Direct Arterial Blood Pressure Research Articles

Cardiovascular effects of sevoflurane in Holstein calves

ObjectiveThe purpose of this study was to determine the cardiovascular effects of sevoflurane in calves. Study designProspective experimental study. AnimalsSix, healthy, 8–12–week–old Holstein calves weighing 80 ± 4.5 (mean ± SEM) kg were studied. MethodsAnesthesia was induced by face–mask administration of 7% sevoflurane in O2. Calves tracheae were intubated, placed in right lateral recumbency, and maintained with 3.7% end–tidal concentration sevoflurane for 30 minutes to allow catheterization of the auricular artery and placement of a Swan–Ganz thermodilution catheter into the pulmonary artery. After instrumentation, administration of sevoflurane was temporarily discontinued until mean arterial pressure was > 100 mm Hg. Baseline values were recorded and the vaporizer output increased to administer 3.7% end–tidal sevoflurane concentration. Ventilation was controlled to maintain normocapnia. The following were recorded at 5, 10, 15, 30 and 45 minutes after collection of baseline data and expressed as the mean value (± SEM): direct systolic, diastolic, and mean arterial blood pressures; cardiac output; mean pulmonary arterial pressure; pulmonary arterial occlusion pressure, heart rate; and pulmonary arterial temperature. Cardiac index and systemic and pulmonary vascular resistance values were calculated using standard formulae. Arterial blood gases were analyzed at baseline, and at 15 and 45 minutes. Differences from baseline values were determined using one–way analysis of variance for repeated measures with post–hoc differences between mean values identified using Dunnet's test (p < 0.05). ResultsMean time from beginning sevoflurane administration to intubation of the trachea was 224 ± 9 seconds. The mean end–tidal sevoflurane concentration at baseline was 0.7 (± 0.11)%. Sevoflurane anesthesia was associated with decreased arterial blood pressure at all sampling times. Mean arterial blood pressure decreased from a baseline value of 112 ± 7 mm Hg to a minimum value of 88 ± 4 mm Hg at 5 minutes. Compared with baseline, arterial pH was decreased at 15 minutes. Pulmonary arterial blood temperature was decreased at 15, 30 and 45 minutes. Arterial CO2 tension increased from a baseline value of 43 ± 3 to 54 ± 4 mm Hg (5.7 ± 0.4 to 7.2 ± 0.3 kPa) at 15 minutes. Mean pulmonary arterial pressure was increased at 30 and 45 minutes. Pulmonary arterial occlusion pressure increased from a baseline value of 18 ± 2 to 23 ± 2 mm Hg at 45 minutes. There were no significant changes in other measured variables. All calves recovered from anesthesia uneventfully. ConclusionWe conclude that sevoflurane for induction and maintenance of anesthesia was effective and reliable in these calves and that neither hypotension nor decreased cardiac output was a clinical concern. Clinical relevanceUse of sevoflurane for mask induction and maintenance of anesthesia in young calves is a suitable alternative to injectable and other inhalant anesthetics.

Bispectral index in dogs anesthetized with isoflurane: comparison with sevoflurane

Bispectral index (BIS) is a numerical value derived from the EEG that is used clinically by anesthesiologists to assess CNS depression in human beings. In a previous study, canine BIS values were inversely related to end-tidal sevoflurane (SEVO) concentration: BIS = 102.7 − (14.2 × [SEVO]); R2 = 0.754. The purpose of this study was to determine the relationship between BIS and end-tidal isoflurane (ISO) in the same dogs used in the SEVO study. ISO minimum alveolar concentration (MAC) was determined using the tail-clamp technique for six English pointer dogs (three males and three females) with a mean ± SD age and weight of 3.7 ± 2.0 years and 20.2 ± 4.8 kg, respectively. One week after MAC determination, BIS was measured at 0.8, 1.0, 1.5, and 2.0 MAC multiples of ISO. Ventilation was controlled and atracurium (0.2 mg kg−1 followed by 6 µg kg−1 minute−1 IV) was administered to eliminate EMG artefact from the EEG. The BIS was determined using an A-2000 monitor (Aspect Medical Systems Inc.). After a 15-minute equilibration period, BIS data were collected for 5 minutes and median BIS values were calculated. Heart rate, direct mean arterial blood pressure (MAP), esophageal temperature, and arterial blood gases were measured at each BIS collection period. End-tidal CO2 and percentage [ISO] were monitored using a calibrated infra-red gas analyzer. Data were analyzed using RM anova (p < 0.05). The mean ISOMAC value was 1.3 ± 0.2%. The BIS values were inversely related to [ISO]: BIS = 93.9 − (25.2 × [ISO]); R2 = 0.614. Mean ± SD BIS values at 0.8, 1.0, 1.5, and 2.0 MAC were 65 ± 8, 60 ± 7, 52 ± 3, and 15 ± 27, respectively. At 2 MAC, three dogs had burst suppression that prevented reliable BIS determination. The BIS values were significantly higher during SEVO at 0.8 and 1.0 MAC compared to ISO. Minor, yet statistically significant, differences between and within anesthetic groups were observed for cardiovascular and arterial blood gas data. We conclude that a predictive relationship exists between BIS and end-tidal [ISO]. However, BIS correlated with end-tidal [SEVO] better than with [ISO]. The BIS appears to be somewhat agent dependent in this group of six dogs. Clinical use of BIS monitoring in dogs may require evaluation of specific anesthetic drug combinations.

The effect of a combination of medetomidine-butorphanol and medetomidine, butorphanol, atropine on glomerular filtration rate in dogs.

The effects of intramuscularly administered medetomidine and butorphanol (MB), and medetomidine, butorphanol, atropine (MBA) on glomerular filtration rate (GFR) were determined in six dogs as measured by 99m-Tc-labeled diethylenetriaminepentaacetic acid (99mTc-DTPA) nuclear scintigraphy. Direct systolic, diastolic, and mean arterial blood pressures and heart rate were measured at regular time intervals before, during, and after GFR calculations. The mean GFR measurement following MB was significantly greater (4.44 ml/min/kg) than following MBA (3.82 ml/min/kg) or saline treatment (3.41 ml/min/kg). There was no significant difference between the mean GFR measurements following MBA injection and following saline injection. Diastolic and mean arterial pressures following MBA injection were significantly higher than the values recorded after either MB or saline alone. Heart rate following MB administration was significantly lower than that recorded for dogs receiving MBA or saline alone. The results of this study indicate that the administration of medetomidine in combination with butorphanol significantly increases total GFR in healthy dogs, while the administration of the combination of medetomidine, butorphanol, and atropine does not.

Acute pulmonary edema after percutaneous balloon valvuloplasty for pulmonary valve stenosis

A 66-year-old man was scheduled for percutaneous balloon valvuloplasty of pulmonary valvular stenosis under general anesthesia in the cardiac catheterization laboratory. The patient had a significant history of cardiorespiratory disease. In 1944, his family physician detected a heart murmur, and in 1955, the patient was referred to a cardiologist and told he had “a narrowed valve.” The patient was then lost to follow-up, and his old hospital records were lost. The patient claimed to have been asymptomatic until he sustained an inferior myocardial infarction in 1999 and was referred to this hospital for further investigations. On admission, the patient admitted to smoking 15 cigarettes per day until his myocardial infarction, and his exercise tolerance was reduced to less than 500 meters during the last few years. His medications were aspirin and atenolol. On examination, the patient was noted to be cyanotic, had clubbing of the fingers, had a raised jugular venous pressure, and had bilateral basal crepitations on chest auscultation. The patient had a soft ejection systolic murmur with a normal second heart sound, and there was no right ventricular heave. Further investigations revealed polycythemia (hemoglobin, 19 g/dL; hematocrit, 57.3%), mild renal impairment (serum creatinine, 143 mmol/ L), and arterial blood gases and lung function testing as shown in Tables 1 and 2. A chest radiograph was normal, and a 12-lead electrocardiogram showed T-wave inversion in leads I through III and no evidence of right ventricular hypertrophy. At cardiac catheterization, the patient was found to have moderate left ventricular dysfunction, with a mild stenosis of the left anterior descending coronary artery and complete occlusion of the dominant right coronary artery. There was a severe pulmonary valve stenosis with a peak-to-peak systolic gradient of 90 mmHg (Fig 1). A small atrioseptal defect or patent foramen ovale was noted and confirmed with transesophageal echocardiography. Transesophageal echocardiography did not show any evidence of right or left ventricular dysfunction, and left ventricular ejection fraction was calculated to be 60%. Oxygen saturations and pressure measurements are shown in Tables 3 and 4. It was decided that the pulmonary stenosis should be treated by percutaneous balloon valvuloplasty. Standard anesthetic monitoring was applied, including a 5‐lead electrocardiogram and direct arterial blood pressure measurement via a 20G radial artery catheter inserted under local anesthesia. Pulse oximetry in air showed a saturation (SpO2) of 92%. After preoxygenation (SpO2 increased to 100%), anesthetic induction consisted of fentanyl, 100 g; etomidate, 16 mg; and vecuronium, 8 mg. After endotracheal intubation, the lungs were ventilated with oxygen, air, and isoflurane, 0.8% to 1.4%, for maintenance of anesthesia. The right internal jugular vein was cannulated with 2 long 14G catheters for monitoring of central venous pressure and easy administration of drugs. During the procedure, 1000 mL of lactated Ringer’s solution was infused. Anesthesia was uneventful, and the angiographic findings compared well with the previous measurements. Balloon pulmonary valvotomy using a 25 mm 40 mm balloon resulted in the peak-to-peak gradient falling to 12 mmHg (Figs 2 and 3, Table 5). The patient’s other cardiovascular parameters were unchanged, and PaO2 improved immediately to 9.65 kPa. The procedure time was 15 minutes. The small atrial septal defect was of little or no significance, and no further procedures were carried out. Neuromuscular blockade was reversed with glycopyrrolate, 500 g, and neostigmine, 2.5 mg, and the patient’s lungs were ventilated with oxygen until adequate spontaneous ventilation was restored and the patient’s trachea could be extubated. Total anesthetic time was 45 minutes. The patient was transferred to the postanesthesia care unit to await transfer to the ward. Within 5 minutes of admission to the postanesthesia care unit, the patient developed a tachycardia (120 beats/min), his respiratory rate increased to 30 breaths/min, and SpO2 decreased to 85%, despite supplemental oxygen by facemask.

The effects of remifentanil on haemodynamic stability during rigid bronchoscopy

We examined the effect of remifentanil on the haemodynamic response to rigid bronchoscopy in 22 adult ASA 2-4 patients, randomly allocated to receive 1.0 microg.kg-1 remifentanil over 1 min followed by 0.5 microg.kg-1.min-1 (remifentanil group) or 2.0 microg.kg-1 fentanyl followed by a saline infusion (control group). Following the initial infusion, all patients received a sleep dose of propofol followed by rocuronium 0.6 mg.kg-1 and their lungs were ventilated using a Sander's injector attached to the rigid bronchoscope. Direct arterial blood pressures, heart rate and ST segment changes on the CM5 lead configuration of the electrocardiograph were measured at 1-min intervals from before induction of anaesthesia until the end of bronchoscopy. Arterial pressures and heart rate were similar in the two groups before and after induction of anaesthesia. Remifentanil attenuated the haemodynamic response to bronchoscopy (p < 0.05 for increases in arterial pressures and heart rate). Four patients in the remifentanil group had ST segment depression compared with eight patients in the control group, but this was not statistically significant.

Vasopressin V1a receptor antagonism does not reverse adrenocorticotrophin-induced hypertension in the rat.

1. The role of arginine vasopressin (AVP) was examined in adrenocorticotrophin (ACTH)-induced hypertension in Sprague-Dawley rats using the non-peptide AVP V1a receptor antagonist OPC 21268. 2. In an acute study, six rats were pretreated with ACTH for 11 days and direct arterial blood pressure (4 h), plasma osmolality and electrolyte concentrations were measured after OPC 21268 gavage. In a chronic study, 40 rats were randomly divided into four groups: (i) sham injection + sham gavage; (ii) ACTH + sham gavage; (iii) sham injection + OPC 21268; or (iv) ACTH + OPC-21268 for 16 days. Systolic blood pressure (SBP), water intake, urine volume (UV), urine osmolality and electrolytes, food intake, bodyweight and plasma osmolality and electrolyte concentrations were measured. 3. In the acute study, direct mean arterial blood pressure did not change with OPC 21268 (122+/-2 and 120+/-3 mmHg at 0 and 240 min, respectively). 4. In the chronic study, OPC 21268 did not affect ACTH-induced rises in blood pressure (from 125+/-2 (control) to 145+/-5 mmHg (group 4) compared with 122+/-3 (control) to 149+/-5 mmHg (group2)). Water intake and UV increased (from 29+/-2 to 83+/-6 mL/day; and from 5+/-1 to 36+/-5 mL/day, respectively) and the change in bodyweight decreased from 0+/-2 to -107+/-7 g. 5. These results suggest that AVP (at the V1a receptor) does not play a significant role in the maintenance of ACTH-induced hypertension.

Analysis of the arterial blood pressure waveform during left ventricular nonpulsatile assistance in animal models.

When the rotary blood pump is used as a left ventricular assist device (LVAD), the arterial blood pressure waveform changes with the LVAD condition. Based on evidence from an in vitro study, the change of the arterial blood pressure waveform during left ventricular assistance was evaluated using animal models. After the left pleural cavity was opened through the fifth intercostal space under general anesthesia, a rotary blood pump was implanted as an LVAD into 6 healthy calves. The direct left carotid arterial blood pressure waveform was measured and recorded by an oscilloscope. The Fast Fourier Transform technique was utilized to analyze the arterial blood pressure waveform and calculate the pulsatility index (PI) and the pulse power index (PPI). Similar to the in vitro study, the PI and PPI decreased exponentially with the increase of the LVAD assist ratio. By using this analysis methodology, a physiologically effective ventricular assistance might be achieved.

Disruption of Subtype 2 Dopamine Receptor (D2-R) Causes Hypotension Independently of Its Action on Sympatetic Nerve System

P51 D 2 -R, known to be involved in the pre-synaptic sympathetic inhibition, is also postulated to be present in the cardiovascular system and to modulate blood pressure via local dopaminergic system. In the present study, we investigated the localization of D 2 -R and the effects of the targeted disruption of both D 2 - long and D 2 - short receptor genes on sympathetic activity and blood pressure. The male homozygous littermates at ages of 6-16 week (KO mice) and the age-matched wild type (WT) control mice were used. We assessed systemic sympathetic activity by 24-h urine norepinephrine (NE) excretion and local sympathetic activity by tissue content of NE in the heart and kidney. RT-PCR revealed that the D 2 -R mRNA was expressed in the heart, the aorta and the kidney as well as in the brain only in WT mice. Urinary NE excretion (KO vs. WT: 8.67± 1.71 vs. 7.78± 0.64 micro-g/day)was not different between KO and WT mice. Renal (KO vs. WT: 390±42 vs.535±155 pg/mg protein,p&lt;0.05)but not cardiac (718±75 vs.697± 193pg/mg protein) content of NE was significantly decreased in KO than in WT mice, reflecting the depletion of stored NE in the renal sympathetic neurons. Conscious systolic tail-cuff blood pressure (KO vs. WT: 102±3.3 vs. 106.6±5.1 mmHg at 16 week, n= 10, p&lt;0.001) and direct mean arterial blood pressure under anesthesia(86±13 vs. 101.4±10, n=5, p&lt;0.05) were significantly lower in KO mice than in WT mice. Heart rate (563±31 vs.549±41), food and water consumption, and 24-hour urine sodium excretion (368±44 vs.359±36 microEq/day)were not different between the KO and WT mice. These results indicate that (1) D 2 -R is expressed in the cardiovascular system, (2) D 2 -R in the kidney is involved in the renal sympathetic control, but (3) disruption of D 2 -R causes hypotension independently of its effects on sympathetic activity.

Effects of pre-emptive atropine on medetomidine induced bradycardia in dogs

The cardiorespiratory effects of atropine (0.04 mg kg−1 IM) administered 10 minutes before IM administration of medetomidine (M) were assessed in 12 healthy dogs (1.52 years old, weighing 18.5-22 kg) randomly assigned to each of six treatments in a crossover study. The groups were medetomidine 10, 20 and 40 μg kg−1 (M1O, M2O, M4O, respectively) with either atropine (A) or saline (S). A one-week interval was allowed between treatments. Direct arterial blood pressure, heart rate, respiratory rate and minute volume were recorded before drug administration, after administration of atropine or saline, and at1, 2, 5, 10, 15, 20, 30, 40, 50, 60 and 70 minutes after administration of medetomidine.

Cardiovascular effects of sevoflurane in Holstein calves

Abstract Objective The purpose of this study was to determine the cardiovascular effects of sevoflurane in calves. Study design Prospective experimental study. Animals Six, healthy, 8–12–week–old Holstein calves weighing 80 ± 4.5 (mean ± SEM) kg were studied. Methods Anesthesia was induced by face–mask administration of 7% sevoflurane in O 2 . Calves tracheae were intubated, placed in right lateral recumbency, and maintained with 3.7% end–tidal concentration sevoflurane for 30 minutes to allow catheterization of the auricular artery and placement of a Swan–Ganz thermodilution catheter into the pulmonary artery. After instrumentation, administration of sevoflurane was temporarily discontinued until mean arterial pressure was > 100 mm Hg. Baseline values were recorded and the vaporizer output increased to administer 3.7% end–tidal sevoflurane concentration. Ventilation was controlled to maintain normocapnia. The following were recorded at 5, 10, 15, 30 and 45 minutes after collection of baseline data and expressed as the mean value (± SEM): direct systolic, diastolic, and mean arterial blood pressures; cardiac output; mean pulmonary arterial pressure; pulmonary arterial occlusion pressure, heart rate; and pulmonary arterial temperature. Cardiac index and systemic and pulmonary vascular resistance values were calculated using standard formulae. Arterial blood gases were analyzed at baseline, and at 15 and 45 minutes. Differences from baseline values were determined using one–way analysis of variance for repeated measures with post–hoc differences between mean values identified using Dunnet's test ( p Results Mean time from beginning sevoflurane administration to intubation of the trachea was 224 ± 9 seconds. The mean end–tidal sevoflurane concentration at baseline was 0.7 (± 0.11)%. Sevoflurane anesthesia was associated with decreased arterial blood pressure at all sampling times. Mean arterial blood pressure decreased from a baseline value of 112 ± 7 mm Hg to a minimum value of 88 ± 4 mm Hg at 5 minutes. Compared with baseline, arterial pH was decreased at 15 minutes. Pulmonary arterial blood temperature was decreased at 15, 30 and 45 minutes. Arterial CO 2 tension increased from a baseline value of 43 ± 3 to 54 ± 4 mm Hg (5.7 ± 0.4 to 7.2 ± 0.3 kPa) at 15 minutes. Mean pulmonary arterial pressure was increased at 30 and 45 minutes. Pulmonary arterial occlusion pressure increased from a baseline value of 18 ± 2 to 23 ± 2 mm Hg at 45 minutes. There were no significant changes in other measured variables. All calves recovered from anesthesia uneventfully. Conclusion We conclude that sevoflurane for induction and maintenance of anesthesia was effective and reliable in these calves and that neither hypotension nor decreased cardiac output was a clinical concern. Clinical relevance Use of sevoflurane for mask induction and maintenance of anesthesia in young calves is a suitable alternative to injectable and other inhalant anesthetics.

The effect of intramuscular dexmedetomidine and medetomidine on cardiorespiratory variables during isoflurane anaesthesia in sheep

The hypoxaemic effects of intravenous alpha2-agonists in sheep are well documented. Based on preliminary trials we hypothesized that intramuscular (IM) administration of medetomidine and dexmedetomidine would lead to less severe side effects than IV administration. Nineteen healthy nonpregnant ewes of various breeds undergoing different orthopaedic procedures were studied. Pre-anaesthetic medication was 15 µg kg−1 dexmedetomidine IM [group A, n = 9] or 30 µg kg−1 medetomidine IM [group B, n = 10] 30 minutes prior to induction of anaesthesia with ketamine (2 mg kg−1) IV. Anaesthesia was maintained with isoflurane in 100% oxygen. End expired anaesthetic concentration (F eiso) and respiratory frequency (fR) were determined with a methane insensitive infrared gas analyser (Anaesthetic Gas Monitor Type 1304, Bruel & Kjaer, Naerum, Denmark). Direct mean arterial blood pressure (MAP) and a lead II ECG were monitored continuously. Arterial blood samples were taken 10 minutes after induction of anaesthesia and then at 30 minute intervals. Data were averaged over time and tested for differences between groups by independent t-tests or anova for repeated measures followed by Bonferroni corrected t-tests. The results are presented as mean ± SD. There were no significant (p < 0.05) differences in bodyweights (A: 53.2 ± 9.5 kg; B: 54.7 ± 3.8 kg), duration of anaesthesia (A: 170 ± 42 minutes; B: 144 ± 33 minutes) or surgery (A: 92 ± 32 minutes, B: 85 ± 31 minutes) between the groups. Average F eiso concentrations required to maintain a surgical plane of anaesthesia were not significantly different between groups (A: 0.82 ± 0.14%; B: 1.00 ± 0.25%). There were no differences in mean fR, mean arterial blood gas values and mean MAP between groups. Heart rates were significantly (p < 0.05) lower in group B over the course of anaesthesia. The PaO2 was more variable in group B 37.0 ± 9.7 kPa (255.45 ± 121.8 mm Hg) than in group A 34.0 ± 16.1 kPa (277.15 ± 72.4 mm Hg) with individual minimum values of 9.33 kPa and 19.2 kPa (70 mm Hg and 144 mm Hg), respectively. Effects of dexmedetomidine and medetomidine on PaO2 seem to be less severe after IM administration compared to IV application ( Kastner et al.) with less variability in dexmedetomidine, enabling stable anaesthesia during orthopaedic surgery in sheep. Acknowledgements: The authors are grateful to ORION corporation, Finland for providing medetomidine and dexmedetomidine.

Anatomic, Radiographic and Physiologic Comparisons of the Internal Carotid and Maxillary Artery in the Horse

The anatomy of the internal carotid and maxillary arteries was examined using angiography, subtraction angiography and arterial cast preparations in three horses. Subtraction angiography was superior to angiography in demonstrating the anatomy of the occipital, external ophthalmic, ethmoidal and palatine arteries. In three horses manipulation of the internal carotid and occipital arteries during angiography resulted in vasospasm which prevented filling of these vessels with contrast. Direct arterial blood pressure measurements of the maxillary artery impinging on the guttural pouches was measured in four anaesthetized and standing horses. Arterial pressure recordings from the maxillary artery indicate there is retrograde blood flow from contralateral vessels into the occluded arterial segment. Vasospasm prevented measurement of arterial pressure in the internal carotid artery.

Acute Myocardial Infarction During Lung Volume Reduction Surgery

Acute Myocardial Infarction During Lung Volume Reduction Surgery

Effect of phenylephrine on histamine-induced bronchoconstriction in dogs.

Although an α-adrenoceptor has been suggested to be involved in the mechanism of asthma, the effect of α1-agonist on the airway is still unclear. In this study we evaluated the effect of phenylephrine on the airway with a direct visualization method using a superfine fiberoptic bronchoscope (SFB). Seven mongrel dogs were anesthetized with pentobarbital (30 mg·kg-1 IV) and paralyzed by pancuronium (0.2mg·kg-1·h-1). The trachea was intubated with an endotracheal tube (ID 7 mm) that has a second lumen for insertion of a SFB (OD 2.2 mm) to monitor the bronchial cross-sectional area (BCA) continuously. The tip of a SFB was placed at the level between the second and third bronchial bifurcation. To assess hemodynamics, the direct arterial blood pressure (ABP) and pulmonary arterial pressure (PAP) were monitored via a femoral arterial catheter and Swan-Granz catheter. Bronchoconstriction was elicited by histamine (10 μg·kg-1+ 500 μg·kg-1·h-1_. At 30 min after the histamine was started, saline or phenylephrine (1, 10, and 100μg·kg-1) was given intravenously. The BCA and hemodynamic variables were assessed before (basal) and 30 min after the histamine was started and 5 min after saline and each phenylephrine dose. Histamine reduced BCA by 40.3±6.3%. Phenylephrine at 10 and 100 μg·kg-1 significantly increased the ABP and PAP; and it significantly decreased the BCA, by 6.5±6.9% and 14.2±7.9%, respectively. Plasma epinephrine and norepinephrine were also significantly reduced following phenylephrine 100 μg·kg-1 IV. The dose of phenylephrine that produced vasopressive actions worsened the histamine-induced bronchoconstriction slightly but significantly. Therefore, phenylephrine should be used with caution in asthmatic patients.

OVERSHOOT PHENOMENON RECORDED BY NEAR INFRARED SPECTROSCOPY IN PATIENTS UNDERGOING CAROTID ENDARTERECTOMY UNDER REGIONAL ANESTHESIA

Introduction: Overshoot in cerebral blood flow has been previously demonstrated using near infrared spectroscopy (NIRS) after reperfusion following global ischemia [1,2]. NIRS was used in this study to monitor changes in cerebral circulation and regional oxyhemoglobin saturation (rSO2) with internal carotid artery (ICA) cross clamping during carotid endarterectomy (CEA) in awake patients under regional anesthesia. Methods: After IRB approval and patient informed consent, 45 patients (26 M and 19 F) aged 49 to 85 years with severe unilateral or bilateral carotid stenosis underwent 50 CEAs under ipsilateral cervical plexus nerve block. Changes in ipsilateral and contralateral rSO2 were monitored by NIRS (INVOS 3100, Somanetics, USA). Neurological status, EKG, pulse oximetry (SpO2) and direct arterial blood pressure were continuously monitored and recorded in one minute intervals. Changes in rSO (2) were recorded in absolute percent change and in relative percent change (change in rSO2/initial rSO2). Results: The duration of ICA cross clamping ranged from 7 to 37 minutes. The rSO2 responses to ICA cross clamping fell into three categories. In the first group of five patients there were no significant changes in ipsilateral rSO2 with cross clamp placement and removal. In the second group, during 24 CEAs, immediately after cross clamp placement rSO2 decreased significantly from baseline level (8% in absolute or 12% in relative values) which was followed by gradual recovery and reached near baseline level after clamp removal. In the third group (overshoot group) of 21 CEAs, rSO2 showed an abrupt reduction (10.2% in absolute, or 16% in relative values) which was significantly greater than the second group (P<0.05), and no spontaneous recovery during clamping occurred in most of these patients (80%). In the third group with cross clamp release, rSO2 increased immediately and overshot baseline level (7.2% in absolute or 12% in relative values, P<0.001) for several minutes and then slowly returned back to baseline levels (Figure 1).Figure 1: [up arrow] Clamp ON [down arrow] Clamp OFFDiscussion: The pattern of the rSO2 curve with overshoot is an indicator of inadequate perfusion during cross clamping resulting in vasomotor paralysis and temporary loss of autoregulation. The overshoot results from the flooding of the clamped hemisphere with oxygenated blood following the release of clamp. This exaggerated blood flow is accompanied by abrupt increase in middle cerebral artery flow velocity verified by Doppler [3]. These patients may be at greater risk from severe cerebral ischemia at the cross clamping, and possible cerebral hemorrhage with clamp release.

The pharmacodynamics of thiopental, medetomidine, butorphanol and atropine in beagle dogs.

This study evaluated the quality of anaesthesia and some of the haemodynamic effects induced by a combination of thiopental, medetomidine, butorphanol and atropine in healthy beagle dogs (n = 12). Following premedication with atropine (ATR, 0.022 mg/kg intravenously (i.v.)) and butorphanol (BUT, 0.22 mg/kg i.v.), medetomidine (MED, 22 micrograms/kg intramuscularly (i.m.)) was administered followed in 5 min by thiopental (THIO, 2.2 mg/kg i.v.). Heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MBP) were monitored continuously with an ECG and direct arterial blood pressure monitor. Atipamezole (ATI, 110 micrograms/kg i.v.) was administered to half of the dogs (n = 6) following surgery to evaluate the speed and quality of arousal from anaesthesia. Anaesthesia was characterized by excellent muscle relaxation, analgesia and absence of purposeful movement in response to surgical castration. Arousal following antagonism of medetomidine was significantly faster (P < 0.05) than in unantagonized dogs. Recoveries were smooth but recovery times following atipamezole administration were highly variable among dogs (sternal time range 6-38 min, standing time range 9-56 min). Medetomidine caused a significant (P < 0.05) increase in SBP, DBP and MBP. Atropine prevented the medetomidine induced bradycardia. In conclusion, this combination provided adequate surgical anaesthesia in healthy beagle dogs. At the dosages used in this study, it seems prudent that this combination should be reserved for dogs free of myocardial disease.

Cardiovascular stability during carotid endarterectomy: endotracheal intubation versus laryngeal mask airway

Study Objective: To compare cardiovascular stability during carotid endarterectomy in groups managed either with laryngeal mask airway (LMA) or endotracheal intubation. Design: Randomized, retrospective, blinded study. Setting: Teaching hospital. Patients: 61 ASA physical status II, III, and IV unpremedicated adult males scheduled for carotid endarterectomy. Interventions: Following standardized anesthetic technique, including intravenous (IV) induction with thiopental sodium 3 to 4 mg/kg, fentanyl 2 to 3 μg/kg), and isoflurane, standard intraoperative cardiovascular monitoring plus direct arterial blood pressure measurements were instituted. Patients were randomly assigned to an endotracheal intubation or LMA group. Measurements and Main Results: Distinct intraoperative episodes of ± 25% increase or decrease of mean arterial blood pressure (MABP) and heart rate (HR) when compared with preinduction baseline values, and the number of such episodes requiring interventional therapy were recorded from a blinded anesthesia record retrospectively. Mean end-tidal isoflurane determination and total case duration enabled calculation of minimum alveolar concentration (MAC) hours of isoflurane administered. The LMA group had a significantly ( p < 0.05) lower incidence of increased MABP and HR episodes and such episodes requiring drug therapy than did the endotracheal intubation group. No difference was found in the length of surgery, mean end-tidal isoflurane concentration, or the total number of MAC hours of isoflurane administered. Conclusions: During carotid endarterectomy, a reduced incidence of hypertensive and tachycardic episodes, as well as such episodes requiring interventional drug therapy, was found in the group whose airway is managed by LMA when compared with endotracheal intubation.

Long-term measurement of arterial blood pressure in conscious mice.

This study describes a technique for the direct daily measurement of arterial blood pressure, sampling of arterial blood, and continuous intravenous infusion in free-moving, conscious, Swiss-Webster mice. Catheters were chronically implanted in the femoral artery and vein, tunneled subcutaneously, exteriorized at the back of the neck in a lightweight tethering spring, and attached to a swivel device at the top of the cage. Time-control experiments (n = 8) demonstrated stable values of mean arterial pressure (MAP, 116 +/- 1 mmHg) and heart rate (HR, 627 +/- 21 beats/min) for up to 35 days after catheter implantation. It was further observed that restraining mice (n = 7) increased MAP by 10 +/- 3 mmHg and HR by 78 +/- 8 beats/min from the values observed under free-moving conditions. To demonstrate the chronic use of the venous catheter, intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME, 8.6 mg.kg-1.day-1, n = 6) for 5 days significantly increased MAP from 117 +/- 4 to 131 +/- 4 mmHg without altering HR. In a final group of mice (n = 5), oral L-arginine (2% in drinking water) increased plasma arginine concentration from 90 +/- 7 to 131 +/- 17 microM and prevented L-NAME hypertension. These experiments illustrate the feasibility of long-term intravenous infusion, direct arterial blood pressure measurements, and arterial blood sampling in conscious mice.

Cross-spectral analysis of cerebral autoregulation dynamics in high risk preterm infants during the perinatal period.

In preterm infants intraventricular hemorrhage occurs predominantly within the perinatal period, which may be due to a "lost autoregulation" of cerebral blood flow (CBF). In this study, perinatal autoregulation dynamics were investigated in high risk preterm infants by cross-spectral analysis (CSA), which is a statistical tool in the analysis of time series. In 15 ventilated preterm infants of 25-32 gestational weeks, a total number of 30 records were made between 24 and 96 h of life. Doppler-derived CBF velocity (CBFv), used as a quantitative measure for CBF, and direct mean arterial blood pressure (MABP) were measured continuously for 10 min. The spectral power of low frequency (LF, 0.02-0.2 Hz) oscillations in CBFv and MABP was quantified by spectral analysis. From the results of CSA, a LF phase-shift between the CBFv and MABP LF oscillations was calculated in each record. Within the study group, the LF spectral power of CBFv and MABP was initially low and increased significantly until 96 h of life. The LF phase-shift was about 0 degrees at 24 h and increased significantly to 55 degrees at 96 h of life. The initially low LF spectral power of CBFv and MABP may indicate a perinatal depression of autonomic nervous centers, which are thought to control LF oscillations of vital parameters. In the light of a high pass filter model for autoregulation, the initially low LF phase-shift may indicate an initially impaired autoregulation, which supports the "lost autoregulation" hypothesis.

Complementation of reduced survival, hypotension, and renal abnormalities in angiotensinogen-deficient mice by the human renin and human angiotensinogen genes.

The aim of this study was to determine whether elements of the human renin-angiotensin system (RAS) could functionally replace elements of the mouse RAS by complementing the reduced survival and renal abnormalities observed in mice carrying a gene-targeted deletion of the mouse angiotensinogen gene (mAgt). Double transgenic mice containing the human renin (HREN) and human angiotensinogen (HAGT) genes were bred to mice heterozygous for the mAgt deletion and the compound heterozygotes were identified and intercrossed. The resulting progeny (n = 139) were genotyped at each locus and the population was stratified into two groups: the first containing both human transgenes (RA+) and the second containing zero or one, but not both human transgenes (RA-). Despite appropriate Mendelian ratios of RA- mice that were wildtype (+/+), heterozygous (+/-), and homozygous (-/-) for the deletion of mAgt at birth, there was reduced survival of RA- mAgt-/- mice to adulthood (P < 0.001 by chi2). In contrast, we observed appropriate Mendelian ratios of RA+ mAgt+/+, RA+ mAgt+/-, and RA+ mAgt-/- mice at birth and in adults (P > 0.05 by chi2). These results demonstrate that the presence of both human transgenes rescues the postnatal lethality in mAgt-/- mice. The renal histopathology exhibited by RA- mAgt-/- mice, including thickened arterial walls, severe fibrosis, lymphocytic infiltration, and atrophied parenchyma, was also rescued in the RA+ mAgt-/- mice. Direct arterial blood pressure recordings in conscious freely moving mice revealed that BP (in mmHg) varied proportionally to mAgt gene copy number in RA+ mice (approximately 20 mmHg per mAgt gene copy, P < 0.001). BP in RA+ mAgt-/- mice (132+/-3, n = 14) was intermediate between wild-type (RA- mAgt+/+, 105+/-2, n = 9) and RA+ mAgt+/+ (174+/-3, n = 10) mice. These studies establish that the human renin and angiotensinogen genes can functionally replace the mouse angiotensinogen gene, and provides proof in principle that we can examine the regulation of elements of the human RAS and test the significance of human RAS gene variants by a combined transgenic and gene targeting approach.