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Biomedical subjects

S Hoka

Publications and source records attributed to S Hoka.

At least 37 records · Page 2Linked to original sources
PubMed1998

Epidural saline solution prior to local anaesthetic produces differential nerve block.

PURPOSE: The loss-of-resistance technique is generally used to identify the epidural space usually with normal saline. However, the effect of epidural saline on anaesthetic spread has not been demonstrated. The purpose of this study was to determine whether epidural saline affected the anaesthetic level and the quality of analgesia. METHODS: Seventy patients undergoing upper abdominal surgery received thoracic epidural anaesthesia combined with general anaesthesia. The patients were randomly allocated into three groups using epidural saline volumes of 1, 5, or 10 ml. Ten minutes after epidural injection of 12 ml mepivacaine 1%, the dermatome levels of hypaesthesia for cold and pinprick were determined by an individual blinded to the amount of saline administered. RESULTS: The levels of hypaesthesia for cold sensation were not different among the three groups (23 [14-44] total bilateral dermatomes blocked with 1 ml saline, 22 [16-41] dermatomes with 5 ml, and 24 [10-36] dermatomes with 10 ml (median [range])). However, the larger volume of saline produced decreased spread of hypaesthesia for pinprick (22 [4-41] dermatomes blocked bilaterally for 1 ml vs 16 [8-24] dermatomes for 10 ml group, P < 0.004). CONCLUSION: Our results suggest that a large volume of saline solution injected in the epidural space to elicit loss-of-resistance dilutes the local anaesthetic solution, resulting in reduced spread of the block to pinprick.

Abdomen↗
PubMed1998

Consideration of the optimal epidural fentanyl doses in abdominal surgery.

STUDY OBJECTIVE: To determine an optimal dose of epidural fentanyl in open abdominal surgery by examining the effects of different doses of epidural fentanyl in combination with or without low concentration of lidocaine on hemodynamic and endocrine responses to surgical stress. DESIGN: Prospective, randomized study. SETTING: University hospital. PATIENTS: 40 ASA physical status I and II patients scheduled for elective abdominal surgery including gastrectomy (n = 20), colectomy (n = 10), liver tumor resection (n = 2), pancreatectomy (n = 3), pancreaticoduodenectomy (n = 1), low anterior resection (n = 3), and cholecystectomy (n = 1). INTERVENTIONS: Patients were randomly allocated to one of two groups: epidural fentanyl with 0.5% lidocaine (Group L + F; n = 25) or epidural fentanyl alone (Group F; n = 15). Both two groups were divided into subgroups; in Group L + F, epidural fentanyl was administered as doses of 0, 0.3, 1, 3, and 5 micrograms/kg in 5 patients each. In Group F, epidural fentanyl was administered as doses of 1, 3, and 5 micrograms/kg in 5 patients each. Hemodynamic data and plasma catecholamine concentrations were compared between before the epidural injection and immediately after peritoneal incision. MEASUREMENTS AND MAIN RESULTS: There was no difference in mean arterial pressure (MAP) and heart rate (HR) between Group L + F and Group F at the time before epidural administration of fentanyl, 20 minutes after epidural fentanyl, and immediately after peritoneal incision. However, there were significant decreases in MAP immediately after skin incision in epidural fentanyl 0 and 3 micrograms/kg in Group L + F patients and also in epidural fentanyl 1 and 3 micrograms/kg in Group F patients. HR significantly decreased in epidural fentanyl 5 micrograms/kg of Group L + F at peritoneal incision (p < 0.05). Plasma epinephrine decreased significantly in fentanyl 3 and 5 micrograms/kg in Group L + F immediately after peritoneal incision (p < 0.05), whereas the increase in norepinephrine was significant in Group F (p < 0.01). Plasma dopamine significantly increased only in fentanyl 1 microgram/kg in Group F (p < 0.05). CONCLUSION: Epidural fentanyl 3 micrograms/kg with 0.5% lidocaine may be most adequate for laparotomy because these doses caused neither bradycardia nor increments of norepinephrine perioperatively.

Abdomen↗
PubMed1998

Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity.

BACKGROUND: Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity. METHODS: In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol. RESULTS: The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups. CONCLUSIONS: The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.

Anesthetics, Intravenous↗
PubMed1997

Removal of retained air during cardiac surgery with transesophageal echocardiography and capnography.

STUDY OBJECTIVE: To evaluate a new method for removal of retained air at the end of cardiopulmonary bypass (CPB) by end-tidal CO2 pressure (PETCO2) and pulmonary arterial pressure (PAP) monitoring, and transesophageal two-dimensional echocardiography (TEE). DESIGN: Prospective study. SETTING: Cardiac surgery unit at a university hospital. PATIENTS: 36 ASA physical status I, II, III patients for open heart surgery. INTERVENTIONS: The CPB reservoir was gradually raised to decrease venous drainage. Accordingly, the right heart began to receive the venous blood and eject it to the pulmonary artery. The vent existing in the left ventricle or the left atrium then collected any whole blood containing air bubbles that came from the pulmonary circulation. The air bubbles were confirmed by TEE to be removed and not to eject from the left ventricle to te systemic circulation. MEASUREMENTS AND MAIN RESULTS: Levels of PETCO2, PaCO2, PAP, and the duration of the removal procedure were measured when a sufficient pulmonary circulation was established and the removal of retained air was considered to be satisfactorily accomplished by the absence of air bubbles, confirmed by TEE for more than 30 seconds. PETCO2 reached 28 +/- 4 mmHg during the removal of air, while PaCO2 reached 35 +/- 6 mmHg (p < 0.05). Mean PAP during removal of air reached 18 +/- 4 mmHg, which was approximately 90% of that before CPB. The duration time of removal of air was 9 +/- 2 min. CONCLUSIONS: PETCO2 and PAP are useful indicators of pulmonary circulation during this procedure for removal of air. PETCO2 of 25 to 30 mmHg and PAP of 90% of the prebypass level have been found to be necessary for the removal of air. Our technique for removal of air using PETCO2, PAP, and TEE enables us to satisfactorily eliminate residual air.

Adolescent↗
PubMed1997

alpha 1-adrenoceptor stimulation is able to reverse halothane-induced cardiac depression in isolated rat hearts.

BACKGROUND: Stimulation of myocardial alpha 1-adrenoceptors has been shown to exert positive inotropic effects through a cyclic AMP-independent mechanism. The purpose of this study was to examine if alpha 1-adrenoceptor stimulation is able to attenuate myocardial depression produced by exposure to halothane, and to test if alpha 1-adrenoceptor stimulation alters myocardial oxygen supply-demand balance in hearts exposed to halothane. METHODS: The effects of phenylephrine were examined in 7 isolated perfused rat hearts. Variables measured were: heart rate, isovolumetric peak left ventricular pressure (LVP), LV dP/dt, coronary arterial flow, myocardial O2 delivery (DO2), myocardial O2 consumption (MVO2) and the ratio of DO2/MVO2. Each heart was exposed to phenylephrine cumulatively 0.1 microM, 0.3 microM, 1 microM and 3 microM under the administration of 1% halothane in the presence of propranolol 1 microM. RESULTS: Halothane 1% decreased the heart rate by 9 +/- 3%, LVP by 37 +/- 3%, and LV dP/dt by 35 +/- 2%. Phenylephrine restored these decreases to the baseline levels. Phenylephrine maintained or further enhanced the reductions in coronary flow and DO2 produced by halothane, resulting in a decrease in the DO2/ MVO2 ratio. CONCLUSION: alpha 1-adrenoceptor stimulation is capable of restoring direct cardiac depressant effects of halothane with a possible impairment of the oxygen supply-demand balance.

Anesthetics, Inhalation↗
PubMed1996

Dose-dependent increases in the renal sympathetic nerve activity during rapid increase in isoflurane concentration in intact, lower airway-deafferented, and baroreceptor-deafferented rabbits.

BACKGROUND: The inhalation of high concentrations of isoflurane has been reported to increase the heart rate and the concentration of serum catecholamines. Although the precise mechanisms for the sympathetic activation of isoflurane have yet to be clearly elucidated, they are considered to possibly originate from the stimulation of airway sensory afferents, the baroreceptor reflex, or the direct stimulation of the central nervous system. To determine how these three mechanisms contribute to sympathetic augmentation, the effects of lower airway deafferentation and baroreceptor deafferentation on the isoflurane-induced changes in the renal sympathetic nerve activity (RSNA) in tracheally intubated rabbits were examined. METHODS: Twenty rabbits were given basal anesthesia. After tracheotomy and during mechanical ventilation, the changes in the heart rate, mean arterial pressure, and RSNA in response to random exposures to 1%, 2%, 3%, and 4% isoflurane were examined. The animals were assigned to one of three groups; 1, the intact group (n = 6); 2, the baroreceptor-deafferented group (n = 9), in which the sinoaortic plus vagal nerves were cut; and 3, the lower airway-deafferented group (n = 5), which underwent a bilateral vagotomy. The exposure to isoflurane was for 10 min in group 1 and 5 min in groups 2 and 3. At least 1 h was allowed for the recovery interval between exposures to isoflurane. RESULTS: The inhalation of isoflurane caused dose-dependent increases in RSNA in all three groups. RSNA during high concentrations of isoflurane began to increase at 1 min, reaching the maximum at 4 or 5 min in group 1 (2.8- and 3.8-fold at 3% and 4% isoflurane, respectively) and group 3 (2.8- and 4.5-fold at 3% and 4% isoflurane, respectively), but it reached the peak at 2 or 3 min in group 2 (1.7- and 2.4-fold at 3% and 4% isoflurane, respectively) after the initiation of inhalation, in association with early slight increases followed by decreases of mean arterial pressure in groups 1 and 2 but only gradual decreases of mean arterial pressure in group 3. The increases in RSNA in group 3 were similar to group 1, however, those in group 2 were significantly attenuated compared with group 1. CONCLUSIONS: The inhalation of isoflurane caused an increase of RSNA in intact, baroreceptor-deafferented, and lower airway-deafferented rabbits. The extent of the increases in RSNA was greater in intact and lower airway-deafferented rabbits than in baroreceptor-deafferented rabbits. Therefore, it is suggested that isoflurane may increase the efferent sympathetic nerve activity via the direct stimulation of the central nervous system and via the arterial baroreceptor reflex reflecting the reduction in arterial blood pressure. The stimulation of the vagally innervated airway may not contribute to the increase in the sympathetic nerve activity by isoflurane.

Afferent Pathways↗
PubMed1996

[Relationship among the heart, vasculature and blood volume at perioperative period: the influence of volatile anesthetics].

Ventricular pressure-volume relationship enables us to understand the relationship among the heart, vasculature, and blood volume, since it provides, on a single plane, the preload, afterload, and cardiac contractility, which are major determinants of stroke volume. In addition, it is also possible to estimate cardio-vascular matching, namely the optimum of cardio-vascular interaction, by an analysis of ventricular pressure-volume relationship. Volatile anesthetics cause circulatory depression due primarily to decreases in cardiac contractility and stressed blood volume. The optimal treatment for it is to restore these decreases produced by volatile anesthetics. Thus, an increase in afterload by vasoactive agents may cause deterioration of cardio-vascular matching. A rationale for optimal perioperative circulatory management can be deduced from understanding a quantitative interaction among the heart, vasculature, and blood volume.

Anesthetics, Inhalation↗
PubMed1995

Effects of phenylephrine and prostaglandin E1 on ventriculo-arterial matching during halothane anaesthesia.

We have investigated the effects of phenylephrine alone and combined with prostaglandin E1 (PGE1) on ventriculo-arterial matching during halothane anaesthesia in dogs. The ratio of left ventricular end-systolic elastance (Ees) to effective arterial elastance (Ea) was used as an index of ventriculo-arterial matching. In group 1 (n = 7), measurements were performed at control, 1.5% halothane, halothane+phenylephrine 1-10 micrograms kg-1 min-1, and halothane+phenylephrine+PGE1 0.2-1.0 or 1.0-2.0 micrograms kg-1 min-1. In group 2 (n = 5), dobutamine 2 and 5 micrograms kg-1 min-1 was infused during halothane anaesthesia. Halothane 1.5% decreased mean arterial pressure (MAP), cardiac output and Ees. Phenylephrine restored MAP, but further decreased cardiac output. The decrease in Ees produced by halothane was reversed by phenylephrine. PGE1 increased cardiac output and reversed the increases in Ea and Ea/Ees during phenylephrine infusion. Dobutamine also reversed halothane-induced decreases in MAP, cardiac output and Ees, and improved Ea/Ees. Our results indicate that combined use of PGE1 with phenylephrine can eliminate the vasoconstrictive property of phenylephrine, resulting in an improvement in ventriculo-arterial matching.

Alprostadil↗
PubMed1995

Changes in end-tidal carbon dioxide tension following sodium bicarbonate administration: correlation with cardiac output and haemoglobin concentration.

An intravenous administration of sodium bicarbonate (NaHCO3) forms excess CO2, resulting in an immediate increase in end-tidal carbon dioxide tension (PETCO2). We hypothesized that the time until PETCO2 reached a maximum, and the magnitude of the increase in PETCO2 are influenced by cardiac output and haemoglobin concentration, respectively. To test this hypothesis, we examined changes in PETCO2 following an intravenous administration of NaHCO3 at different levels of cardiac output and haemoglobin concentration. We administered 0.2 mmol.kg-1 of 8.4% NaHCO3 into the vena cava in 15 anesthetized dogs under mechanical ventilation of 20 breaths per min. Cardiac output was increased by dopamine infusion, and decreased by blood withdrawal under halothane anaesthesia. Haemoglobin concentrations were changed by haemodilution with hydroxyethyl starch. When control measurements were taken, time-max (the time until the increase in PETCO2 reached a maximum) was 4 +/- 0.2 breaths-time, and delta CO2-max (the magnitude of the increase in PETCO2) was 0.90 +/- 0.04 kPa (6.6 +/- 0.3 mmHg). Cardiac output was inversely correlated with time-max (r = 0.94, P < 0.0001), while it revealed a poor correlation with delta CO2-max. Haemoglobin concentration showed a significant correlation with delta CO2-max (r = 0.736, P < 0.005), but not with time-max. We concluded that the time course and the magnitude of changes in PETCO2 following intravenous administration of NaHCO3 reflect changes in cardiac output and haemoglobin concentration, respectively.

Anesthesia, Inhalation↗
PubMed1995

Coronary artery spasm induced under lumbar epidural anaesthesia.

A case of coronary artery spasm during lumbar epidural anaesthesia prior to surgery is presented. Three paroxysmal episodes of ST segment elevation in lead II without changes in V5 developed concomitantly when the patient complained of chest discomfort. A denervation of the cardiac sympathetic nerve seems to be the primary genesis of the attack in a patient prone to such events.

Adult↗
PubMed1994

L-arginine attenuates ketamine-induced increase in renal sympathetic nerve activity.

BACKGROUND: It has been reported that ketamine produces sympathoexcitation by directly stimulating the central nervous system. It also has been shown that nitric oxide (NO) may play a role in signal transduction of the nervous system. Therefore, we hypothesized that the sympathoexcitation of ketamine may be linked to central NO formation. To test this hypothesis, we examined the effects of L-arginine, a substrate of NO formation, on renal sympathetic nerve activity (RSNA) during ketamine anesthesia. METHODS: Using 45 rabbits given basal anesthesia with alpha-chloralose, we measured changes in heart rate, mean arterial pressure, and RSNA in response to intravenous ketamine (1 mg/kg) and investigated the effect of intravenous L-arginine and D-arginine (bolus 30 mg/kg followed by continuous 30 mg.kg-1.min-1). The animals were divided into intact, sinoaortic- and vagal-deafferented, and spinal cord-transected groups. RESULTS: Ketamine caused significant increases in RSNA (172 +/- 16%), heart rate (12 +/- 2 beats/min), and mean arterial pressure (8 +/- 1 mmHg) in the intact rabbits. Ketamine also increased RSNA in sinoaortic- and vagal-deafferented rabbits, but not in spinal cord-transected rabbits. L-Arginine attenuated the ketamine-induced increase in RSNA in intact and deafferented rabbits, whereas D-arginine had no effect on RSNA. In addition, NG-nitro-L-arginine methyl ester, a NO synthase inhibitor, increased RSNA and the increase was attenuated by L-arginine. CONCLUSIONS: Ketamine may act centrally to increase sympathetic outflow, and the sympathoexcitation may be attenuated by increasing NO formation with L-arginine in the central nervous system.

Animals↗
PubMed1994

The difference of isoflurane and halothane in ventriculoarterial coupling in dogs.

Effective arterial elastance (Ea) and left ventricular end-systolic elastance (Ees) are used as indices of cardiac afterload and cardiac contractility, respectively. We compared the effects of two volatile anesthetics, halothane and isoflurane, on ventriculoarterial coupling using an index of Ea/Ees in 20 mongrel dogs. Ees was obtained using a single-beat estimation technique. Ea was estimated as the ratio of the mean arterial pressure to stroke volume. Basal anesthesia consisted of pentobarbital and alpha-chloralose. Dogs were further anesthetized either with halothane 1 minimum alveolar anesthetic concentration (MAC) and 2 MAC (n = 10) or with isoflurane 1 MAC and 2 MAC (n = 10). Halothane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 35.5% +/- 4.9%, 18.3% +/- 12.6%, and 39.7% +/- 10.8%, respectively. Isoflurane 2 MAC significantly decreased the cardiac output, Ea, and Ees by 37.9% +/- 4.0%, 38.7% +/- 6.4%, and 43.0% +/- 6.0%, respectively. The decreases in cardiac output and Ees were not significantly different between halothane and isoflurane. Halothane increased Ea/Ees from 0.83 +/- 0.05 to 1.22 +/- 0.13, whereas isoflurane maintained the Ees/Es at a constant level. Our results suggest that mechanical efficiency is well maintained during isoflurane anesthesia because it has an equivalent effect on left ventricular contractility and arterial properties, whereas halothane can impair mechanical efficiency by depressing left ventricular contractility more than the arterial system.

Animals↗
PubMed1993

Intra-operative blood pressure control by prostaglandin E1 in patients with hypertension and ischemic heart disease--a multi-center study.

The purpose of this multi-center study was to evaluate the efficacy and safety of prostaglandin E1 (PGE1) administration in achieving deliberate hypotension and in treating intraoperative hypertension for patients with a history of hypertension and ischemic heart disease. PGE1 (0.08 microg.kg(-1).min(-1)) decreased systolic blood pressure from 125 +/- 29 to 106 +/- 22 mmHg (mean +/- SD) in the deliberate hypotension group (n = 158) and from 155 +/- 34 to 125 +/- 32 mmHg in the antihypertension group (n = 55). The heart rate significantly increased from 80 +/- 15 to 85 +/- 18 beats.min(-1) in the deliberate hypotension group, but was not significantly altered in the antihypertension group. The time required to obtain the desired level of blood pressure was approximately 20 min in the deliberate hypotension group. When the infusion was stopped, blood pressure returned approximately to the preinfusion level within about 20 min. No rebound hypertension was observed. PGE1 significantly increased the urine flow in patients who had a low urine flow before PGE1 infusion. Thirteen out of 213 patients (5.6%) had side effects such as excessive hypotension (1%), phlebitis (3%), and unexpected tachycardia (1%), which were alleviated gradually after discontinuation of PGE1 infusion. No dysarrhythmia and further ST segment changes in the electrocardiograms were observed. These findings suggest that PGE1 can be safely used to control arterial blood pressure during surgery in patients having preoperative hypertension and ischemic heart disease.

Journal Article↗
PubMed1993

Changes in venous capacitance during prostaglandin E1-induced hypotension; comparisons with trinitroglycerin.

The purpose of this study was to examine the effects of prostaglandin E1 (PGE1) on venous capacitance during controlled hypotension. Trinitroglycerin (TNG) was used as a control agent. In rats anesthetized with ketamine, mean arterial pressure was lowered to 70 mmHg and subsequently 50 mmHg by intravenous infusion of PGE1 or TNG. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was significantly decreased by PGE1 from 7.9 +/- 0.3 to 6.9 +/- 0.3 mmHg at mean arterial pressure of 70 mmHg and to 6.9 +/- 0.2 mmHg at mean arterial pressure of 50 mmHg. The decrease in MCFP by PGE1 at mean arterial pressure of 70 mmHg was not significantly different from TNG. However, the decrease in MCFP by PGE1 at mean arterial pressure of 50 mmHg was significantly less than that by TNG. The results suggest that the venous capacitance may be increased by PGE1 to a similar degree with TNG at doses to produce a comparable level of moderate hypotension, but the increase in venous capacitance may be less in PGE1 than TNG at doses to produce deep hypotension.

Journal Article↗
PubMed1993

Effects of high salt intake on control of hindlimb vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats.

1. This study aimed to examine whether a high salt diet alters control of vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). 2. SHR and WKY aged 8 weeks were fed either high (8%) or normal salt (0.4%) diet for 4 weeks. Arterial baroreflex control of hindlimb vascular resistance was assessed by examining reflex-induced vasodilation and vasoconstriction in response to phenylephrine and nitroprusside, respectively, in the constant-flow perfused hindlimb of urethane-anesthetized rats. 3. Tonic influence of the cardiopulmonary vagal afferents was evaluated by examining the effects of vagotomy on hindlimb vascular resistance and on the gain of arterial baroreflex control of hindlimb vascular resistance. 4. The gain of the arterial baroreflex control of hindlimb vascular resistance in response to both phenylephrine and nitroprusside were not significantly different between SHR receiving high and normal salt diets, and between WKY receiving high and normal salt diets. 5. Vagotomy increased hindlimb vascular resistance in all four groups of rats. However the high salt diet than those in SHR on a normal salt diet but similar between the two groups of WKY. Vagotomy increased the slope of arterial baroreflex control of hindlimb vascular resistance in SHR receiving a normal salt diet and the two groups of WKY but not in SHR receiving a high salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1993

The effect of the pericardium on right and left ventricular diastolic functions during isoflurane anesthesia.

We examined the effects of the pericardium on diastolic function of the right and left ventricles during isoflurane anesthesia. The diastolic properties of the ventricles were assessed by indices of isovolumetric relaxation such as -dP/dt, -dP/dt25, and time constant for relaxation, and by end-diastolic pressure. In seven mongrel dogs, anesthesia was initially induced by the administration of pentobarbital and maintained with alpha-chloralose. Two 7F microtipped pressure transducers were inserted into the right and left ventricles, and a flow-directed pulmonary artery catheter was placed in the pulmonary artery. After a left thoracotomy, opening and closing the pericardium was performed at 0% isoflurane, 1.3% isoflurane, and 2.6% isoflurane. Isoflurane 1.3% and 2.6% produced a decrease in cardiac output in association with a decrease in -dP/dt and an increase in time constant for relaxation of both ventricles, suggesting that isoflurane may depress isovolumetric relaxation of both ventricles. Isoflurane also increased end-diastolic pressure of the left ventricle. With 0% isoflurane, pericardial opening did not significantly change the diastolic properties of either ventricle and other hemodynamics. Pericardial opening at 1.3% and 2.6% isoflurane increased cardiac output without any significant changes in -dP/dt and time constant of either ventricle, but with significant decreases in end-diastolic pressures of both ventricles. We conclude that the pericardium may have a constraining effect on the diastolic properties, especially end-diastolic pressure, but not on isovolumetric relaxation of both ventricles during isoflurane anesthesia.

Anesthesia, Inhalation↗