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Biomedical subjects

N Fuke

Publications and source records attributed to N Fuke.

18 recordsLinked to original sources
PubMed1999

[A classification of shock based on hemodynamic profiles].

Shock is a syndrome of numerous etiologies. The treatment of shock syndrome depends on the etiology and circulatory pathophysiology. From the viewpoint of circulatory physiology, the mechanism of circulatory failure can be attributed to three factors: blood volume; cardiac contractility; and vascular resistance. Balloon-tipped pulmonary artery (Swan-Ganz) catheters can distinguish between these factors in the clinical setting and allows physicians to treat shock patients most appropriately and logically. The author proposes a treatment-oriented classification of shock based on Swan-Ganz catheter findings and divides shock into three types: hypovolemic; cardiogenic; and low-resistant shock. All clinicians who treat shock must have qualified knowledge of and experience in handling this beneficial but invasive monitoring device.

Catheterization, Swan-Ganz↗
PubMed1994

The effects of intravenous clonidine on regional myocardial function in a canine model of regional myocardial ischemia.

This study was performed to investigate the effects of clonidine on regional myocardial function in a canine model of regional myocardial ischemia. Myocardial systolic shortening (%SS) was used as an index of regional myocardial function. In eight dogs after thoracotomy, the left circumflex coronary artery (LCX) was occluded by screw clamp until regional myocardial function became impaired. After partial occlusion of the LCX, cumulative doses of clonidine (1.25, 2.5, and 5.0 micrograms/kg) were administered intravenously. After administration of clonidine, heart rate, mean arterial blood pressure (MAP), and norepinephrine concentration decreased in a dose-dependent manner. At a dose of 5.0 micrograms/kg of clonidine, the LCX flow and systolic shortening of the LCX area decreased to 76% and 81% of the poststenotic values (P < 0.05, respectively), whereas no significant changes were observed at a dose of 1.25 and 2.5 micrograms/kg. These results suggest that clonidine administration and an associated decrease in arterial blood pressure deteriorates regional myocardial function of the ischemic myocardium.

Animals↗
PubMed1988

Burn injury to rat increases nicotinic acetylcholine receptors in the diaphragm.

Thermal injury induces aberrant responses to neuromuscular (NM) blocking drugs, and it has been speculated that an increase in nicotinic acetylcholine receptors (AchR) may contribute to the altered response. Using the diaphragmatic muscle as a representative of skeletal muscle, the changes in AchR were examined. The diaphragm, rather than limb muscles, was chosen to avoid the effects of wound contracture-induced immobilization and denervation of limb, which can also increase AchR in skeletal muscle. Study of changes in diaphragm also tested the hypothesis that increase in AchR are the result of a generalized systemic effect, and not limited to area of burn. Following a 45-55% body surface area thermal injury to the trunk (not limbs) of rats, AchR changes in the diaphragm were studied at 10, 14, 21, and 28 days after injury and compared to uninjured (control) rats. The AchR changes in the diaphragmatic muscle was assayed using 125I-alpha-bungarotoxin as the specific ligand. At 10, 14, and 21 days after thermal injury, the animals had an arrest in weight growth and the AchR concentration was increased to (mean +/- SE) 155 +/- 15% (P less than 0.02), 160 +/- 16% (P less than 0.003), and 141 +/- 16% (0.05 less than P less than 0.1), respectively, compared to control. At 28 days, probably because of wound healing and burn wound contracture, the size of thermally injured area was significantly (P less than 0.001) reduced to 19 +/- 4% of body surface area, and weight increased (P less than 0.001) compared to preburn weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Burn injury to trunk of rat causes denervation-like responses in the gastrocnemius muscle.

Thermal injury results in dystropic changes in skeletal muscle and abnormal pharmacological responses to neuromuscular relaxants, each of which suggests a denervation-like phenomenon. In the rat thermal injury model we examined whether, as in denervation states, increases in nicotinic acetylcholine receptors (AChR) and hyposensitivity to d-tubocurarine (dTc) are found. While anesthetized, thermal injury was imposed to trunk only. At 10, 14, and 21 days after injury the effective doses of dTc for left gastrocnemius tension suppression to 95% of control tension (ED95) were 0.213 +/- 0.039, 0.305 +/- 0.070, and 0.214 +/- 0.032 mg/kg, respectively. These values were significantly higher (P less than 0.05) than control values (0.155 +/- 0.006 mg/kg). The AChR concentrations in the left gastrocnemius, quantitated by 125I-alpha-bungarotoxin binding, increased at 10, 14, and 21 days to 182 +/- 20% (P less than 0.001), 166 +/- 22% (P less than 0.03), and 164 +/- 18% (P less than 0.001) of control, respectively. AChR concentrations in the right gastrocnemius also increased subsequent to thermal injury. Changes in effective dose of dTc for 50 and 95% twitch suppression in the left gastrocnemius correlated significantly with changes in AChR concentrations for the same muscle (r = 0.73 and 0.81, P less than 0.001, respectively). This study confirms the hypothesis that the systemic effects of thermal injury include an increase in AChR at sites distant from thermal injury, which may account for the skeletal muscle dysfunction and aberrant responses to neuromuscular relaxants.

Animals↗
PubMed1987

Concentration-dependent interaction of theophylline with d-tubocurarine.

The interaction of theophylline with d-tubocurarine chloride (dTC) was examined in rabbits. After steady-state subtherapeutic (less than 10 mg/l), therapeutic (10-20 mg/l), and toxic (greater than 20 mg/l) concentrations of theophylline, dose-response curves for dTC were determined and compared with controls that received no theophylline. At therapeutic concentrations of theophylline the effective dose for 50% inhibition of twitch (ED50) for dTC (mean +/- SE, 0.115 +/- 0.016 mg/kg) was significantly shifted to the left in comparison with the control (0.165 +/-0.008 mg/kg). The ED50 of dTC for the subtherapeutic group was 0.143 +/- 0.011 mg/kg, which was less than the control but not of statistical significance (P = 0.1). The ED50 for the toxic theophylline group was 0.168 +/- 0.003 mg/kg, which was not significantly different from controls but significantly different from the theophylline therapeutic and subtherapeutic groups. Thus, toxic concentrations of theophylline reversed the potentiating effects of therapeutic and subtherapeutic concentrations of dTC dose-response curves. Therefore, depending on concentration, theophylline exhibits a biphasic interaction with dTC. Surgical patients on theophylline may require less dTC intraoperatively. More importantly, the use of theophylline in the postoperative period to reverse anesthetic effects may result in recurarization.

Acetylcholine↗
PubMed1984

[The effect of high frequency jet ventilation on intracranial pressure in the patients with severe head injury].

The effect of high frequency jet ventilation (HFJV) on intracranial pressure (ICP) in the series of seven patients with severe head injury was studied. These patients received mechanical ventilation for respiratory failure accompanied with neural damage or circulatory shock and for ICP control by decreasing PaCO2. ICP was measured continuously by subarachnoid catheter method connected to Gould P-50 strain-gage transducer and controlled by hyperventilation and/or osmotic diuretics during acute phase. Arterial pressure, central venous pressure and intratracheal pressure were measured continuously in the same way. Arterial blood gases were analysed by BG-I of Technicon Co. Ltd. At the weaning from respirator, two methods were applied. One was conventional IMV (with PEEP) and/or CPAP by using IMV mode of Servo 900 respirator or T-piece together with PEEP valve and another was new-fashioned HFJV. Mean intratracheal pressure (mPit) was fixed at 0 mmHg (control value), 5, 10 and 15mmHg in both methods by adjusting PEEP valve or driving pressure of HFJV. The result is that in the same patients ICP was significantly lower during HFJV than IMV/CPAP when mPit was 5 and 10mmHg. Only three cases having been studied at 15mmHg of mPit because circulatory condition would not permit it, significant difference of ICP between HFJV and IMV/CPAP was not detected. PaCO2, being suspected to be the cause of lower ICP of HFJV group, was studied too. But blood gas analysis showed no significant difference neither PaCO2 nor PaO2. The fluctuation of CVP reflecting the change of intrathracic pressure was smaller in HFJV group than in IMV/CPAP group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

PaO2 and intratracheal pressure in oscillatory ventilation in experimental respiratory failure.

In order to study the effect of high frequency ventilation on the pulmonary gas exchange in respiratory failure, we measured the PaO2 and other pulmonary gas exchange parameters for ventilatory rates of 0.5, 1.2, 4.8, and 16 Hz in dogs, to which acute respiratory failure was created by intravenous infusion of oleic acid. Either the mean intratracheal pressure or the end-tidal intratracheal pressure was controlled. A loud-speaker ventilator of our own design was modified so as to enable variation of the intratracheal pressure. Ventilation was measured using an ultrasonic instrument which counts the number of turbulent eddies. The tidal volume was set slightly higher than that was determined for healthy animals, but the resulting PaCO2 values were consistently higher than normal when PaO2 values were low. With the mean intratracheal pressure kept constant at 5, 10, and 15 cm H2O, PaO2 values with the FIO2 of 1 were between 41 and 46 at mPit of 5, 65 and 82 at 10 cm H2O, 278 and 423 at 15 cm H2O. No increase in PaO2 was observed with the increase in respiratory frequencies. If anything, a slight reduction in PaO2 at 8 and 16 Hz was observed, though not statistically significant. With the end-tidal intratracheal pressure constant, PaO2 varied but again correlated well with the mPit.

Animals↗