The effects of prostaglandin E1 on systemic and cerebral oxygenation before and during cardiopulmonary bypass

The purpose of this study was to examine the effects of a small dose of prostaglandin E1 on systemic and cerebral oxygenation. Thirty patients for coronary artery bypass graft surgery were randomly divided into two groups: Group 1 received PGE1 25 ng.kg-1.min-1. Group 2 received PGE1 50 ng.kg-1.min-1. After measuring baseline hemodynamics and mixed (SvO2) and juglar (SjvO2) venous oxygen saturations, administration of PGE1 at a rate of 25 ng.kg-1.min-1 or 50 ng.kg-1.min-1 was started before and during CPB. In group 2, mean arterial pressure (MAP) decreased during CPB, while in group 1, MAP was unchanged during CPB. There was no change in SjvO2 both in group 1 and group 2 before and during CPB. The administration of PGE1 at a rate of 25 ng.kg-1.min-1 during CPB was suitable for the maintenance of SvO2 and SjvO2.     

Effects of prostaglandin E1 infusion during cardiopulmonary bypass

Effects of continuous prostaglandin E1 (PGE1) infusion 0.03 micrograms.kg-1.min-1 on hemodynamics, body temperature and urine output during cardiopulmonary bypass (CPB) were studied. Systemic vascular resistance was kept significantly lower in PGE1 administration group than control group. Differences between core and peripheral temperature decreased faster in the PGE1 administration group than the control group. Mean arterial pressure was stable at 40mmHg during CPB in the PGE1 group and 60mmHg in the control group. However, there were no significant differences in urine output between the PGE1 administration group (10.8ml.kg-1.h-1) and the control group (9.4ml.kg-1.h-1). This study indicates that continuous PGE1 infusion (0.03 micrograms.kg-1.min-1) is a method of choice for vasodilation and improvement of peripheral perfusion during hypothermia of CPB.     

Prostaglandin E1 infusion fails to inhibit the increase of serum granulocyte elastase and myeloperoxidase and the decrease of plasma angiotensin converting enzyme in patients undergoing open-heart surgery]

We studied whether prostaglandin E1 (PGE1) could inhibit the increase of serum granulocyte elastase (GEL) and myeloperoxidase (MPO), and the decrease of plasma angiotensin converting enzyme (ACE) induced by oxygenator in 19 patients undergoing open-heart surgery. The patients were randomly allocated into 2 groups: one group (PGE1 group, n = 9) received a continuous infusion of PGE1 at a rate of 30 ng.kg-1.min-1 during cardiopulmonary bypass (CPB), and the other group (control group, n = 10) received saline infusion. GEL, MPO and ACE were measured serially at 8 points: before induction of anesthesia (as baseline), immediately before initiation of CPB, 10 min after initiation, 60 min after initiation, immediately after the end of CPB, 60 min after CPB, 120 min after CPB, and on the first postoperative day. Serum levels of GEL and MPO during 120 min after the end of CPB in both groups increased significantly compared with the baseline values. There was no significant difference between the two groups. Plasma levels of ACE in both groups decreased significantly immediately after the end of CPB compared with values taken 10 min after the initiation of CPB. There was no significant difference between the groups. We conclude that the infusion of PGE1 30 ng.kg-1.min-1 failed to inhibit the increase of GEL as well as MPO, and the decrease of ACE.     

The effects of prostaglandin E1 on the granulocyte elastase, white blood cells and platelets in head-neck surgery

We studied whether prostaglandin E1 (PGE1) inhibits the granulocyte elastase increase, white blood cell increase and platelet decrease caused by surgical stimuli in 30 head-neck surgical patients. The patients were divided into a group of no PGE1 infusion (C group) and two groups of PGE1 infusion (infusion of 10 ng.kg-1.min-1 in P 10 group and infusion of 30 ng.kg-1.min-1 in P 30 group). PGE1 was infused intravenously using a syringe pump during operation. The granulocyte elastase, white blood cells and platelets were measured at 4 points: before induction of anesthesia, before surgery, 4 hours after the start of surgery or the infusion of PGE1, and on the first postoperative day. Granulocyte elastase was maintained at significantly higher levels during and after surgery in 3 groups. White blood cells correlated with granulocyte elastase in 3 groups (especially in C group; Granulocyte elastase = 1.48 X white blood cells + 23.5, r = 0.672). Platelets decreased significantly in the first postoperative day in C and P 10 group. PGE1 has a tendency to inhibit dose-dependently the postoperative decrease in platelets. We conclude that 30 ng.kg-1.min-1 infusion of PGE1 did not inhibit granulocyte elastase release from white blood cells, but has a tendency to inhibit postoperative platelet decrease.     

Effects of small doses of prostaglandin E(1) on systemic hemodynamics and jugular venous oxygen saturation during cardiopulmonary bypass

STUDY OBJECTIVE: To examine the effects of small doses of prostaglandin E(1) (PGE(1)) on systemic hemodynamics and cerebral oxygenation during cardiopulmonary bypass(CPB). DESIGN: Randomized, prospective study. SETTING: Cardiac surgery at Saitama Cardiovascular and Pulmonary Center. PATIENTS: Forty patients who underwent elective coronary artery bypass surgery. INTERVENTIONS: The study was performed at the stable CPB period. Patients were randomly divided into four groups: control group (n = 10) received an infusion of saline, PGE(1) 10 group (n = 10) received an infusion of PGE(1) 10 ng/kg/min, PGE(1) 25 group (n = 10) received an infusion of PGE(1) 25 ng/kg/min, and the PGE(1) 50 group (n = 10) received an infusion of PGE(1) 50 ng/kg/min. MEASUREMENTS: After measuring the baseline partial pressure of the arterial oxygen saturation (SpO(2)), mixed venous oxygen saturation (SvO(2)), and jugular venous oxygen saturation (SjvO(2)), blood gases, and cardiovascular hemodynamic values, PGE(1) was infused intravenously at rate of between 10 and 50 ng/kg/min. PGE(1) infusion continued 30 minutes after the start of drug infusion, and the blood gas analysis and cardiovascular hemodynamic values were simultaneously determined together with the hemodynamic values at 2, 5, 10, 20, and 30 minutes during drug infusion. At 30 minutes after discontinuation of the drug infusion, the blood gas analyses were simultaneously determined together with the hemodynamic values. MAIN RESULTS: Mean arterial pressure (MAP) in PGE(1) 25 and 50 groups was decreased 20 and 30 minutes after the start of PGE(1) infusion compared with the baseline value (p < 0.05). In contrast, SvOm(2) in PGE(1) 25 and 50 groups was increased 20 and 30 minutes after the start of PGE(1) infusion compared with the baseline value (p < 0.05). There was no change in SjO(2) value despite a decrease in MAP during the study. CONCLUSIONS: Cerebral oxygenation estimated by SjvO(2) was maintained despite a decrease in MAP during the administration rate of PGE(1) between 10 and 50 ng/kg/min.     

The effects of prostaglandin E1 on myeloperoxidase and alpha 1-protease inhibitor in head-neck surgery]

To investigate whether prostaglandin E1 (PGE1) 30 ng.kg-1.min-1 inhibits the release of lysosomal enzyme from granulocytes by surgical stimuli, we measured myeloperoxidase and alpha 1-protease inhibitor (alpha 1-PI) in 32 patients for head neck surgery. The patients were divided into two groups; no PGE1 infusion group (C group) and PGE1 30 ng.kg-1.min-1 infusion group (P group). PGE1 was infused intravenously using a syringe pump during operation. MPO and alpha 1-PI were measured at 4 points: before induction of anesthesia, before surgery, 4 hours after the start of surgery or the infusion of PGE1, and on the first postoperative day. MPO was maintained at significantly higher levels during and after surgery in both groups. alpha 1-PI decreased significantly during operation and increased for 10% in the first postoperative day in both groups. There were no significant differences between groups in MPO and alpha 1-PI levels. We conclude that the infusion of PGE1 30 ng.kg-1.min-1 did not completely inhibit the release of lysosomal enzyme from granulocytes by surgical stimuli.     

Effects of prostaglandin E1 and dibutyryl cyclic AMP on hemodynamics after cardiopulmonary bypass in valve replacement surgery]

In view of vasodilating action of prostaglandin E1 (PGE1) and dibutyryl cyclic AMP (DBcAMP) we investigated the effect of each agent on hemodynamics after weaning from cardiopulmonary bypass (CPB) comparing with the effect in control group. PGE1 and DBcAMP were administered to patients who underwent valve replacement surgery with continuous low dose infusion at an average rate of 0.026 micrograms.kg-1.min-1 and 7.25 micrograms.kg-1.min-1 respectively. Following result was obtained. In PGE1 administered group, a significant reduction in pulmonary vascular resistance (PVR) and a significant decrease in mean arterial pressure (MAP) were observed during CBP, while there were no significant differences in other parameters, such as platelet counts, differences between core and peripheral temperature (delta T), urine output, systemic vascular resistance (SVR), cardiac index (CI), right-to-left shunt (Qs/Qt), oxygen delivery (DO2) and oxygen consumption (VO2). However, CI and platelet counts tended to increase but delta T and SVR tended to decrease. In DBcAMP administered group, there were no significant differences in all parameters compared with those of control group, showing a tendency of less improvement in hemodynamics than in PGE1 group. We have shown that the use of PGE1 rather than DBcAMP as vasodilator agent seems advantageous during open-heart surgery in patients especially with severe pulmonary hypertension, but it tends to cause severe hypotension during CPB.     

Hemodynamic effects of dopamine during thoracic epidural analgesia in man

The cardiovascular effects of dopamine were studied before and during thoracic epidural analgesia (TEA) in eight patients prior to abdominal aortic surgery. Dopamine was infused at rates of 2, 4, and 8 micrograms X kg-1 X min-1. Mean plasma dopamine concentration increased proportionally to the infusion rate. Before TEA, dopamine 8 micrograms X kg-1 X min-1 decreased systemic vascular resistance 4 +/- 4 mmHg min X 1-1 (m +/- SD) (P less than 0.05), but increased mean arterial pressure 15 +/- 12 mmHg (P less than 0.01), cardiac output 1.9 +/- 1.0 1 X min-1 (P less than 0.01), heart rate 10 +/- 9 beats X min-1 (P less than 0.05), and plasma norepinephrine concentration 544 +/- 252 pg X ml-1 (P less than 0.01). After the induction of TEA, which extended above the T2 dermatome and below the L2 dermatome, saline and albumin were infused to maintain central venous and pulmonary capillary wedge pressures. TEA reduced mean arterial pressure from 96 +/- 18 to 55 +/- 8 mmHg (P less than 0.01), cardiac output from 4.7 +/- 0.9 to 3.9 +/- 0.9 1 X min-1 (P = 0.05), systemic vascular resistance from 21 +/- 6 to 14 +/- 3 mmHg min X 1-1 (P less than 0.05), and plasma norepinephrine concentration from 394 +/- 141 to 207 +/- 73 pg X ml-1 (P less than 0.01). The plasma epinephrine concentration was reduced 49% after the induction of TEA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of lidocaine on arterial and venous circulation of limbs in man]

The effects of intravenous lidocaine on limb arteries and veins were investigated in a placebo-controlled study. Seven young healthy volunteers, 23 to 28-years-old, were included. Electrocardiogram, arterial pressure and arm and leg blood flows were recorded continuously. Systolic and diastolic blood pressures were measured in the left arm by finger photoplethysmography. Limb blood flow and the limb venous system were studied by venous occlusive plethysmography. The venous parameters studied were venous tone, lowest closing pressure, venous volume at 30 mmHg, and venous distensibility. After an initial bolus of 1.5 mg.kg-1 lidocaine had been given, 30, and then 60, micrograms.kg-1.min-1 were given for one hour each. Plasma noradrenaline and serum lidocaine titres were measured before giving the lidocaine, and at the end of each one hour period. Placebo consisted in a two hour infusion of 0.25 ml.min-1 normal saline. Lidocaine titres were 1.64 +/- 0.40 microgram.ml-1 after one hour, and 2.55 +/- 0.69 microgram.ml-1 after two hours. Lidocaine increased vascular resistances in both the forearm (+81% to +93%) and the calf (+38% to +57%). There was a concomitant increase in mean arterial blood pressure (+21% to +28%) without any change in heart rate. There was a significant dose-dependent increase in plasma noradrenaline levels during the second period of the lidocaine infusion with respect to the preinfusion period and the same period during the placebo infusion. Venous capacitance measured before any infusion had been started was greater in the leg than in the arm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of continuous infusion of diltiazem on cardiovascular responses to laryngoscopy and intubation]

We studied the cardiovascular responses to laryngoscopy and intubation in 30 patients who received continuous infusion of either diltiazem 10 micrograms.kg-1.min-1, 40 micrograms.kg-1.min-1 or saline as control group during 20 min before induction. Heart rate, arterial pressure, rate pressure product (RPP), pressure rate quotient (PRQ) were measured starting 20 min before induction to 3 min after tracheal intubation. The increases in arterial pressure and RPP following tracheal intubation were reduced significantly in patients receiving diltiazem 40 micrograms.kg-1.min-1, but they were not reduced in patients receiving diltiazem 10 micrograms.kg-1.min-1 compared with control. We conclude that continuous infusion of diltiazem during 20 min before induction is effective for preventing the increases in arterial pressure and RPP following tracheal intubation, and the optimal infusion rate is from 10 to 40 micrograms.kg-1.min-1.     

Cerebrospinal fluid concentrations of propofol during anaesthesia in humans

The concentration of propofol in and surrounding the human brain during propofol anaesthesia is unknown. We measured simultaneously the concentration of propofol in cerebrospinal fluid (CSF) from an indwelling intraventricular catheter and the concentration in arterial blood in five neurosurgical patients before, during induction (at 2.5 and 5 min) and during a maintenance propofol infusion (at 15 and 30 min). After induction of anaesthesia with propofol 2 mg kg-1, anaesthesia was maintained with an infusion of 8 mg kg-1 h-1 for 15 min and then reduced to 6 mg kg-1 h-1. The plasma concentration of propofol increased rapidly during induction and reached a plateau concentration of mean 2.24 (SD 0.66) micrograms ml-1 after 5 min. The concentration of propofol in CSF showed a slower increase during induction and remained almost constant at 35.5 (19.6) ng ml-1 at 15-30 min after induction. The CSF concentration of propofol that we measured was 1.6% of the plasma concentration and consistent with the high protein binding of the drug in plasma.      

Anesthetic management with propofol,fentanyl TCI and BIS in two cases of secondary hyperthyroidism due to TSH secretion from pituitary adenomas

We managed two patients with secondary hyperthyroidism due to TSH secretion from pituitary adenomas using total intravenous anesthesia with propofol and fentanyl. Both propofol and fentanyl were infused with target-controlled infusion (TCI) systems. The anesthesiologists controlled the target concentration of propofol to maintain the bispectral index (BIS) in a range from 40 to 60, and the target concentration of fentanyl was kept within a range of 2.0 to 3.0 ng.ml-1. Propranolol was injected in 0.4 mg increments to a total dosage of 2.4 to 3.2 mg. Prostaglandin E1 (PGE1) was infused at a rate from 0.01 to 0.04 microgram.kg-1.min-1 to maintain a stable heart rate and stable systemic blood pressure. The anesthetic effects were excellent in both patients. The necessary concentration of propofol during anesthesia was 2.5 to 4.0 micrograms.ml-1, and the emergence concentration of propofol was 1.4 to 1.7 micrograms.ml-1. These values were almost equal to those obtained in patients without thyroid disease. In conclusion, we could maintain the anesthesia for the patients with hyperthyroidism safely and stably by titrating the concentration of propofol and fentanyl based on the BIS value, and by administrating propranolol and PGE1 to avoid hypertension and tachycardia.     

Hypothermia after cardiopulmonary bypass in man: effects of prostaglandin E1 and phentolamine

The "afterdrop" in body temperature (TEMP) following adequate rewarming from hypothermic cardiopulmonary bypass (CPB) is frequently observed. This temperature drop sometimes accompanied by shivering results in increased myocardial oxygen demand. We investigated the relations between the afterdrop and use of vasodilators after CPB. For vasodilator therapy, PGE1 at the rate of 0.025-0.088 microgram.kg-1.min-1 (Prostaglandin Low Doses, PLD; n = 8), 0.107-0.136 microgram.kg-1.min-1 (Prostaglandin High Doses, PHD; n = 7), or phentolamine at 4.1-5.9 micrograms.kg-1.min-1 (PHENT; n = 8) were intravenously infused in 23 adult patients after CPB. During three hour period after CPB, esophageal, rectal, and forehead TEMP are lower in PHENT than in PGE1 groups. There were significant differences between PHD and PHENT group. Finger tip TEMP was lower in PGE1 groups than in PHENT group. There were significant differences between PHD and PHENT group. There were no differences in systemic arterial pressure, cardiac index (CI) and systemic vascular resistance (SVR) at any point between PHD and PHENT groups. It is concluded that PHENT increases the peripheral skin blood flow and TEMP but decreases the visceral TEMP possibly due to vasodilatation of the skin vessels, while PGE1 decreases skin blood flow and TEMP but increases the visceral TEMP, although SVR clearly decreases at the same rate in the two groups.     

The effects of milrinone on hemodynamics in patients undergoing cardiac surgery

The phosphodiesterase inhibitor, milrinone is used to treat low cardiac output syndrome, especially after cardiac surgery. But there were few reports about the precise hemodynamic effects at separation from cardiopulmonary bypass (CPB). We examined the hemodynamic effects of milrinone in 24 patients undergoing elective coronary artery bypass graft (CABG). Patients were assigned to the milrinone group (n = 12) and the control group (n = 12). Before separation from CPB, milrinone was administered as a loading dose of 50 micrograms.kg-1 into the reservoir of CPB at rectal temperature 33.5 degrees C and simultaneously a continuous infusion of 0.5 microgram.kg-1.min-1 was started. In addition, dopamine and nitroglycerine were administered in both groups. Hemodynamic measurements were performed before CPB, just after the weaning from CPB, 15, 30, 60 minutes after the weaning from CPB. Cardiac index increased significantly (P < 0.01) in the milrinone group as compared with the control group. Systemic vascular resistance index and mean arterial pressure decreased significantly (P < 0.0001, P < 0.05, respectively) in the milrinone group as compared with the control group. There were no significant differences in heart rate, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, mean right atrial pressure, stroke volume index, and pulmonary vascular resistance index between the two groups. These hemodynamic effects showed that milrinone supported cardiac performance after CPB for CABG.     

Effects of Cardiopulmonary Bypass and Prostacyclin on Plasma Catecholamines, Angiotensin II and Arginine-Vasopressin

Infusion of prostacyclin during cardiopulmonary bypass (CPB) reduces platelet activation, diminishes postoperative blood loss and decreases arterial blood pressure. In spite of continuous prostacyclin infusion, there is a delayed gradual rise in arterial pressure and resistance from low initial levels. We measured epinephrine (E), norepinephrine (NE), serotonin (5-HT), angiotensin II (ATII) and arginine-vasopressin (AVP) in plasma and carried out hemodynamic studies in 19 patients operated for coronary vascular disease. Eight patients served as a control group and were subjected to routine CPB. Eleven patients received prostacyclin 50 ng/kg/min during CPB. E and NE increased four- to sixfold during CPB from about 0.5 ng/ml (P less than 0.001). There was no difference between the groups. During CPB AVP increased sixfold from about 20 pg/ml in both groups (P less than 0.001), decreased early after CPB and increased again to high levels 3 h after CPB. The combined action of E, NE and AVP is of likely importance for the rise in systemic vascular resistance and/or need of vasodilation during CPB in the control group. ATII did not increase in the control group, but increased fourfold to about 20 pg/ml (P less than 0.01) during CPB in the prostacyclin group. The addition of AT II to E, NE and AVP seems responsible for the gradual return of arterial pressure and resistance during prostacyclin infusion. Postoperative hypertension and/or need of vasodilation 3 h after CPB was associated with high AVP levels in both groups. Hypotension caused by prostacyclin infusion did not increase E, NE or AVP above levels produced by CPB and moderate hypotension alone.     

Continuous infusion of prostaglandin E1 facilitates weaning from cardiopulmonary bypass

Vasodilators expedite the rewarming process and facilitate weaning from cardiopulmonary bypass (CPB). We continuously infused prostaglandin E1 (PG-E1) at 0.02-0.05 microgram.kg-1.min-1 (n = 11) or phentolamine (PHENT) at 5-10 micrograms.kg-1.min-1 (n = 13) during rewarming from mild hypothermic CPB. Rectal temperature was 33.3 +/- 1.7 degrees C in PG-E1 group vs. 31.3 +/- 1.3 degrees C in PHENT group at 30 minutes, and 34.0 +/- 1.2 degrees C vs. 32.7 +/- 1.1 degrees C at 40 minutes from the start of rewarming. There were significant differences (P less than 0.01 at 30 min, P less than 0.05 at 40 min) in rectal temperature between the two groups. There were no differences in perfusion index of CPB, arterial perfusion temperature, mean arterial pressure, systemic vascular resistance as well as esophageal, forehead or palm skin temperatures at any point between the two groups. The required time for weaning from CPB was significantly shorter in PG-E1 than in PHENT group (P less than 0.01, 36 +/- 8 min vs. 46 +/- 11 min). Our results also strongly suggest that PG-E1 preferentially improves splanchnic blood flow.     

Phenylephrine Increases Cerebral Blood Flow during Low-flow Hypothermic Cardiopulmonary Bypass in Baboons

Background: Although low-flow cardiopulmonary bypass (CPB) has become a preferred technique for the surgical repair of complex cardiac lesions in children, the relative hypotension and decrease in cerebral blood flow (CBF) associated with low flow may contribute to the occurrence of postoperative neurologic injury. Therefore, it was determined whether phenylephrine administered to increase arterial blood pressure during low-flow CPB increases CBF.

Methods: Cardiopulmonary bypass was initiated in seven baboons during fentanyl, midazolam, and isoflurane anesthesia. Animals were cooled at a pump flow rate of 2.5 l *symbol* min-1 *symbol* m-2 until esophageal temperature decreased to 20 degrees C. Cardiopulmonary bypass flow was then reduced to 0.5 l *symbol* min-1 *symbol* m-2 (low flow). During low-flow CPB, arterial partial pressure of carbon dioxide (PCO2) and blood pressure were varied in random sequence to three conditions: (1) PCO2 30-39 mmHg (uncorrected for temperature), control blood pressure; (2) PCO2 50-60 mmHg, control blood pressure; and (3) PCO2 30-39 mmHg, blood pressure raised to twice control by phenylephrine infusion. Thereafter, CPB flow was increased to 2.5 l *symbol* min-1 *symbol* m-2, and baboons were rewarmed to normal temperature. Cerebral blood flow was measured by washout of intraarterial133 Xenon before and during CPB.

Results: Phenylephrine administered to increase mean blood pressure from 23+/-3 to 46+/-3 mmHg during low-flow CPB increased CBF from 14+/-3 to 31+/-9 ml *symbol* min-1 *symbol* 100 g-1, P < 0.05. Changes in arterial PCO2 alone during low flow bypass produced no changes in CBF.     

Haemodynamic changes and circulating histamine concentrations following protamine administration to patients and dogs

Haemodynamic changes and the circulating concentrations of histamine associated with the intravenous infusion of protamine were measured in six adult patients undergoing elective aortocoronary bypass graft surgery and twelve halothane-anaesthetized dogs. Administration of protamine (4.7 mg X kg-1) over five minutes to patients at the conclusion of cardiopulmonary bypass did not produce haemodynamic changes or alterations in the arterial or mixed venous concentrations of histamine. Likewise, the administration of protamine (4.5 mg X kg-1) over five minutes to six dogs produced no haemodynamic changes or alterations in the arterial concentrations of histamine. Conversely, administration of protamine (4.5 mg X kg-1) as a rapid intravenous injection to six other dogs produced a decrease (about 30 per cent below control) in systolic, diastolic and mean arterial pressure (p less than 0.05) at 2.5 minutes following the injection. These decreases in blood pressure were paralleled by increases in the arterial concentration of histamine from 295 +/- 71 pg X ml-1 (mean +/- SD) before protamine to 860 +/- 6,465 pg X ml-1 (p less than 0.05) 2.5 minutes after protamine. Haemodynamic changes and the arterial concentration of histamine were not different from control five minutes after protamine administration. It is concluded that administration of protamine over five minutes to patients or dogs does not evoke significant haemodynamic changes or alterations in circulating concentrations of histamine. Conversely, rapid injection of protamine to dogs evokes transient decreases in blood pressure that are paralleled by increases in the arterial concentrations of histamine.     

Effects of oral clonidine premedication and postoperative i.v. infusion on haemodynamic and adrenergic responses during recovery from anaesthesia

The effects of clonidine, a central alpha 2-adrenoreceptor agonist, on haemodynamic and catecholamine changes were assessed during emergence from anaesthesia, a period which is associated with increased sympathetic nervous discharge, hypertension and tachycardia. According to a double-blind randomized design, 32 patients received either clonidine, preoperatively given by oral route (3.5 micrograms.kg-1) and postoperatively by i.v. infusion (0.3 microgram.kg-1.h-1), or a placebo. Perioperative management was similar in both groups. Measurements were made in the recovery room, before starting clonidine or placebo infusions for evaluation of clonidine premedication, and then during infusion as follows: when core temperature reached 37 degrees C; then 2 h, and 6 h later. Prior to starting infusions, mean blood pressure (88 +/- 15 vs 103 +/- 14 mmHg) (11.7 +/- 2.0 vs 13.7 +/- 1.9 kPa), heart rate (67 +/- 8 vs 87 +/- 17 beats.min-1) and plasma norepinephrine levels (462 +/- 393 vs 615 +/- 361 pg.ml-1) were lower in the clonidine group. Only at the latest measurement (6 h after core temperature reached 37 degrees C) did clonidine elicit significant effects. The values during clonidine infusion compared to placebo were at this time: mean blood pressure (73 +/- 10 vs 86 +/- 13 mmHg) (9.7 +/- 1.3 vs 11.5 +/- 1.7 kPa), heart rate (71 +/- 6 vs 93 +/- 13 beats.min-1) and plasma norepinephrine levels (240 +/- 224 vs 451 +/- 111 pg.ml-1). Our results suggest that: 1) preoperative clonidine may improve the haemodynamic profile associated with anaesthetic discontinuation, but 2) i.v. infusion (0.3 microgram.kg-1.h-1) did not prolong this effect during the early postoperative period in the face of the sympathetic nervous discharge of recovery.     

Haemodynamic and catecholamine responses to calcitonin gene-related peptide during volatile anaesthesia

PURPOSE: Calcitonin gene-related peptide (CGRP) produces vasodilatation, hypotension, and tachycardia. Tachycardia induced by CGRP may be due to sympathetic activation. Volatile anaesthetics attenuate activation of arterial baroreflexes. We examined the haemodynamic and endocrine effects of CGRP infusion (4 micrograms.kg-1) during anaesthesia with either enflurane or isoflurane in dogs. METHODS: Measurements of haemodynamic variables and hormone assays for plasma catecholamines were made before, during, and after CGRP infusion. Anaesthesia consisted of induction with 25 mg.kg-1 pentobarbital, followed by either enflurane (n = 7) or isoflurane (n = 7) to achieve a 1.0 end-tidal minimum alveolar concentration in oxygen 100%. RESULTS: Mean arterial pressure and systemic vascular resistance decreased (P < 0.01) and the reductions in both variables were similar during CGRP infusion in both groups. Cardiac index (CI) was increased (P < 0.01) in the enflurane group throughout the study while CI increased (P < 0.01) only during infusion in the isoflurane group. Heart rate (HR) remained unchanged (from 135 +/- 6 bpm to 134 +/- 7 bpm) in the enflurane group but tended to increase (from 162 +/- 9 bpm to 171 +/- 9 bpm) in the isoflurane group during infusion. Intergroup differences in HR were found (P < 0.05). Plasma epinephrine concentrations increased (from 42.4 +/- 12.7 pg.ml-1 to 115.3 +/- 41.8 pg.ml-1, P < 0.01) during infusion in the isoflurane group. However, these increases were suppressed (from 46.6 +/- 23.2 pg.ml-1 to 64.7 +/- 32.4 pg.ml-1) to a greater extent in the enflurane group. CONCLUSION: The haemodynamic responses, except for HR, of CGRP infusion are similar during enflurane and isoflurane anaesthesia. Suppression of tachycardia induced by CGRP is greater with enflurane than with isoflurane. The differences in HR may be due to the roles of catecholamine responses resulting from the anaesthetic-induced sympathetic suppression.