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Biomedical subjects

N Matsumiya

Publications and source records attributed to N Matsumiya.

At least 19 recordsLinked to original sources
PubMed1995

Efficacy of an epidural test dose in adult patients anesthetized with isoflurane: lidocaine containing 15 micrograms epinephrine reliably increases arterial blood pressure, but not heart rate.

When continuous epidural anesthesia is combined with general anesthesia, the only objective sign of intravascular migration of the epidural catheter are the increments of heart rate (HR) or arterial blood pressure after a local anesthetic test dose containing epinephrine. However, the efficacy of a simulated intravenous (IV) test dose in adult patients under general anesthesia has not been determined. Thirty adult patients were randomly assigned to one of two groups, each of which was anesthetized with 1% end-tidal isoflurane and nitrous oxide after endotracheal intubation. The epinephrine group (n = 15) was given 3 mL of 1.5% lidocaine with epinephrine (1:200,000) IV to simulate an IV administered epidural test dose. The saline group (n = 15) was identical to epinephrine group, but received 3 mL of normal saline IV. HR and arterial blood pressure were measured at 20-s intervals for 4 min after IV injection. In the epinephrine group, significant increases in HR compared with the baseline value were observed from 40 to 80 s after the IV test dose with a mean maximum HR increase of 24 +/- 2 bpm (mean +/- SEM) occurring at 48 +/- 3 s. However, 5 of 15 patients in the epinephrine group developed HR increments smaller than 20 bpm (sensitivity 67%). Since HRs were essentially unchanged in the saline group, specificity, positive predictive value (+PV), and negative predictive value (-PV) were 100%, 100%, and 75%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Efficacy of simulated epidural test doses in adult patients anesthetized with isoflurane: a dose-response study.

A recent study demonstrated that an epidural test dose containing 15 micrograms epinephrine was an imperfect marker for intravascular injection during isoflurane anesthesia based on the conventional heart rate (HR) criterion (positive if > or = 20 bpm increase). We have determined the effects of epinephrine doses and isoflurane concentrations on these efficacies in healthy adult patients during isoflurane anesthesia. Eighty patients were randomly assigned to one of four groups according to the simulated test dose injected intravenously (IV) under 1% end-tidal isoflurane and nitrous oxide after endotracheal intubation. The saline group (n = 20) received 3 mL normal saline; the epinephrine 7.5 group (n = 20) received 3 mL 1.5% lidocaine containing 7.5 micrograms epinephrine; the epinephrine 15 and epinephrine 22.5 groups (n = 20 each) received an identical dose and volume of lidocaine but containing 15 and 22.5 micrograms epinephrine, respectively. HR and systolic blood pressure (SBP) were monitored invasively for 4 min after IV injection of the study drug. Although none in the saline group developed a HR increase > or = 20 bpm, 2, 14, and 12 patients elicited positive responses in the epinephrine 7.5, 15, and 22.5 groups (10%, 70%, and 60% sensitivities), respectively. If a positive HR response was defined by an increase of 10 bpm, sensitivities were 55%, 100%, and 100% in the epinephrine 7.5, 15, and 22.5 groups, respectively. On the other hand, none in the saline group, 12 in the epinephrine 7.5 group, and all patients in the epinephrine 15 and 22.5 groups developed maximum SBP increases > or = 15 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Agonists↗
PubMed1992

[The relation between upper respiratory tract infection and mild hypoxemia during general anesthesia in children].

Anesthesiologists often face the problem of a child with symptoms of an acute upper respiratory infection (URI) presenting for surgery. Anesthesia in the presence of uncomplicated URI may not be contraindicated. However, we experienced three cases of such children in which lung atelectasis developed after the induction of general anesthesia. Because continuous monitoring of arterial oxygen saturation by pulse oximetry (SpO2) was useful for detecting mild hypoxemia in these patients, we retrospectively examined the possible association between URI symptoms and SpO2 in 63 children. Patients with symptoms of URI showed a significantly high incidence of decreased SpO2 to below 95% for 5 minutes. Our results suggest that, with URI symptoms even uncomplicated, symptomatic patients have increased risks for the development of mild hypoxemia during anesthesia.

Anesthesia, General↗
PubMed1992

[Effect of high dose-fentanyl on cerebrospinal fluid pressure in patients with normal intracranial pressure under halothane anesthesia].

The effect of high dose fentanyl on cerebrospinal fluid pressure (CSFP) was studied in 16 consented patients scheduled for major surgery with thoracotomy. In all patients, CSFP was measured through a 23G spinal needle at L3/L4 intervertebral space on the lateral position under light halothane-nitrous oxide-oxygen anesthesia (halothane 0.2-0.3%). After the control values were taken fentanyl, 50 micrograms.kg-1 (n = 8) or 100 micrograms.kg-1 (n = 8) was administered intravenously in 15 min. After the administration of both doses of fentanyl, CSFP decreased but not significantly. Mean blood pressure and cerebral perfusion pressure (CPP) decreased significantly within 5 min after the beginning of fentanyl administration but CPP did not decrease below 50 mmHg in any cases. These results indicate that high dose fentanyl has little influence on intracranial pressure in normal patients and could be used safely for neuroanesthesia.

Aged↗
PubMed1991

Conjugated superoxide dismutase reduces extent of caudate injury after transient focal ischemia in cats.

We tested the efficacy of preischemic and postischemic systemic treatment with 30,000 units polyethylene glycol-conjugated superoxide dismutase in a reperfusion model of focal cerebral ischemia. Forty-one anesthetized cats underwent 2 hours' occlusion of the left middle cerebral artery and both common carotid arteries followed by 4 hours of reperfusion. Cats were blindly assigned to one of three groups: treatment with vehicle (10% polyethylene glycol in saline, n = 17), pretreatment with drug 3 hours before ischemia (n = 12), and posttreatment with drug at the time of reperfusion (n = 12). Size of the ischemic injury was calculated from 2,3,5-triphenyltetrazolium chloride staining. Injury in the caudate nucleus was significantly reduced with pretreatment (28 +/- 6% of ipsilateral caudate volume, mean +/- SEM) compared with the vehicle (56 +/- 8%). Posttreatment did not significantly ameliorate caudate injury (46 +/- 10%). Between the first and second hours of ischemia ipsilateral caudate blood flow determined using microspheres increased significantly from 11 +/- 4 to 16 +/- 5 ml/min/100 g with pretreatment, but blood flow remained constant throughout ischemia with vehicle (8 +/- 2 ml/min/100 g) and posttreatment (10 +/- 3 ml/min/100 g). The size of cortical injury (vehicle, 17 +/- 5%; pretreatment, 11 +/- 3%; posttreatment, 17 +/- 5% of hemispheric volume) did not differ significantly among groups. Somatosensory evoked potential recovery did not differ among groups. We conclude that pretreatment with conjugated superoxide dismutase can ameliorate the extent of injury in an end-artery region, such as the caudate nucleus, in a reperfusion model of focal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Consistency of cerebral blood flow and evoked potential alterations with reversible focal ischemia in cats.

To enhance the consistency of the ischemic insult caused by reversible transorbital middle cerebral artery occlusion, we investigated the variability of somatosensory evoked potential amplitudes and regional cerebral blood flow in 26 anesthetized cats using four procedures to induce transient ischemia. These procedures included 60 minutes of left middle cerebral artery occlusion with or without left common carotid artery occlusion and 120 minutes of left middle cerebral artery occlusion with or without bilateral common carotid artery occlusion. Blood flow in the left middle cerebral artery territory was markedly and consistently reduced to less than 20 ml/min/100 g with simultaneous occlusion of the left middle cerebral artery and both common carotid arteries. The standard deviation of blood flow with this procedure (5.4) was less than that with the other three procedures (13-25). The amplitudes of ipsilateral somatosensory evoked potentials were decreased to approximately 20% of control during ischemia with all four procedures. During reperfusion, amplitudes recovered more slowly, to half of control, after both procedures involving 120 minutes of ischemia. After 120 minutes of reperfusion, the range of amplitudes was smallest in the group exposed to middle cerebral artery occlusion with bilateral common carotid artery occlusion. The degree of recovery of the somatosensory evoked potentials correlated with residual blood flow in both the ipsilateral middle cerebral artery territory and in the white matter during ischemia. We conclude that the most consistent model of focal ischemia and reperfusion in cats in which there is partial recovery of somatosensory evoked potentials is occlusion of one middle cerebral artery and both common carotid arteries for 120 minutes.

Animals↗
PubMed1989

[Influence of four opioids on pulmonary oxygenation and naloxone's effects in mechanically ventilated dogs].

In order to examine effects of opioids on pulmonary oxygenation during constant ventilation, we investigated changes in PaO2 following four different opioids and after reversal with naloxone in mechanically ventilated, lightly anesthetized dogs. The systemic administration of morphine 1.0mg.kg-1, buprenorphine 0.03mg.kg-1, butorphanol 0.1mg.kg-1, and cyclazocine 0.05mg.kg-1, did not affect PaO2, although these opioids decreased mean arterial pressure and heart rate significantly. Naloxone 0.04mg.kg-1 after four opioids affected the hemodynamics, significantly, but it did not cause any detrimental effects on pulmonary oxygenation. Although naloxone alone did not affect mean arterial pressure and heart rate at all, subsequent morphine decreased mean arterial pressure and heart rate significantly. Neither naloxone nor subsequent morphine produced any change in PaO2. The results suggest that reversal with naloxone may not cause any significant influences on pulmonary oxygenation in mechanically ventilated and anesthetized patients.

Animals↗
PubMed1987

Carbon dioxide elimination during circulatory arrest.

To learn modes of CO2 elimination during cardiac arrest, we continuously measured end-tidal CO2 concentration (ETCO2) in acutely arrested dogs with constant ventilation. A decrease in peak ETCO2 during cardiac arrest in each dog showed a washout biexponential function when graphed on semilog paper. The average half-times of each compartment were 19.2 +/- 3.1 (SD) sec for the fast compartment and 108.1 +/- 23.8 sec for the slow compartment; the fast compartment of the CO2 elimination curve suggested that CO2 was eliminated from the functional residual capacity, while the slow compartment indicated CO2 elimination from the pulmonary capillary blood and tissue stores. Neither pretreatment with sodium bicarbonate (1 mEq/kg iv) nor a 5-min cardiorespiratory arrest altered the mode of CO2 elimination. The ETCO2 also reflected the potential effects of external cardiac compressions on pulmonary blood flow, as previously reported. Besides mixed venous blood CO2 flowing back to the lungs by cardiac compressions, it should be noted that both alveoli and pulmonary capillary blood CO2 are also reflected in the ETCO2 during the first minute of CPR.

Animals↗
PubMed1984

The effects of subarachnoid lidocaine and phenylephrine on spinal cord and cerebral blood flow in dogs.

To investigate the central nervous system circulation during spinal anesthesia, local spinal cord blood flow (SCBF) and cerebral blood flow (CBF) were measured simultaneously by the hydrogen clearance technique following subarachnoid lidocaine, phenylephrine, or a combination of both. The mean control values of SCBF and CBF were 22.4 +/- 7.9 ml X 100 g-1 X min-1 and 53.1 +/- 12.0 ml X 100 g-1 X min-1, respectively, in dogs lightly anesthetized with halothane. The subarachnoid administration of lidocaine solutions (1, 2, 3, and 5%), 1 ml, failed to produce statistically significant changes in SCBF (P greater than 0.05). Whereas, when phenylephrine (0.1, 0.2, 0.3, and 0.5%), 1 ml, was injected into the spinal subarachnoid space, SCBF decreased significantly with concentrations greater than 0.2% (P less than 0.05). When a mixture of lidocaine (24 mg) and phenylephrine (1 mg) was administered into the subarachnoid space, SCBF decreased significantly and returned to control within 60-90 min. CBF did not change significantly with any of the injections, remaining within less than +/- 12% of control. Dextrose solutions in water (5 and 7.5%), which were used for dilution of the drugs, did not affect either SCBF or CBF. These results indicate that local spinal cord blood flow can be affected significantly during spinal anesthesia when phenylephrine is added to the local anesthetic solution. However, the circulatory effects of drugs injected into the spinal subarachnoid space appear to be restricted to the local spinal cord per se and do not involve other parts of the CNS.

Anesthesia, Spinal↗
PubMed1983

[Mechanism of morphine-induced suppression of central nervous system blood flow].

Narcotic agonists such as morphine are well known to decrease cerebral blood flow and metabolism. To investigate a possible mechanism for this action of narcotics, cerebral blood flow (CBF) and spinal cord blood flow (SCBF) were simultaneously measured by the hydrogen clearance technique following intravenous or subarachnoid administration of morphine and subsequent naloxone in lightly anesthetized dogs. The effects of new opiate agonist + antagonists, cyclazocine and buprenorphine, alone or in a combination with naloxone on those CNS blood flow were also investigated. Morphine, 1 mg/kg iv, produced significant decreases in both CBF and SCBF (p less than 0.01), which were reversed by naloxone, 40 micrograms/kg. Naloxone per se did not produce any change in both. Cyclazocine, 50 micrograms/kg iv, also produced significant decreases in both CBF and SCBF (p less than 0.05), but the decreased CBF was not reversed by naloxone. Buprenorphine, 30 micrograms/kg, showed variable changes in both CBF and SCBF, resulted insignificant reduction. However, spinal subarachnoid administration of morphine, 0.2 mg, with which profound analgesia can be obtained in human adults, did not cause any changes in SCBF as well as CBF. These results suggest that narcotic analgesics affect SCBF similar to CBF and morphine decreases CNS blood flow via the activation of supraspinal opiate receptors.

Animals↗
PubMed1983

Effects of intravenous or subarachnoid morphine on cerebral and spinal cord hemodynamics and antagonism with naloxone in dogs.

In order to elucidate the possible mechanism(s) by which opiates may affect cerebral and spinal circulation, and cerebral metabolism, cerebral blood flow (CBF) and spinal cord blood flow (SCBF) were measured simultaneously following intravenous or subarachnoid administration of morphine in dogs lightly anesthetized with halothane. The mean values of CBF and SCBF, using hydrogen clearance methods, were 52.3 +/- 14.7 ml . 100 g-1 . min-1 (mean +/- 1 SD) and 22.3 +/- 9.0 ml . 100 g-1 . min-1, respectively. Morphine hydrochloride, 1 mg/kg, when given intravenously, reduced both CBF and SCBF to approximately 73% of the control values (P less than 0.01). These changes were accompanied by decreases in the cerebral metabolic rates for oxygen (CMRO2) and glucose (CMRglucose). The circulatory effects and, in part, the metabolic effects, were reversed by naloxone 40 microgram/kg iv. Prior administration of naloxone blocked the morphine effects on CBF and SCBF and suppressed the effects on CMRO2 and CMRglucose. The decreases in blood pressure (MAP) and heart rate (HR) were similar following morphine iv with or without prior administration of naloxone. However, when 0.2 mg morphine was injected into the spinal subarachnoid space, the above variables remained unaffected. Neither naloxone alone, nor its subsequent intravenous administration following spinal morphine, affected cerebral and spinal circulatory or cerebral metabolic indices. These results indicate that intravenous morphine affects both cerebral and spinal cord blood flow via the opiate receptors at supraspinal sites of action.

Animals↗