Ó 2014 Eur J Oral Sci

Eur J Oral Sci 2015; 123: 24–29 DOI: 10.1111/eos.12162 Printed in Singapore. All rights reserved

European Journal of Oral Sciences

Effect of changes in end-tidal carbon dioxide tension on oral tissue blood flow during dexmedetomidine infusion in rabbits

Reina Okada, Nobuyuki Matsuura, Masataka Kasahara, Tatsuya Ichinohe Department of Dental Anesthesiology, Tokyo Dental College, Chiba, Japan

Okada R, Matsuura N, Kasahara M, Ichinohe T. Effect of changes in end-tidal carbon dioxide tension on oral tissue blood flow during dexmedetomidine infusion in rabbits. Eur J Oral Sci 2015; 123: 24–29. © 2014 Eur J Oral Sci A decrease in arterial carbon dioxide tension induces an increase in masseter muscle blood flow and a decrease in mandibular bone marrow blood flow during general anesthesia. In addition, dexmedetomidine infusion reduces oral tissue blood flow. In this study we investigated how end-tidal carbon dioxide tension (ET-CO2) changes influence on oral tissue blood flow during continuous dexmedetomidine infusion in rabbits. Eleven male Japan White rabbits were anesthetized with sevoflurane. Then, ET-CO2 was set at 30 mmHg and adjusted to 40 and 60 mmHg, and heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, and blood flow in other oral tissues were measured. Following this, the ETCO2 was returned to 30 mmHg and dexmedetomidine was infused over 60 min. The measurements were repeated. Most parameters increased, regardless of whether or not dexmedetomidine was present, and heart rate and masseter muscle blood flow decreased in an ET-CO2-dependent manner. Dexmedetomidine infusion suppressed ET-CO2-dependent masseter muscle blood flow change. Masseter muscle blood flow during ET-CO2 at 30 mmHg with dexmedetomidine was the same as that during ET-CO2 at 40 mmHg without dexmedetomidine. Our findings suggest that dexmedetomidine infusion and slight hypocapnia under general anesthesia suppress an increase in masseter muscle blood flow as well as reducing mandibular bone marrow blood flow. These results may be of significance for decreasing bleeding during oral and maxillofacial surgery.

Control of intra-operative bleeding is important during oral and maxillofacial surgery because the operative field includes bone marrow, mucosa, and skeletal muscles in which blood flow is abundant. The surgeon can shorten operating times and avoid risks from blood transfusions if bleeding is reduced and the operative field is clearly sighted. Although hypotensive anesthesia has been used to control intra-operative bleeding (1–4), there have been reports of serious complications, including brain damage (5–7). We have therefore been conducting research on safer methods to control bleeding in oral tissues (8–11). HANDA et al. (12) previously reported increased blood flow in masseter muscle tissue, as well as decreased blood flow in the common carotid artery and in mandibular bone marrow tissue, when arterial carbon dioxide tension was decreased during general anesthesia. With use of dexmedetomidine, a highly selective alpha-2 receptor agonist (13–15), SAZUKA et al. (16) reported a decrease in oral tissue blood flow that was

Reina Okada, Department of Dental Anesthesiology, Tokyo Dental College, 1-2-2, Masago, Mihama-ku, Chiba 261-8502, Japan E-mail: [email protected] Key words: blood flow; carbon dioxide; dexmedetomidine; sevoflurane Accepted for publication November 2014

dependent on the administration rate of dexmedetomidine during both sevoflurane and propofol anesthesia in rabbits. KAWAAI et al. reported that paratal mucosal blood flow in humans was decreased following the administration of dexmedetomidine (17). RICHA et al. (18) reported that bleeding decreased by using dexmedetomidine during maxillofacial surgery. FALE et al. (19) measured cerebral blood flow with dexmedetomidine infusion during isoflurane anesthesia or pentobarbital anesthesia, and reported that administration of dexmedetomidine during isoflurane anesthesia decreased cerebral blood flow but had no effect on cerebrovascular reactivity to hypercapnia. However, as yet, there are no reports on how the regulation of arterial carbon dioxide tension during dexmedetomidine infusion affects oral tissue blood flow. We hypothesized that dexmedetomidine infusion might modify arterial carbon dioxide tension-dependent changes of oral tissue blood flow under general anesthesia because, unlike the cerebral circulation, there are no autoregulatory

Oral tissue blood flow

mechanisms in oral tissue blood flow, and dexmedetomidine might influence vasoconstriction through sympathetic activation by hypercapnia. In this study, we investigated how changes in end-tidal carbon dioxide tension (ET-CO2) during infusion of dexmedetomidine affect oral tissue blood flow in rabbits.

Material and methods This study was conducted with the approval of the Ethics Review Board of the Animal Experiments Committee of Tokyo Dental College (approval number: 242505). Eleven male Japan White rabbits, each around 2.5 kg in weight, were used in the study. The rabbits were anesthetized with 3.0% isoflurane (Forane; Abbott Japan, Tokyo, Japan) and oxygen at 4 l min 1. After local anesthesia was achieved with 0.5 ml of 1% lidocaine hydrochloride (Xylocaine; AstraZeneca, Osaka, Japan), the rabbits were tracheostomized and a 20-Fr pediatric tracheal tube was inserted and fixed. During surgery, artificial ventilation was maintained at 30–50 ml tidal volume and the ventilation rate was around 30 breaths per min. A 22-G indwelling catheter was inserted in the left auricular marginal vein as a route for drug administration, and the following were continuously infused: acetated Ringer’s solution at 10 ml kg 1 h 1, and rocuronium bromide (Eslax; Schering-Plough, Tokyo, Japan) at 14 lg kg 1 min 1. After local anesthesia with 0.5 ml of 1% lidocaine hydrochloride, the right femoral artery was dissected and a 20-G catheter was inserted. A pressure transducer (P231D; Gould, Oxnard, CA, USA) was used to monitor the systolic blood pressure, diastolic blood pressure, and mean arterial pressure continuously, and the heart rate was calculated from the pressure waveform. The probe (Type 3SB) of an ultrasound blood flow meter (T108; Transonic, Ithaca, NY, USA) was attached to the left common carotid artery and blood flow was measured. The ET-CO2 was measured using a capnometer (Capnomac; Datex, Helsinki, Finland). The masseter muscle and the mandibular periosteum were exposed by making an incision into the left inferior margin of the mandible; to avoid the vasodilatory action of lidocaine hydrochloride, local anesthesia was not performed. The periosteum was detached and a round bar (ISO 008; Morita, Saitama, Japan) was used to create a small opening from the bone surface to the mandibular bone marrow. The probe of a hydrogen clearance tissue blood flow meter (UHE-100; Unique Medical, Tokyo, Japan) was inserted into the mandibular bone marrow, masseter muscle, left upper alveolar tissue, and left lower alveolar tissue, and the blood flow in each tissue was measured. The laser-emitting surface of the probe (Type C) of a laser Doppler blood flow meter (ALF21; Unique Medical) was securely attached to the left dorsal lingual mucosa and the tongue mucosal blood flow was measured. After these preparations were complete, isoflurane inhalation was discontinued and anesthesia was maintained with 1.8% sevoflurane (Sevofrane; Maruishi Pharmaceutical, Osaka, Japan) and oxygen at 3 l min 1. Rectal temperature was maintained between 39.0 and 39.5°C during the experiment by use of a heat lamp. This study involved changing the ET-CO2 without changing the ventilation conditions. Therefore, the ETCO2 was set at 30 mmHg when the experiment began and was adjusted to 40 mmHg for 15 min and then to

25

60 mmHg for 15 min by using CO2 inhalation. After the measurements, described below, were made at an ET-CO2 of 60 mmHg, the ET-CO2 was returned to 30 mmHg and hemodynamic variables were confirmed to be the same as those at the start of the experiment. Then, dexmedetomidine was infused at an initial loading dosage of 6 lg kg 1 h 1 for 10 min and subsequently at a maintenance dose of 0.4 lg kg 1 h 1 for 1 h, and the measurements described below were again repeated at 30, 40, and 60 mmHg ET-CO2 in a similar manner but without dexmedetomidine infusion. The following measurements were made. For hemodynamic parameters, we measured the heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure, and common carotid artery blood flow. These parameters, as well as tongue mucosal blood flow, were continuously recorded on a polygraph (Series 360; NEC Sanei, Tokyo, Japan). For oral tissue blood flow, we measured tongue mucosal blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow. Each parameter measured using the hydrogen clearance tissue blood flow meter was analyzed using a datacollection analysis system (UCO; Unique Medical). The measurements at 40 and 60 mmHg ET-CO2 were compared with the measurement at 30 mmHg ET-CO2, and in the presence or absence of dexmedetomidine infusion (N30, N40, and N60: no dexmedetomidine infusion at an ET-CO2 of 30, 40, and 60 mmHg; D30, D40, and D60: dexmedetomidine infusion at an ET-CO2 of 30, 40, and 60 mmHg). Furthermore, we calculated, by dividing mean arterial pressure with each oral tissue blood flow value, the tongue mucosal vascular resistance, the mandibular bone marrow vascular resistance, the masseter muscle vascular resistance, the upper alveolar tissue vascular resistance, and the lower alveolar tissue vascular resistance (16, 20). We set N30 vascular resistance as 100% and expressed the values for N40, N60, D30, D40, and D60 as the percentage change in oral tissue vascular resistance. We performed statistical analysis of each parameter using one-way ANOVA and the Student–Newman–Keuls test. We plotted the relationship between ET-CO2 and tissue blood flow using linear regression and investigated the differences in the slopes of the regression lines obtained in the presence and absence of dexmedetomidine using a paired t-test. All results were expressed as mean  SD, and the significance level was set at P < 0.05.

Results When ET-CO2 was increased from 30 to 60 mmHg, systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, tongue mucosal blood flow, mandibular bone marrow blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow increased in an ET-CO2dependent manner, whereas heart rate and masseter muscle blood flow decreased in an ET-CO2-dependent manner. Heart rate, tongue mucosal blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow were significantly lower in D30 than in N30. When ET-CO2 was raised from D30

Data are expressed as mean  SD. D30, D40, and D60, end-tidal carbon dioxide tension (ET-CO2) at 30, 40, and 60 mmHg with dexmedetomidine infusion; N30, N40, and N60, ET-CO2 at 30, 40, and 60 mmHg without dexmedetomidine infusion. P < 0.05: *vs. N30; **vs. D30. †vs. without dexmedetomidine infusion.

          22.9 19.6 7.2** 6** 9.4 3.6† 4.1**† 6.1**† 7**† 11.4**†                     Heart rate (beats per min) Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) Mean arterial pressure (mmHg) Common carotid artery blood flow (ml min 1) Tongue mucosal blood flow (ml/100 g min 1) Mandibular bone marrow blood flow (ml/100 g min 1) Masseter muscle blood flow (ml/100 g min 1) Upper alveolar tissue blood flow (ml/100 g min 1) Lower alveolar tissue blood flow (ml/100 g min 1)

299 111.4 51.7 77.9 33.4 28.5 34.5 67.6 33.7 39.1

25.5 16.9 5.3 8.4 9.2 4.8 4.8 8.3 3.9 10.6

275 114.2 55.5 80 35.3 29.7 44.1 53.9 44 52.9          

31.2* 17.6 5.6 7.8 9.8 4.4 6.4* 7.2* 5.7* 12.1*

261 123.8 65.5 89.3 43.1 33.1 54.3 40.6 53.8 66.9

         

29.9* 17.2* 5.9* 7.7* 12.5* 4.2* 8.1* 7.2* 6.8* 14.7*

278 109.9 53.4 76.4 35.1 23.8 29.2 51.7 26 34.4

         

28.2† 18.2 5.1 5.5 7.7 3.9† 3.3† 7.6† 4.3† 9.7†

263 113.8 58.4 81.2 38.2 25.4 38.2 40.6 34.3 46

D40 D30 N60 N40 N30

ET-CO2 without dexmedetomidine infusion

When dexmedetomidine was not infused, systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, tongue mucosal blood flow, mandibular bone marrow blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow increased in an ET-CO2-dependent manner, and heart rate and masseter muscle blood flow decreased in an ET-CO2-dependent manner. According to HANDA et al. (12), increasing the ET-CO2 during isoflurane anesthesia increases systolic blood pressure, diastolic blood pressure, common carotid artery blood flow, and mandibular bone marrow blood flow and decreases heart rate and masseter muscle blood flow, but does not change blood flow in the mandibular periosteum. Although sevoflurane was used as the inhalation anesthetic in this study, the ET-CO2-dependent changes in hemodynamic variables without dexmedetomidine infusion, seen here, were broadly the same as those in the study by HANDA et al. (12). Dexmedetomidine infusion produces the following changes in hemodynamic variables: an increase in blood pressure as a result of peripheral vasoconstriction caused by stimulation of alpha-2B receptors during the initial high-dose infusion, followed by a decrease in blood pressure as a result of suppression of sympathetic nervous activity caused by stimulation of alpha-2A receptors during infusion of the lower maintenance dose. Heart rate has also been reported to decrease (13, 18). SAZUKA et al. (16) reported that with continuous dexmedetomidine infusion under sevoflurane anesthesia, heart rate, systolic blood pressure, mean arterial pressure, common carotid artery blood flow, tongue mucosal blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow decrease, but the rate of decline in heart rate, systolic blood pressure, mean arterial pressure, and common carotid artery

Table 1

Discussion

Hemodynamic variables and tissue blood flow

ET-CO2 with dexmedetomidine infusion

252 118.7 65.8 87 45.2 30 46.9 31.4 42.4 56.4

D60

to D60, systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, tongue mucosal blood flow, mandibular bone marrow blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow increased in an ET-CO2-dependent manner and heart rate and masseter muscle blood flow decreased in an ET-CO2-dependent manner (Table 1). Vascular resistance changed in an ET-CO2-dependent manner with and without dexmedetomidine: masseter muscle vascular resistance increased, whereas mandibular bone marrow vascular resistance, upper alveolar tissue vascular resistance, and lower alveolar tissue vascular resistance decreased (Table 2). When the slope of the regression line, which expresses the ET-CO2-dependent change in oral tissue blood flow, was compared between conditions with and without dexmedetomidine, we observed reductions for masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow (Table 3).

32.6** 20.5**† 9.3** 10** 12.1** 2.9**† 7.7**† 5.9**† 8.8**† 12.4**†

Okada et al.

Variable

26

Oral tissue blood flow

27

Table 2 Changes in oral tissue vascular resistance ET-CO2 without dexmedetomidine infusion

ET-CO2 with dexmedetomidine infusion

Variable

N30

N40

N60

D30

D40

D60

Tongue mucosal vascular resistance (%) Mandibular bone marrow vascular resistance (%) Masseter muscle vascular resistance (%) Upper alveolar tissue vascular resistance (%) Lower alveolar tissue vascular resistance (%)

100 100

98.5  5.4 80.9  8.3*

99.0  11.3 73.9  12.6*

119.5  20.8† 117.2  17.7†

118.3  19.5† 94.4  10.2**†

107.1  19.0 83.7  15.0**†

100 100 100

129.9  16.9* 79.1  8.1* 76.1  10.9*

200.2  63.2* 72.3  6.8* 67.3  11.9*

130.1  18.1 129.9  22.1† 112.5  13.6†

177.1  30.5**† 106.8  24.5**† 89.0  11.5**†

249.8  66.8**† 93.4  28.0**† 78.0  16.0**†

Data are expressed as mean  SD. D30, D40, and D60, end-tidal carbon dioxide tension (ET-CO2) at 30, 40, and 60 mmHg with dexmedetomidine infusion; N30, N40, and N60, ET-CO2 at 30, 40, and 60 mmHg without dexmedetomidine infusion. P < 0.05: *vs. N30; **vs. D30. †vs. without dexmedetomidine infusion.

Table 3 Regression line slopes Dexmedetomidine infusion Variable Tongue mucosal blood flow Mandibular bone marrow blood flow Masseter muscle blood flow Upper alveolar tissue blood flow Lower alveolar tissue blood flow

No

Yes

P

0.15  0.08

0.21  0.14

0.276

0.64  0.21

0.57  0.25

0.123

0.87  0.33

0.65  0.22

0.003*

0.64  0.14

0.53  0.23

0.045*

0.90  0.28

0.70  0.27

0.014*

Data are expressed as mean  SD. * P < 0.05 vs. without dexmedetomidine infusion.

blood flow is less than that for oral tissue blood flow. In the present study, dexmedetomidine infusion stimulated decreases in tongue mucosal blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow at all ET-CO2 levels; heart rate, systolic blood pressure, and mean arterial pressure also tended to decrease but these decreases were not always statistically significant. As in the report by SAZUKA et al. (16), although systemic circulation was suppressed only slightly, oral tissue blood flow decreased significantly. In this study, the reduction in systolic blood pressure and mean arterial pressure caused by continuous infusion with dexmedetomidine was not significant, and common carotid artery blood flow did not decrease. We attribute this to the maintenance dose of 0.4 lg kg 1 h 1 used in this study, which was lower than the dose of 2 lg kg 1 h 1 used in the study of CHANG et al. (21) and the dose of 5 lg kg 1 h 1 used in the study of COSAR et al. (22). In the present study, dexmedetomidine infusion resulted in ET-CO2-dependent increases in systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, tongue

mucosal blood flow, mandibular bone marrow blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow and in ET-CO2-dependent decreases in heart rate and masseter muscle blood flow. A comparison of the calculated regression line slopes showed that dexmedetomidine infusion suppressed the ET-CO2-dependent changes in masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow; it tended to suppress the change in mandibular bone marrow blood flow, although this effect was not statistically significant. This suggests that dexmedetomidine infusion suppresses the ET-CO2dependent increases in upper alveolar tissue blood flow, lower alveolar tissue blood flow, and mandibular bone marrow blood flow and that the change in blood flow might be offset by the suppression of the ET-CO2dependent decrease in masseter muscle blood flow. Regarding the percentage change in vascular resistance, there was an increase in masseter muscle vascular resistance in association with the ET-CO2dependent decrease in masseter muscle blood flow, and decreases were observed in mandibular bone marrow vascular resistance, upper alveolar tissue vascular resistance, and lower alveolar tissue vascular resistance in association with the ET-CO2-dependent increases in mandibular bone marrow blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow, regardless of whether or not dexmedetomidine was administered. This suggests that the ET-CO2-dependent changes in mandibular bone marrow blood flow, masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow are caused by variation in vascular resistance. However, SAZUKA et al. (16) noted that the reduction in oral tissue blood flow with dexmedetomidine administration may involve a reduction in cardiac output based on the suppression of sympathetic nervous activity as a result of the agonistic action of dexmedetomidine on alpha-2A receptors, in addition to the peripheral vasoconstriction caused by the agonistic action of dexmedetomidine on alpha-2B receptors. FALE et al. (19) reported that administration of dexmedetomidine to isoflurane-anesthetized dogs decreases

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Okada et al.

cerebral blood flow but does not affect cerebrovascular reactivity to hypercapnia. In the present study, when dexmedetomidine was administered to sevoflurane-anesthetized rabbits, we observed suppression of the ETCO2-dependent change in masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow, but not in mandibular bone marrow blood flow and tongue mucosal blood flow. The difference in the effect of dexmedetomidine on vascular reactivity under CO2 loading between cerebral and oral tissues may be a result of the fact that whereas dexmedetomidine does not fully suppress the mechanism that autoregulates cerebral blood flow, there is no such autoregulatory mechanism of blood flow in oral tissues. ZORNOW et al. reported that dexmedetomidine infusion reduced cerebral blood flow and tended to reduce intracranial pressure (23, 24). The common carotid artery branches into the external and internal carotid arteries, with the external carotid artery mainly supplying blood flow to the face and the internal carotid artery controlling cerebral blood flow (25). Although cerebral blood flow was not measured in the present study, the reduced blood flow may indicate that blood flow was redistributed to the face, assuming that dexmedetomidine infusion decreased cerebral blood flow without changing common carotid artery blood flow. However, in the present study, continuous dexmedetomidine infusion decreased blood flow in all oral tissues. Further research is needed on the impact of dexmedetomidine on the distribution of cervicofacial blood flow. The sevoflurane concentration for maintenance anesthesia in the present study was set to 1.8%, on the basis of 0.5 minimum alveolar concentration (MAC) with reference to the sevoflurane MAC value used for New Zealand White rabbits in research by SCHELLER et al. (26). The rate of the maintenance dose of rocuronium bromide was set with reference to 14 lg kg 1 min 1, the rate used by TERAKAWA et al. to achieve stable muscle relaxation in rabbits (27). D30 masseter muscle blood flow was equivalent to N40 masseter muscle blood flow, whereas D30 mandibular bone marrow blood flow was lower than N40 mandibular bone marrow blood flow. This suggests that the concomitant use of dexmedetomidine and slight hypocapnia during general anesthesia can suppress the increase in masseter muscle blood flow as a result of reduced ET-CO2 and can reduce mandibular bone marrow blood flow that could help to control bleeding during oral and maxillofacial surgery. Dexmedetomidine is currently not indicated for general anesthesia and its use is limited to sedation during and after removal of artificial ventilation in an intensive care unit, as well as sedation during surgery or procedures under local anesthesia without intubation. However, even with general anesthesia, dexmedetomidine has been reported to have numerous useful actions, including analgesic effects, because of its stimulation of alpha-2A receptors (13), effects of reducing the inhalation anesthetic MAC (28), and organ-protective effects (29). If its indications are expanded during general

anesthesia in the future, dexmedetomidine could be a useful pharmacological agent for, among other uses, the control of bleeding during oral surgery. In conclusion, dexmedetomidine infusion reduces blood flow in oral tissues and suppresses ET-CO2dependent changes in masseter muscle blood flow, upper alveolar tissue blood flow, and lower alveolar tissue blood flow. Acknowledgements – This work was partly supported by JSPS KAKENHI Grant Number 25463147. Conflicts of interest – The authors declare that they have no conflicts of interest.

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22. COSAR M, ESER O, FIDAN H, SAHIN O, BUYUKBAS S, ELA Y, YAGMURCA M, OZEN OA. The neuroprotective effect of dexmedetomidine in the hippocampus of rabbits after subarachnoid hemorrhage. Surg Neurol 2009; 71: 54–59. 23. ZORNOW MH, FLEISCHER JE, SCHELLER MS, NAKAKIMURA K, DRUMMOND JC. Dexmedetomidine, an alpha 2-adrenergic agonist, decreases cerebral blood flow in the isoflurane-anesthetized dog. Anesth Analg 1990; 70: 624–630. 24. ZORNOW MH, SCHELLER MS, SHEEHAN PB, STRNAT MA, MATSUMOTO M. Intracranial pressure effects of dexmedetomidine in rabbits. Anesth Analg 1992; 75: 232–237. 25. KAMIJO Y. 3 Angiology in oral anatomy, 1st edn (in Japanese). Tokyo: Anatome, 1965; 426. 26. SCHELLER MS, SAIDMAN LJ, PARTRIDGE BL. MAC of sevoflurane in humans and the New Zealand white rabbit. Can J Anaesth 1988; 35: 153–156. 27. TERAKAWA Y, ICHINOHE T, KANEKO Y. Rocuronium and vecuronium do not affect mandibular bone marrow and masseter muscular blood flow in rabbits. J Oral Maxillofac Surg 2010; 68: 15–20. 28. FRAGEN RJ, FITZGERALD PC. Effect of dexmedetomidine on the minimum alveolar concentration (MAC) of sevoflurane in adults age 55 to 70 years. J Clin Anesth 1999; 11: 466–470. 29. KUNISAWA T. Pharmacokinetics and pharmacodynamics of dexmedetomidine. (in Japanese). J Jpn Soc Clin Anesth 2010; 30: 181–189.

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Effect of changes in end-tidal carbon dioxide tension on oral tissue blood flow during dexmedetomidine infusion in rabbits.

A decrease in arterial carbon dioxide tension induces an increase in masseter muscle blood flow and a decrease in mandibular bone marrow blood flow du...
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