 min throughout the surgery. In addition, the CPB venous line temperature (CPBT), a reasonable indicator of mixed venous blood temperature during CPB and believed to best reflect core temperature during stabilized hypothermia on CPB, was recorded during the period of total CPB. RESULTS: PAT began to change immediately after the start of cooling or rewarming, closely matching the CPBT ( r = 0.98). During either situation, the other four temperatures lagged behind PAT ( P < 0.05); however, NPT followed PAT more closely than the other three temperatures ( P < 0.05). During stabilized hypothermia, PAT, NPT, and FHT, but not UBT, closely matched the CPBT, with gradients of less than 0.5 degrees C. CONCLUSION: During induction of profound hypothermia and its reversal on total CPB with the heart in situ, a PA catheter thermistor, presumably because of its placement immediately behind the superior vena cava, would provide a reliable measure of the mixed venous blood temperature. During stabilized profound hypothermia, PAT, NPT, and FHT, but not UBT, serve as a reliable index of core temperature.

Aged↗

PubMed2004

Important role of superoxide dismutase in EDHF-mediated responses of human mesenteric arteries.

The endothelium synthesizes and releases several vasodilator substances, including prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF). We have identified hydrogen peroxide (H2O2) as an EDHF in mouse and human mesenteric arteries and porcine coronary microvessels. We also have recently demonstrated that Cu,Zn-SOD plays an important role in EDHF synthesis in mouse mesenteric arteries. However, it remains to be determined whether SOD also plays an important role in EDHF-mediated responses of human arteries. In this study, we addressed this point in human mesenteric arteries. We used small mesenteric arteries of patients who underwent gastrectomy operations. Isometric tensions and membrane potentials were recorded in the presence of indomethacin and N-nitro-L-arginine to inhibit the synthesis of prostacyclin and NO, respectively. Pretreatment with Tiron, a cell-permeable SOD-mimetic, significantly enhanced the EDHF-mediated relaxations and hyperpolarizations to bradykinin, and this effect was abolished by catalase, indicating that this enhancing effect was achieved by H2O2. By contrast, Tiron did not affect endothelium-independent relaxations, indicating that the enhancing effect of Tiron is not caused by the enhancement of vascular smooth muscle responses. These results indicate that SOD plays an important role in EDHF-mediated relaxations and hyperpolarizations of human mesenteric arteries.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMed2004

[Changes in serum Na+ and blood hemoglobin levels during three types of transurethral procedures for the treatment of benign prostatic hypertrophy].

BACKGROUND: Transurethral holmium YAG laser resection of the prostate (HoLR-P) and transurethral electrovaporization of the prostate (TUV-P) have recently received increasing attention as an effective minimally invasive approach for the treatment of prostatic hypertrophy. However, less information is available regarding the intraoperative changes in the serum Na+ and blood hemoglobin levels during either HoLR-P or TUV-P. METHODS: Intraoperative changes in serum Na+ and blood hemoglobin levels were investigated in 17 patients undergoing transurethral resection of the prostate (TUR-P, n = 7), HoLR-P (n = 7) or TUV-P (n = 3). The 3% D-sorbitol solution was used as the irrigating fluid in all the patients. RESULTS: In three patients, severe hyponatremia (118-123 mEq x l(-1)) developed abruptly (< or = 15 min) at various time points during TUR-P with (n = 1) or without (n = 2) cystostomy. However, no clinical symptoms were observed after development of the hyponatremia in those awake patients. No large (> 10 mEq x l(-1)) decreases in the Na+ level were observed in any of the patients undergoing HoLR-P or TUV-P. In patients undergoing TUR-P and HoLR-P, percent changes in serum Na+ level significantly correlated with those in blood hemoglobin level, but not with the resection time; the slopes were significantly larger than unity. CONCLUSIONS: The TUR syndrome is less likely to occur during HoLR-P or TUV-P. During TUR-P, the onset of severe hyponatremia appears to be unpredictable, and may not necessarily be accompanied by clinical symptoms. Frequent measurements of the serum Na+ level appear essential for early detection of severe hyponatremia.

Aged↗

PubMed2003

Evidence for protein kinase C-mediated activation of Rho-kinase in a porcine model of coronary artery spasm.

OBJECTIVE: We have recently demonstrated that protein kinase C (PKC) and Rho-kinase play important roles in coronary vasospasm in a porcine model. However, it remains to be examined whether there is an interaction between the two molecules to cause the spasm. METHODS AND RESULTS: A segment of left porcine coronary artery was chronically treated with IL-1beta-bound microbeads in vivo. Two weeks after the operation, phorbol ester caused coronary spasm in vivo and coronary hypercontractions in vitro at the IL-1beta-treated segment; both were significantly inhibited by hydroxyfasudil, a specific Rho-kinase inhibitor. Guanosine 5'-[gamma-thio]triphosphate (GTPgammaS), which activates Rho with a resultant activation of Rho-kinase, enhanced Ca2+ sensitization of permeabilized vascular smooth muscle cells, which were resistant to the blockade of PKC by calphostin C. The GTPgammaS-induced Ca2+ sensitization was greater in the spastic segment than in the control segment. Western blot analysis revealed that only PKCdelta isoform was activated during the hypercontraction. CONCLUSIONS: These results demonstrate that PKC and Rho-kinase coexist on the same intracellular signaling pathway, with PKC located upstream on Rho-kinase, and that among the PKC isoforms, only PKCdelta may be involved. Thus, the strategy to inhibit Rho-kinase rather than PKC may be a more specific and useful treatment for coronary spasm.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2003

Long-term inhibition of Rho-kinase suppresses angiotensin II-induced cardiovascular hypertrophy in rats in vivo: effect on endothelial NAD(P)H oxidase system.

Intracellular signaling pathway mediated by small GTPase Rho and its effector Rho-kinase plays an important role in regulation of vascular smooth muscle contraction and other cellular functions. We have recently demonstrated that Rho-kinase is substantially involved in angiotensin II-induced gene expressions and various cellular responses in vitro. However, it remains to be examined whether Rho-kinase is involved in the angiotensin II-induced cardiovascular hypertrophy in vivo and, if so, what mechanisms are involved. Long-term infusion of angiotensin II for 4 weeks caused hypertrophic changes of vascular smooth muscle and cardiomyocytes in rats. Both changes were significantly suppressed by concomitant oral treatment with fasudil, which is metabolized to a specific Rho-kinase inhibitor, hydroxyfasudil, after oral administration. Angiotensin II caused a perivascular accumulation of macrophages and Rho-kinase activation, both of which were also significantly suppressed by fasudil. Vascular NAD(P)H oxidase expression (nox1, nox4, gp91phox, and p22phox) and endothelial production of superoxide anions were markedly increased by angiotensin II, both of which were also significantly suppressed by fasudil. Thus, fasudil ameliorated the impaired endothelium-dependent relaxations caused by angiotensin II without affecting vasodilator function of vascular smooth muscle. These results provide evidence that Rho-kinase is substantially involved in the angiotensin II-induced cardiovascular hypertrophy in rats in vivo. The suppression of endothelial NAD(P)H oxidase upregulation and resultant superoxide production and the amelioration of endothelial vasodilator function may be involved in this process.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2003

Unproductive cleavage and the inactivation of protease-activated receptor-1 by trypsin in vascular endothelial cells.

1 Using fura-2 fluorometry of [Ca(2+)](i) in response to thrombin, trypsin and protease-activated receptor activating peptides (PAR-APs), we determined whether trypsin cleaves protease-activated receptor 1 (PAR1) and activates it in the endothelial cells of the porcine aortic valves and human umbilical vein. 2 Once stimulated with thrombin, the subsequent application of trypsin induced a [Ca(2+)](i) elevation similar to that obtained without the preceding stimulation with thrombin in the valvular endothelial cells. However, the preceding stimulation with trypsin abolished the subsequent response to thrombin, but not to bradykinin or substance P. 3 The response to PAR1-AP (SFLLRNP) was significantly (P<0.05) reduced by the preceding stimulation with thrombin and PAR1-AP in the valvular endothelial cells, while, importantly, it remained unaffected by the preceding stimulation with either trypsin or PAR2-AP (SLIGRL). The response to PAR2-AP was reduced by the preceding stimulation with trypsin and PAP2-AP. PAR1-AP attenuated the subsequent responses not only to thrombin and PAR1-AP but also to trypsin and PAR2-AP, while PAR2-AP specifically attenuated the subsequent responses to trypsin and PAR2-AP. 4 In human umbilical vein endothelial cells, a higher affinity PAR1-AP (haPAR1-AP) (Ala-pF-Arg-Cha-HArg-Tyr-NH(2)) specifically attenuated the responses to thrombin but not trypsin. On the other hand, the response to haPAR1-AP was significantly (P<0.05) attenuated by the preceding stimulation with thrombin but not trypsin. 5 In conclusion, trypsin cleaved PAR1 but did not activate it in the endothelial cells. Moreover, the trypsin-cleaved PAR1 was no longer responsive to thrombin.

Animals↗

PubMed2003

Quantitative analysis of left ventricular regional wall motion with color kinesis during abdominal aortic cross-clamping.

OBJECTIVES: The authors aimed to establish a technique for quantitative analysis of regional wall motion abnormality (RWMA) using color kinesis (CK) of transesophageal echocardiography (TEE) in surgical patients. This technique was used to determine whether RWMAs develop de novo after infrarenal aortic cross-clamping in patients undergoing vascular surgery with a preoperative dipyridamole thallium stress test (DTST). DESIGN: An observational study. SETTING: University hospital. PARTICIPANTS: Thirty-eight patients undergoing infrarenal abdominal aortic aneurysm resection or aortofemoral bypass. MEASUREMENTS AND MAIN RESULTS: CK images of the left ventricle (LV) were obtained from the midventricular transgastric short-axis view before and after infrarenal aortic cross-clamping using TEE and analyzed off-line using custom software. The predictive value of the category "reversible perfusion defect" (RD) was also estimated from DTST for predicting new RWMAs with CK. CK analysis is suitable for clinical use based on the comparison with conventional two-dimensional echocardiogram measurements and interobserver variability. CK analysis showed all 7 patients with persistent perfusion defects on DTST had RWMAs. New RWMAs occurred in 2 of 9 patients with RD and in 2 of 15 patients with normal DTST, indicating that there was no significant difference between RD and normal DTST in the incidence of new RWMAs. CONCLUSIONS: A new method is available for clinical use, which is capable of visualizing RWMAs. These results suggest that new RWMAs introduced by aortic cross-clamping occur irrespective of the risk as assessed by preoperative DTST. CK with the new analysis method might be a useful tool to quantitatively evaluate RWMAs during surgery.

Aorta, Abdominal↗

PubMed2003

Performance evaluation of a new pulse oximeter during mild hypothermic cardiopulmonary bypass.

UNLABELLED: Newly developed pulse oximeters (POs) are designed to display accurate SpO(2) during motion and hypoperfusion. We compared the performance of a new PO, the Masimo SET Radical (M), with a conventional PO, the Nihon Kohden AY-900P (N), during hypothermic cardiopulmonary bypass. Eighteen patients were studied prospectively. PO failure was defined as failure to show no SpO(2) value or show incorrect SpO(2) values for longer than 3 min continuously. PO failure occurred in 4 and 14 patients with M and N, respectively (P = 0.0022). All 4 patients in whom PO failure developed with M were among the 14 patients with N. No SpO(2) was provided for 4% +/- 12% of the duration of aorta cross-clamping with M and 36% +/- 39% with N (P = 0.002). Skin temperature and mean arterial blood pressure when PO failure started to occur and ended were similar between M and N. PO failure easily developed in patients with preoperative diuretic therapy or with intraoperative hyperlactatemia in N, but not in M. M was able to display accurate SpO(2) values significantly more frequently and longer than N during mild hypothermic cardiopulmonary bypass with nonpulsatile flow, suggesting that M is more useful for monitoring SpO(2) during hypoperfusion. IMPLICATIONS: We compared the performance of a new pulse oximeter with that of a conventional pulse oximeter during hypothermic cardiopulmonary bypass with nonpulsatile flow. The newly developed device displayed accurate SpO(2) significantly more frequently and longer than a conventional oximeter. Newly developed pulse oximeters seem to be more useful for monitoring SpO(2) during hypoperfusion.

Aged↗

PubMed2003

Mechanisms of direct inhibitory action of isoflurane on vascular smooth muscle of mesenteric resistance arteries.

BACKGROUND: Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries. METHODS: Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the beta-escin membrane-permeabilized strips. RESULTS: Isoflurane (3-5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 microM) or KCl (40 mM). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl- channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the beta-escin-permeabilized strips. CONCLUSIONS: In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl- channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.

Anesthetics, Inhalation↗

PubMed2003

Pivotal role of Cu,Zn-superoxide dismutase in endothelium-dependent hyperpolarization.

The endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several vasodilating factors, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF). We have recently identified that endothelium-derived H2O2 is an EDHF in mesenteric arteries of mice and humans and in porcine coronary microvessels. However, the mechanism for the endothelial production of H2O2 as an EDHF remains to be elucidated. In this study, we tested our hypothesis that Cu,Zn-superoxide dismutase (Cu,Zn-SOD) plays a pivotal role in endothelium-dependent hyperpolarization, using control and Cu,Zn-SOD-/- mice. In mesenteric arteries, EDHF-mediated relaxations and hyperpolarizations were significantly reduced in Cu,Zn-SOD-/- mice with no inhibitory effect of catalase, while endothelium-independent relaxations and hyperpolarizations were preserved. Endothelial H2O2 production also was significantly reduced in Cu,Zn-SOD-/- mice. In Langendorff isolated heart, bradykinin-induced increase in coronary flow was significantly reduced in Cu,Zn-SOD-/- mice, again with no inhibitory effect of catalase. The exogenous SOD mimetic tempol significantly improved EDHF-mediated relaxations and hyperpolarizations and coronary flow response in Cu,Zn-SOD-/- mice. These results prove the novel concept that endothelial Cu,Zn-SOD plays an important role as an "EDHF synthase" in mice, in addition to its classical role to scavenge superoxide anions.

Animals↗

PubMed2003

[Usefulness of monitoring forehead deep-tissue temperature as an index of core temperature in adult patients undergoing laparotomies under general anesthesia--investigation in operating rooms with air-movement control system using vertical flow].

BACKGROUND: Acute changes in air temperature in the vicinity of the patents' forehead may impair clinical usefulness of the forehead deep-tissue thermometry. We thus investigated usefulness of monitoring the forehead deep-tissue temperature as an index of core temperature in 12 adult patients undergoing laparotomies in operating rooms with air-movement control system using vertical flow. METHODS: Nasopharyngeal, forehead deep-tissue, palm deep-tissue, and fingertip skin-surface temperatures were recorded during surgery every 5 minutes in operating rooms where room temperature was thermostatically controlled at approximately 25 degrees C. The patients were not actively warmed with forced-air warmers, but covered with cotton blankets where possible. The deep-tissue and fingertip skin-surface temperatures were compared with the nasopharyngeal temperature using regression and Bland and Altman's analyses. RESULTS: The four temperatures continued decreasing during surgery, and the nasopharyngeal temperature decreased to below 36 degrees C 2 hours after induction of anesthesia. Only the forehead deep-tissue temperature satisfactorily correlated with the nasopharyngeal temperature (r = 0.76, n = 300, P < 0.0001). The difference between nasopharyngeal and forehead temperatures was +0.26 degree C, and its standard deviation was 0.34 degree C. CONCLUSIONS: The forehead deep-tissue temperature has sufficient accuracy and precision for clinical use in operating rooms with air-movement control system using vertical flow. However, the core temperature appears to be slightly underestimated with the forehead deep-tissue thermometry.

Adult↗

PubMed2002

Persistent hypertension does not alter the cerebral blood flow and glucose utilization in young-adult Dahl salt-sensitive rats.

The Dahl- Iwai salt-sensitive (DS) rat develops hypertension due to a high-salt diet without any structural alterations of the brain arteries and arterioles. We investigated the effect of persistent hypertension on the regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCGU) in the DS rats. The rats were fed either a high-salt diet (HSD; 8% NaCl, n = 5) or a low-salt diet (LSD; 0.3% NaCl, n = 6) from 8 to 16 weeks of age, and the HSD group developed hypertension lasting for 1 month. At 16 weeks of age, the rCBF was measured in the sensorimotor and visual cortices using the hydrogen clearance method, and the rCGU was measured in 26 different brain structures using the [(14)C]deoxyglucose method. The mean arterial pressure was significantly higher in the HSD group (168+/-7 mm Hg) than in the LSD group (139+/-3 mm Hg) (P < 0.01). The mean rCBF and the rCGU values tended to be lower in the HSD group than in the LSD group; however, there were no statistically significant differences except for the reduced rCGU value in the nucleus accumbens. These results suggest that hypertension itself does not alter either the rCBF or the rCGU in young-adult DS rats. This indicates that the functional / structural changes of the cerebral arteries and arterioles that are associated with hypertension appear to be responsible for altered rCBF and rCGU in other animal models of hypertension.

Animals↗