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Biomedical subjects

K Samii

Publications and source records attributed to K Samii.

At least 145 records · Page 8Linked to original sources

Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans.

The role of variation of venous return on baroreflex control of heart rate during lumbar epidural anesthesia was investigated in 12 unpremedicated patients. Group 1 patients (n = 6) received 8 ml of 0.5% plain bupivacaine in the epidural space (L3-4) (mean upper level of analgesia at T10). Group 2 patients (n = 6) received 8 ml of saline at the same level in the epidural space. Following the epidural injection, phenylephrine (PHE) and nitroglycerin (NTG) were employed to alter the stimulation of baroreceptor sites before and during application of lower body positive pressure (LBPP). Plasma bupivacaine, catecholamines, renin activity, and vasopressin were assayed. In contrast to saline, epidural bupivacaine induced a decrease in systolic arterial and right atrial pressures (-11 +/- 4 and -3.2 +/- 0.7 mmHg, respectively, mean +/- SEM) without change in heart rate, an increase in baroreflex slopes during PHE and NTG injections (+5.9 +/- 1.6 ms/mmHg and +2.8 +/- 0.9 ms/mmHg, respectively), and a decrease in plasma norepinephrine (-248 +/- 89 pg/ml). The application of LBPP restored hemodynamic and reflex variables to preepidural analgesia values, whereas plasma catecholamines decreased further. Plasma renin activity and vasopressin were not modified at any time in either groups. This study indicates that lumbar epidural anesthesia enhances cardiac vagal tone mainly through a decrease in venous return.

Adult↗

Effects of lidocaine on myocardial contractility and baroreflex control of heart rate in conscious dogs.

The effects of intravenous lidocaine (30 and 60 micrograms X kg-1 X min-1 during 30 min) at steady-state plasma levels (1.9 +/- 0.2 and 3.5 +/- 0.2 micrograms/ml, respectively) were investigated in conscious dogs, previously instrumented for measurements of arterial and left ventricular (LV) pressures, isometric myocardial contractility indexes (LV peak rate of tension development [dP/dt] and LV [dP/dt]/DP40), and heart rate. In addition, before and at the end of lidocaine infusions, arterial baroreflex responses were tested by bolus injections of nitroglycerin and phenylephrine. Whereas LV peak dP/dt and LV (dP/dt)/DP40 were significantly decreased after the low dosage of lidocaine, these indexes returned to control values after the 10th min of infusion of the high dosage. Moreover, eight out of 14 dogs exhibited continuous tremors, tachycardia, hypertension, and increase in contractility after the 10th min of lidocaine infusion (60 micrograms X kg-1 X min-1), although their lidocaine plasma levels (3.7 +/- 0.2 micrograms/ml) did not differ from those of the whole group. When these dogs were pretreated by combined alpha- and beta-adrenoceptor blocking drugs, none of them had tremors, and there was a constant depressant effect on cardiac chronotropism and inotropism. A specific enhancement of baroreflex sensitivity after phenylephrine injection was observed at the high lidocaine dosage. It is concluded that a central stimulation of both components of the autonomic nervous system modulates the direct effects of therapeutic plasma levels of lidocaine on cardiac chronotropism and inotropism in conscious dogs.

Animals↗

Epidural morphine in children: pharmacokinetics and CO2 sensitivity.

The effects of epidural morphine (50 micrograms X kg-1) after abdominal and urologic surgery were studied in 20 children ranging in age from 2 to 15 yr and weighing between 9 and 54 kg. The onset and the duration of analgesia were 30 +/- 12 min and 19.5 +/- 8 h, respectively (mean +/- SD). Side effects were pruritus (4/20), nausea and vomiting (8/20), and urinary retention (4/14). No apnea was observed. Ventilation control was studied in seven children. No significant change in resting respiratory variables occurred after both surgery and epidural morphine injection. However, the slope of the ventilatory response to CO2 was significantly (P less than 0.05) decreased after surgery but before morphine, as compared with its preoperative control value (0.84 +/- 0.44 versus 1.51 +/- 0.72 l X min-1 X mmHg-1), and remained low for 22 h after epidural morphine (0.90 +/- 0.57 l X min-1 X mmHg-1). Sixty minutes after morphine injection, the plasma morphine concentration was always less than 12 ng X ml-1 in the seven children studied. Pharmacokinetic parameters were similar to those observed after epidural injection of morphine in adults, except for a shorter terminal half-life (73.8 +/- 41.6 min) attributed to a greater total body clearance of morphine in the children (28.3 +/- 3.4 ml X min-1 X kg-1). It is concluded that epidural morphine provides effective and prolonged analgesia in children after abdominal and urologic surgery and that it is associated with prolonged respiratory depression that requires close monitoring for at least 24 h.

Adolescent↗

Effects of epidural anesthesia on catecholamines, renin activity, and vasopressin changes induced by tilt in elderly men.

Mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin changes induced by a 30-degree head-up tilt were studied before and during epidural anesthesia with bupivacaine in eight elderly patients (ages 58-82 yr). The tilt performed before epidural anesthesia did not modify mean arterial pressure, heart rate, plasma catecholamines, renin activity, and vasopressin at 5 and 15 min. During epidural anesthesia, the superior level of analgesia ranged from T4 to T10. Epidural anesthesia induced significant (P less than 0.05) decreases from control values in mean arterial pressure and plasma norepinephrine (from 85 +/- 6 to 67 +/- 8 mmHg and from 600 +/- 108 to 307 +/- 77 pg/ml, respectively, mean +/- SEM) without significant changes in heart rate, plasma epinephrine, renin activity, and vasopressin. However 5 and 15 min after tilt, significant decreases from pretilt values were measured in mean arterial pressure (from 67 +/- 8 to 57 +/- 6 and 55 +/- 6 mmHg, respectively) and in heart rate (from 70 +/- 8 to 63 +/- 7 and 62 +/- 7 beats/min). Simultaneously, an increase in plasma vasopressin (from 14.8 +/- 5.5 to 36.2 +/- 10.3 and 40.0 +/- 10.5 pg/ml) was recorded, whereas plasma norepinephrine and epinephrine remained unchanged. Posttilt plasma renin activity values at 5 and 15 min were increased significantly when compared with the preepidural values (2,752 +/- 1,168, 2,410 +/- 1,214 and 713 +/- 190 pg X ml-1 X h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Ventilatory response to CO2 following intravenous and epidural lidocaine.

The authors determined the effects of intravenous infusion and epidural administration of lidocaine on the control of ventilation in two groups of eight healthy unpremedicated subjects. In the intravenous group, an injection of 1.5 mg/kg lidocaine was followed by an infusion at a rate of 60 micrograms X kg-1 X min-1 for 30 min. The slope of the ventilatory response to CO2 was significantly increased (P less than 0.05) from its control value (2.65 +/- 1.22 1 X min-1 X mmHg-1 [mean +/- SD]) at the end of the infusion (58%), while plasma lidocaine level was at 3.14 +/- 0.82 microgram/ml. The correlation between individual plasma lidocaine levels and the changes in the slope of the ventilatory response to CO2 was significant (r = 0.58, n = 24, P less than 0.01). In the epidural group, after the administration of 5 mg/kg of lidocaine, the slope of the ventilatory response to CO2 increased significantly (P less than 0.05) from its control value (1.52 +/- 0.75 1 X min-1 X mmHg-1) at 15 (+22%) and 25 min (+42%), while plasma lidocaine levels were at 1.79 +/- 0.42 and 2.22 +/- 0.47 microgram/ml, respectively. In both groups, resting minute ventilation and end-tidal CO2 values remained unchanged. These results suggest that epidural lidocaine has a stimulating effect on the ventilatory control mechanisms that results from the systemic effect of the drug.

Adult↗

Ventilatory response to CO2 following axillary blockade with bupivacaine.

The systemic effect of bupivacaine on the control of ventilation was studied in eight ASA I (six male, two female) unpremedicated healthy subjects aged 30-55 yr (mean 43.5 yr) and weighing 59-82 kg (mean 69 kg) after axillary blockade with bupivacaine 0.5% without epinephrine, 3 mg/kg. The slope of the ventilatory response to CO2 was significantly increased (P less than 0.05) from its control value (1.77 +/- 1.03 l X min-1 X mmHg-1 [mean +/- SD]) 30 min (+19 +/- 32%) and 60 min (+32 +/- 37%) after axillary blockade, while plasma bupivacaine levels were 1.65 +/- 0.82 and 1.40 +/- 0.60 micrograms/ml, respectively. The correlation between individual plasma bupivacaine levels and the changes in the slope of the ventilatory response to CO2 was significant (r = 0.57, n = 16, P less than 0.05). Resting minute ventilation and end-tidal CO2 values did not change significantly. These results suggest that bupivacaine has a systemic stimulating effect on the ventilatory control mechanisms.

Adult↗

Antidiuretic hormone response to osmotic stimulus under fentanyl anaesthesia.

The effect of fentanyl anaesthesia on the plasma antidiuretic hormone (ADH) response to osmotic stimulus was studied in eight patients. Eight g (137 mmol) NaCl were rapidly injected intravenously the day before anaesthesia and blood samples were collected 5, 10, 20 and 30 min after the injection. This protocol was repeated in the same subjects, under anaesthesia with thiopental, nitrous oxide and fentanyl before surgical incision. Plasma ADH markedly increased after NaCl administration and was significantly correlated with plasma sodium (r = 0.67, P less than 0.005) when the patients were awake, whereas it did not change over 30 min and was not correlated with plasma sodium (r = 0.18, P greater than 0.05) under fentanyl anaesthesia. This inhibitory effect of anaesthesia occurred in spite of a significant fall in the mean arterial pressure during the study. In order to eliminate the role of overnight fasting, premedication and fluid load, the same protocol was performed in six control patients who were fasted overnight, premedicated and fluid loaded. These results demonstrate that fentanyl anaesthesia abolishes the plasma ADH response to both osmotic and low arterial pressure stimuli.

Adult↗

Effect of analgesia on respiratory muscle function after upper abdominal surgery.

The effects of three methods of analgesia (intravenous morphine, epidural lidocaine and epidural morphine) on vital capacity (VC), forced expiratory volume in 1 s (FEV1) and maximal expiratory and inspiratory pressures (MEP and MIP) at the mouth were studied in 12 high respiratory risk patients following upper abdominal surgery. VC, FEV1, MEP and MIP markedly decreased following laparotomy. VC and FEV1, were partially restored by epidural analgesia and remained unchanged following intravenous morphine. MEP and MIP remained unchanged after each of the three methods of analgesia. This suggests the existence of a non-analgesic dependent dysfunction of inspiratory and expiratory muscles following upper abdominal surgery.

Aged↗

Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperative pain.

The effects of upper abdominal surgery on diaphragmatic function were studied in 5 patients. During quiet tidal breathing, the volume displacement of the abdomen within the tidal volume (Vab/Vt) and the ratio of abdominal and transdiaphragmatic pressure changes (delta Pab/delta Pdi), taken as an index of the diaphragmatic contribution to the breathing process, decreased significantly on the first postoperative day (p less than 0.001); in 2 patients, a cephalad paradoxical motion of the diaphragm during inspiration was observed. Diaphragmatic dysfunction also occurred during maximal inspiratory efforts as shown by the significant fall in maximal static transdiaphragmatic pressure (Pdimax) and cephalocaudal diaphragmatic displacement on the first (p less than 0.001) and third (p less than 0.001) postoperative days. On the first postoperative day, opiate epidural analgesia did not modify Vab/VT, delta Pab/delta Pdi, and Pdimax. These parameters spontaneously returned towards control values on the seventh postoperative day. We conclude that upper abdominal surgery induces a marked diaphragmatic dysfunction lasting about 1 wk and that it is not suppressed by postoperative pain relief. The mechanism of this dysfunction remains to be determined. It may be the main cause of the postoperative pulmonary restrictive pattern.

Abdomen↗

[Post-operative respiratory function after subcutaneous and epidural morphine analgesia (author's transl)].

In 20 elderly patients who underwent cholecystectomy post-operative analgesia was obtained with morphine given either subcutaneously (n = 10) or epidurally (n = 10). Both groups were comparable as to age and pre-operative respiratory function values. On the first post-operative day, vital capacity, forced expiratory volume in one second and and paO2 were significantly higher in the epidural morphine group (respectively 70 +/- 6 p. cent and 68 +/- 6 p. cent of pre-operative values, and 74 +/- 3 mmHg) (mean +/- s.e.m.) than in the subcutaneous morphine group, where the corresponding figures were 52 +/- 4 p. cent, 48 +/- 5 p. cent and 63 +/- 2 mmHg respectively. PaCO2 was unchanged in both groups. These data indicate that epidural morphine analgesia to some extent reduces the post-operative respiratory dysfunction observed after abdominal surgery.

Aged↗

[Pharmacology of narcotics administered by the epidural or intrathecal route (author's transl)].

Owing to the presence of specific opiate receptors in the spinal cord, analgesia can be obtained with epidural or intrathecal injections of morphine derivatives. The duration of analgesia depends upon the degree of water solubility of the compound. Compounds with low coefficient of distribution in lipids (e.g. morphine) do not readily cross the blood-brain barrier and have a prolonged action, whereas the duration of analgesia induced by highly lipid-soluble compounds, such as dextromoramide and phenoperidine, is not very different from that obtained with more conventional routes of administration. The fact that large amounts of narcotics are taken up by the spinal cord explains that central effects are relatively rare. However, side-effects may be observed, and their frequency mainly depends upon the quantity of narcotic injected. These side-effects reduce the number of indications, which cannot yet be precisely determined. Epidural and intrathecal analgesia appears to be particularly useful during the post-operative period in patients liable to respiratory complications.

Analgesia↗

Plasma pharmacokinetics of morphine after i.m., extradural and intrathecal administration.

Eighteen patients received morphine 0.2 mg kg-1 in 0.9% saline i.m. (n = 6), extradurally (n = 6), or in a 10% dextrose solution intrathecally (n = 6) for pain relief operation. Plasma unmetabolized morphine was isolated by extraction using liquid-solid chromatography and measured by radioimmunoassay. Conjugated morphine was calculated from the difference between total immunoreactive morphine and unmetabolized morphine. Initial vascular absorption was significantly less in the intrathecal group than in the i.m. and extradural groups. This accounts for persistence of plasma unmetabolized morphine at 24 h and for more prolonged analgesia in the intrathecal group. Prolonged analgesia observed following extradural and intrathecal administration was caused by a small quantity of unmetabolized morphine. Extradural and i.m. groups showed the same pharmacokinetic patterns although extradural analgesia is much more prolonged. Morphine glucuronide appeared later in blood in the intrathecal group than in the two other groups.

Epidural Space↗