Propofol But Not Desflurane Maintains Rat Cerebral Arteriolar Responses to Acetylcholine During Acute Hyperglycemia.

BACKGROUND: Acute hyperglycemia causes vascular endothelial dysfunction in various organs including the cerebral vessels. It is associated with increased mortality and morbidity in the perioperative period. The impact of anesthetic agents on cerebral vasodilatory responses during hyperglycemia remains unclear. We investigated endothelial function in rat cerebral arterioles during acute hyperglycemia, under propofol or desflurane anesthesia. MATERIALS AND METHODS: A closed cranial window preparation was used to measure changes in pial arteriole diameter induced by topical application of acetylcholine (ACh), an endothelium-dependent vasodilator, in rats anesthetized with propofol or desflurane. Pial arteriole responses to ACh were measured during normoglycemia and hyperglycemia. We then investigated whether the response of cerebral arterioles to acute hyperglycemia under propofol anesthesia were related to propofol or its vehicle, intralipid. RESULTS: ACh resulted in a dose-dependent dilation of cerebral arterioles during propofol and desflurane anesthesia under normoglycemic conditions. The vasodilatory effects of ACh were also maintained under hyperglycemic conditions during propofol anesthesia, but the vasodilator response to ACh was significantly impaired during hyperglycemia compared with normoglycemia with desflurane anesthesia. The vasodilatory effects of ACh were maintained during normoglycemia and hyperglycemia in rats receiving propofol or intralipid. CONCLUSIONS: Rat pial arteriole responses to ACh are maintained during conditions of acute hyperglycemia with propofol anesthesia but suppressed compared with normoglycemia with desflurane anesthesia.

A practical guide for anesthetic management during intraoperative motor evoked potential monitoring.

Postoperative motor dysfunction can develop after spinal surgery, neurosurgery and aortic surgery, in which there is a risk of injury of motor pathway. In order to prevent such devastating complication, intraoperative monitoring of motor evoked potentials (MEP) has been conducted. However, to prevent postoperative motor dysfunction, proper understanding of MEP monitoring and proper anesthetic managements are required. Especially, a variety of anesthetics and neuromuscular blocking agent are known to attenuate MEP responses. In addition to the selection of anesthetic regime to record the baseline and control MEP, the measures to keep the level of hypnosis and muscular relaxation at constant are crucial to detect the changes of MEP responses after the surgical manipulation. Once the changes of MEP are observed based on the institutional alarm criteria, multidisciplinary team members should share the results of MEP monitoring and respond to check the status of monitoring and recover the possible motor nerve injury. Prevention of MEP-related adverse effects is also important to be considered. The Working Group of Japanese Society of Anesthesiologists (JSA) developed this practical guide aimed to help ensure safe and successful surgery through appropriate anesthetic management during intraoperative MEP monitoring.

Cerebrovascular reactivity to hypercapnia during sevoflurane or desflurane anesthesia in rats.

BACKGROUND: Hypercapnia causes dilation of cerebral vessels and increases cerebral blood flow, resulting in increased intracranial pressure. Sevoflurane is reported to preserve cerebrovascular carbon dioxide reactivity. However, the contribution of inhaled anesthetics to vasodilatory responses to hypercapnia has not been clarified. Moreover, the cerebrovascular response to desflurane under hypercapnia has not been reported. We examined the effects of sevoflurane and desflurane on vasodilatory responses to hypercapnia in rats. METHODS: A closed cranial window preparation was used to measure the changes in pial vessel diameters. To evaluate the cerebrovascular response to hypercapnia and/or inhaled anesthetics, the pial vessel diameters were measured in the following states: without inhaled anesthetics at normocapnia (control values) and hypercapnia, with inhaled end-tidal minimal alveolar concentration (MAC) of 0.5 or 1.0 of either sevoflurane or desflurane at normocapnia, and an MAC of 1.0 of sevoflurane or desflurane at hypercapnia. RESULTS: Under normocapnia, 1.0 MAC, but not 0.5 MAC, of sevoflurane or desflurane dilated the pial arterioles and venules. In addition, under both 1.0 MAC of sevoflurane and 1.0 MAC of desflurane, hypercapnia significantly dilated the pial arterioles and venules in comparison to their diameters without inhaled anesthetics. The degrees of vasodilation were similar for desflurane and sevoflurane under both normocapnia and hypercapnia. CONCLUSIONS: Desflurane induces cerebrovascular responses similar to those of sevoflurane. Desflurane can be used as safely as sevoflurane in neurosurgical anesthesia.

Endothelium-dependent vasodilation in the cerebral arterioles of rats deteriorates during acute hyperglycemia and then is restored by reducing the glucose level.

PURPOSE: Acute hyperglycemia in patients with traumatic brain injury correlates with a poor neurological outcome. We investigated the endothelium function of rat cerebral arterioles during acute hyperglycemia and after reducing the glucose levels using insulin. We also examined whether or not oxidative stress was involved in the cerebral arteriole response to acute hyperglycemia. METHODS: In isoflurane-anesthetized, mechanically ventilated rats, we used closed cranial window preparation to measure the changes in the pial arteriolar diameter following the topical application of acetylcholine (ACh) or adenosine. We examined the pial arteriolar vasodilator response before hyperglycemia, during hyperglycemia, and after reducing the glucose level using insulin. After intravenous pretreatment with an NADPH oxidase inhibitor (apocynin or diphenylene iodonium), we reexamined the pial arteriolar vasodilator response following the topical application of ACh. RESULTS: Under control conditions, the topical application of ACh dose-dependently dilated the cerebral arterioles. The vasodilatory responses to topical ACh were impaired during hyperglycemia and improved after the administration of insulin. The vasodilatory responses to topical adenosine were not affected by the glucose levels. In the apocynin or diphenylene iodonium pretreatment group, the topical application of ACh dilated the cerebral arterioles during hyperglycemia. CONCLUSION: Acute hyperglycemia induces a dysfunction of the endothelium-dependent vasodilation of rat cerebral arterioles. The dysfunction can be reversed by improving the acute hyperglycemia and it can be prevented entirely by the administration of NADPH oxidase inhibitors. These results could suggest that controlling the glucose levels works protectivity to endothelium function of cerebral arterioles.

A case of anaphylaxis apparently induced by sugammadex and rocuronium in successive surgeries.

Rocuronium is the agent most frequently involved in perioperative anaphylaxis, and sugammadex has also been known to induce anaphylactic reactions. We describe a case of successive anaphylactic episodes that seemed to be induced by clinical doses of rocuronium and sugammadex. The patient was a 19-year-old woman who had a medical history of asthma, but no history of surgery. She had been injured in a fall, and several surgeries were scheduled for multiple bone fractures. At the first surgery under general anesthesia, she developed anaphylaxis 5 min after sugammadex administration. A second general anesthesia for treatment of calcaneal fracture was induced uneventfully without neuromuscular blockade after 10 days. A third general anesthesia was scheduled to reinforce the spinal column 12 days after the first surgery. She developed anaphylaxis 8 min after rocuronium administration. The level of plasma histamine was elevated, but serum tryptase level remained normal. This surgery was canceled and rescheduled without use of a neuromuscular blockade. Skin tests were performed in a later investigation. The patient showed positive results on intradermal tests for sugammadex and rocuronium, supporting a diagnosis of allergic reactions to both drugs. Clinicians must be aware that anaphylactic reactions can be induced by both sugammadex and rocuronium.

Anaphylactic shock due to intravesical administration of pirarubicin hydrochloride for the fifth time.

We report the first case of anaphylaxis induced by intravesical administration of pirarubicin hydrochloride during spinal anesthesia. The patient was a 64-year-old woman being followed up for transitional cell carcinoma of the bladder. Anaphylaxis occurred the fifth time pirarubicin hydrochloride was administered intravesically. Pirarubicin hydrochloride, an anthracycline antitumor antibiotic that is widely used for intravesical instillation chemotherapy, is administered at the end of surgery. Because this is about the time that the patient is leaving the operating room, attention to patient monitoring tends to be divided. Because anaphylaxis may occur at this time, staff should remain vigilant of the risk of anaphylaxis.

[Motor Evoked Potential and Somatosensory Evoked Potential during Spine and Spinal Surgery].

Spine and spinal cord surgery carries a significant risk of neurological impairment Intraoperative neurological monitoring should now include not only somatosensory evoked potential (SEP), but also motor evoked potential (MEP). While SEP monitors the posterior cord, MEP provides better information regarding the status of the anterior/anterolateral cord. The multimodality SEP and MEP monitoring essentially covers physiological changes of the entire cord, and thereby reduces the risk of development of irreversible neural injury. A 50% drop in SEP amplitude is the universally accepted warning criteria. Conversely, different warning criteria for MEP have been proposed because of MEP especially sensitive to the effects of anesthetic agents. Although evidence lacks that intraoperative evoked potential reduces the rate of neurologic deficits, it is recommended to monitor MEP for spine and spinal surgery, when the spinal cord is considered to be at risk. The anesthesiologist must be familiar with SEP and MEP monitoring to increase the preciseness of the monitoring.

[Monitored Anesthesia Care for Deep Brain Stimulation and Embolization of Brain Arteriovenous Malformation].

The aim of monitored anesthesia care (MAC) in neurosurgery and interventional neuroradiology is to provide optimal surgical conditions including patient immobility and comfort, facilitate intraoperative neuromonitoring, and rapidly treat any complication. The anesthetist has a crucial role in facilitating procedures, and this requires an understanding of specific procedures, their potential complications, and their management. Choice of anesthetic technique varies between centers with little data to support any specific technique. Dexmedetomidine is useful as a sedative and hypnotic for patients undergoing procedures without the need for tracheal intubation. We usually use dexmedetomidine in MAC.

Effects of topical and intravenous JM-1232(-) infusion on cerebrovascular reactivity in rats.

A novel short-acting benzodiazepine receptor agonist, JM-1232(-), has been shown to have a sedative/hypnotic effect and wide safety margin. However, its effect on cerebral vessels is not well known. Therefore, we investigated the cerebrovascular reactivity to topical and intravenous JM-1232(-) and during hypotension or hypercapnia with intravenous administration of JM-1232(-). We used a closed cranial window preparation to measure the changes of cerebral pial arteriolar diameters in isoflurane-anesthetized Sprague-Dawley rats. We first measured the direct effect of topical JM-1232(-). We then determined the effect of intravenous JM-1232(-) and then we measured the response to hypercapnia before and after JM-1232(-) infusion. Finally, we measured the reaction to stepwise induction of hypotension before and after JM-1232(-) infusion. Topical infusion of JM-1232(-) dilated pial arterioles. Intravenous infusion of JM-1232(-) changed pial arterioles by 4.5 ± 2.7 %, 5.0 ± 3.9 %, and -2.8 ± 2.6 % (at 0.1, 0.3, and 1.0 mg/kg/min, respectively). Hypercapnia dilated pial arterioles before and after JM-1232(-) infusion. The diameters of pial arterioles did not change during hypotension before or after intravenous JM-1232(-) infusion. These results indicate that topical JM-1232(-) has a dilative effect on pial arterioles and that intravenous administration of JM-1232(-) may not affect cerebrovascular reactivity to hypotension or hypercapnia.

Nicorandil protects pial arterioles from endothelial dysfunction induced by smoking in rats.

BACKGROUND: Our aims are to investigate the effect of nicorandil, which is used for angina prevention and treatment, on the endothelial dysfunction induced by acute smoking and to clarify the underlying mechanism. MATERIALS AND METHODS: A closed cranial window preparation was used to measure changes in pial vessel diameters in Sprague-Dawley rats. The responses of arterioles were examined to an endothelium-dependent vasodilator acetylcholine (ACh) before smoking. After intravenous nicorandil (200 µg/kg bolus infusion and then 60 µg/kg/min continuous infusion; n=6) or saline (control; n=6) pretreatment, the pial vasodilator response to topical 10 M ACh infusion was reexamined both before and 1 hour after 1-minute cigarette smoking. Thereafter, either glibenclamide or N-ω-nitro-L-arginine methyl ester (L-NAME) was infused 20 minutes before nicorandil infusion. In the glibenclamide (n=6) or L-NAME; n=6 pretreatment group, the pial vasodilator response to topical ACh was examined before and after smoking. Percentage changes in pial vessel diameters were used for the statistical analysis. RESULTS: Cerebral arterioles were dilated during topical ACh infusion. After smoking, 10 M ACh constricted cerebral arterioles (-7.7±1.8%). After smoking, in the nicorandil-pretreatment group, 10 M ACh dilated cerebral pial arterioles by 10.5±3.0%. When given before nicorandil infusion, glibenclamide, but not L-NAME, abolished the preventive effects of nicorandil against smoking-induced endothelial dysfunction in pial vessels. CONCLUSIONS: Acute cigarette smoking causes dysfunction of endothelium-dependent pial vasodilatation, and nicorandil prevents this effect of smoking. The mechanism underlying this protective effect may depend mainly on adenosine triphosphate-sensitive potassium-channel activation.

Continuous cardiac output measurement with a Doppler-equipped pulmonary artery catheter.

BACKGROUND: We developed a Doppler-equipped pulmonary artery catheter that provides continuous measurement of the true main pulmonary blood flow velocity independent of the angle of incidence formed by the pulmonary artery catheter and the main pulmonary artery blood flow. This device uses 2 orthogonally positioned Doppler transducers that allow trigonometric correction for differences in the angle of blood flow between each transducer. We tested the accuracy of the Doppler-equipped pulmonary artery catheter by comparing its cardiac output measurements with those done by conventional techniques in animals. METHODS: The Doppler-equipped pulmonary artery catheter was evaluated in dogs. A pair of ultrasound Doppler transducers positioned at a fixed angle (90°) was mounted on the distal part of the thermodilution pulmonary artery catheter. The Doppler shifts (Δf1, Δf2) were detected by the 2 transducers sampling at 2 closely spaced points in the main pulmonary artery. The values of Δf1 and Δf2 were used to compute 2 velocity measurements. The true flow velocity of the main pulmonary artery was calculated with the following equation: V(pulm) = {(V(transducer1))(2) + (V(transducer2))(2)}(1/2) (V(pulm) = true main pulmonary artery velocity; V(transducer1) and V(transducer2) = velocity detected by transducers 1 and 2, respectively). The flow velocities were calculated by using a phase differential technique. Cardiac output was calculated as V(pulm) multiplied by a coefficient value. The coefficient value was calculated by dividing cardiac output, derived from conventional techniques, by V(pulm) at the beginning of each experiment. After thoracotomy, an electromagnetic flowprobe was placed around the main pulmonary artery in dogs. Cardiac output was simultaneously measured by the Doppler-equipped pulmonary artery catheter (CO-Doppler), and the electromagnetic flowmeter (CO-EMF) or the thermodilution technique (CO-Thermo). Cardiac output was manipulated by dobutamine and propranolol. RESULTS: CO-Doppler was highly correlated with CO-EMF (y = 1.16 × -0.26, r(2) = 0.99, P < 0.001) and CO-Thermo (y = 1.24 × -0.90, r(2) = 0.85, n = 48, P < 0.001). The bias between CO-EMF and CO-Doppler was -0.02 L/min; 95% limits of agreement were -0.32 to 0.28 L/min. The percentage error was 16%. The bias between CO-Thermo and CO-Doppler was 0.18 L/min; 95% limits of agreement were -0.62 to 0.98 L/min. CONCLUSIONS: The newly developed Doppler-equipped pulmonary artery catheter with 2 orthogonally positioned Doppler transducers allowed accurate and continuous measurements of cardiac output independent of the angle of incidence formed by the pulmonary artery catheter and the main pulmonary artery blood flow.

[Preoperative assessment of the patient with restrictive lung disease].

Restrictive lung disease is characterized by a reduction in total lung capacity. Pulmonary conditions such as interstitial lung disease related to connective tissue disease, idiopathic interstitial pneumonia (IIP), lung resection, and pulmonary fibrosis could cause restrictive disease. In addition, extrapulmonary disorders are caused by chest wall limitations, muscle dysfunction, or pleural disease. Preoperative medical history of associated diseases or symptoms prompts the anesthesiologist to the directed evalution. With regard to the restrictive lung disease, IIP is the most important disease for an anesthesiologist to know. IIP is known to be combined with primary lung cancer and is associated with an increased risk of postoperative acute exacerbation. Acute exacerbation of IIP is a serious postoperative complication and the consequence is extremely poor. Therefore, both surgeons and anesthesiologists must aim to prevent acute exacerbation of IIP Although it is difficult to predict the development of acute exacerbation of IIP, we should avoid or postpone the surgery in patients demonstrating an active phase of IIP. Besides, we should give enough explanation of the risk of postoperative acute exacerbation to the patient with IIP.

Comparative effects of cilostazol and aspirin on the impairment of endothelium-dependent cerebral vasodilation caused by acute cigarette smoking in rats.

We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that a reduction of oxidative stress by agents such as valsartan, fasudil, or apocynin prevented this impairment. Here, our aim was to investigate the comparative effects of two antiplatelet drugs used for stroke-prevention [a phosphodiesterase-3 inhibitor (cilostazol) and a cyclooxygenase inhibitor (aspirin)] on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure the changes in pial vessel diameters induced by topical application of acetylcholine (ACh) following intraperitoneal injection of 0.5% carboxymethyl cellulose sodium salt (CMC; vehicle control for the antiplatelet drugs). After 1-min smoking (1 mg-nicotine cigarette), the arteriolar responses to ACh were reexamined. Finally, after intraperitoneal cilostazol or aspirin (each in 0.5% CMC) pretreatment, we reexamined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-relatedly dilated by topical ACh (10(-6) and 10(-5 )M). One hour after 1-min smoking, 10(-5 )M ACh (a) constricted cerebral pial arterioles in the control group and in the aspirin-pretreatment group (responses not significantly different from each other), but (b) dilated cerebral pial arteries in the cilostazol pretreatment groups (responses significantly different from those obtained without cilostazol pretreatment). Thus, cilostazol (but not aspirin) may prevent the smoking-induced impairment of endothelium-dependent vasodilation in cerebral pial arterioles.

The association between the initial end-tidal carbon dioxide difference and the lowest arterial oxygen tension value obtained during one-lung anesthesia with propofol or sevoflurane.

OBJECTIVE: The purpose of this study was to examine the correlation between the lowest PaO(2) value recorded during the first 45 minutes of one-lung ventilation (OLV) and the end-tidal CO(2) (ETCO(2)) difference between two-lung ventilation (TLV) and the early phase of OLV. DESIGN: A prospective, randomized study. SETTING: A university hospital. PARTICIPANTS: Thirty-six patients scheduled for elective thoracic surgery. INTERVENTIONS: Thoracic surgery patients were randomly assigned to 1 of 2 groups (group P [n = 18], maintained with propofol; group S [n = 18], maintained with sevoflurane). After setting up, the authors measured arterial blood gases at F(I)O(2) = 1.0 as follows: during TLV and at 5 minutes, 15 minutes, 30 minutes, and 45 minutes after the start of OLV. ETCO(2) was recorded just before and at 3 minutes after the start of OLV. The authors examined the relationship between the initial ETCO(2) difference and the lowest PaO(2) value recorded during the first 45 minutes of OLV. MEASUREMENTS AND MAIN RESULTS: There was a significant negative correlation between the lowest PaO(2) (x) value and the initial ETCO(2) difference (y) during OLV in each group (group P: y = -0.0203x + 7.2571, r(2) = 0.5351; group S: y = -0.0257x + 7.3158, r(2) = 0.6129). This correlation was not significantly different between the groups. CONCLUSION: The present study indicates that the ETCO(2) difference between TLV and early OLV has an association with impaired oxygenation later during OLV. This would be a simple and clinically convenient predictor of the lowest PaO(2) value likely to be reached during one-lung anesthesia with either propofol or sevoflurane.

Rho-kinase inhibitor and nicotinamide adenine dinucleotide phosphate oxidase inhibitor prevent impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.

INTRODUCTION: We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that blocking the angiotensin II (Ang II) type 1 (AT1) receptor with valsartan prevented this impairment. Our aim was to investigate the effects of a Rho-kinase inhibitor (fasudil) and a Nicotinamide Adenine Dinucleotide PHosphate (NADPH) oxidase inhibitor (apocynin) on smoking-induced endothelial dysfunction in cerebral arterioles. METHOD: In Sprague-Dawley rats, we used a closed cranial window preparation to measure changes in pial vessel diameters following topical acetylcholine (ACh) before smoking. After one-minute smoking, we again examined the arteriolar responses to ACh. Finally, after intravenous fasudil or apocynin pre-treatment we re-examined the vasodilator responses to topical ACh (before and after cigarette smoking). RESULTS: Under control conditions, cerebral arterioles were dose-dependently dilated by topical ACh (10(-6) M and 10(-5) M). One hour after a one-minute smoking (1 mg-nicotine cigarette), 10(-5) M ACh constricted cerebral arterioles. However, one hour after a one-minute smoking, 10(-5) M ACh dilated cerebral pial arteries both in the fasudil pre-treatment and the apocynin pre-treatment groups, responses that were significantly different from those obtained without fasudil or apocynin pre-treatment. CONCLUSION: Thus, inhibition of Rho-kinase and NADPH oxidase activities may prevent the above smoking-induced impairment of endothelium-dependent vasodilation.

Human atrial natriuretic peptide prevents the increase in pulmonary artery pressure associated with aortic unclamping during abdominal aortic aneurysmectomy.

OBJECTIVE: To assess the effect of human atrial natriuretic peptide (HANP) on the pulmonary and systemic circulations during infrarenal abdominal aortic aneurysmectomy. DESIGN: A prospective, randomized study. SETTING: A university hospital. PARTICIPANTS: Forty-five patients undergoing infrarenal abdominal aortic aneurysmectomy. INTERVENTIONS: Abdominal aortic aneurysmectomy patients were randomly assigned to 1 of 3 groups (n = 15 for each group). They were infused with normal saline solution (SA), 0.02 microg/kg/min of HANP (LH), or 0.05 microg/kg/min of HANP (HH), starting 5 minutes after clamping. Hemodynamic variables were measured before/after clamping and unclamping. MEASUREMENTS AND MAIN RESULTS: Both mean pulmonary arterial pressure (MPAP) and the pulmonary vascular resistance index (PVRI) increased (v baseline) in the SA group. HANP attenuated the rises in MPAP and PVRI dose dependently (LH and HH groups v SA). Mean arterial pressure and systemic vascular resistance index were not significantly different among the 3 groups. CONCLUSION: HANP, infused during aortic clamping and abdominal aortic aneurysmectomy, attenuates the rises in pulmonary artery pressure and vascular resistance without severe systemic hypotension. This may result from direct and/or indirect pulmonary vascular effects of HANP because no HANP-induced changes in endothelin-1, angiotensin-II, and thromboxane B(2) were detected.

The effects of transient cerebral ischemia on vasopressin-induced vasoconstriction in rabbit cerebral vessels.

BACKGROUND: Vasopressin is a drug of choice for use during cardiopulmonary resuscitation because several experimental studies have shown that it is better than epinephrine at increasing systemic perfusion pressure and improving cerebral perfusion pressure without increasing myocardial oxygen consumption. We used a pial window preparation to determine the effects of vasopressin when applied topically to pial vessels and whether any effects were altered after cerebral ischemia in rabbits (n = 27). METHODS: We first examined the effects of topical application of arginine-vasopressin (AVP) (10(-11) M, 10(-9) M, 10(-7) M, and 10(-5) M, sequentially). We then examined the effects of topical application of AVP (10(-9) M and 10(-7) M, sequentially) before and after a 5-min intervention consisting of cerebral ischemia produced by inflation of a neck tourniquet plus systemic hypotension or systemic hypotension alone. RESULTS: Pial arteriolar diameters were (a) dilated by 10(-11) M AVP [7% +/- 11% (P = 0.014 versus baseline)], but constricted by 10(-9) M, 10(-7) M, and 10(-5) M AVP [7% +/- 14%, 20% +/- 14%, and 16% +/- 16% (each P < 0.05), respectively], and (b) constricted before hypotension (7% +/- 10% at 10(-9) M, 20% +/- 15% at 10(-7) M) or ischemia (7% +/- 11% at 10(-9) M, 21% +/- 15% at 10(-7) M). However, after the 5-min of ischemia, the decrease in diameter induced by 10(-7) M AVP was significantly reduced but not by hypotension alone [hypotension control group: 7% +/- 10% at 10(-9) M, 19% +/- 14% at 10(-7) M; ischemia group: 5% +/- 11% at 10(-9) M, 10% +/- 13% at 10(-7) M (P = 0.35 versus hypotension control)]. CONCLUSIONS: Topical application of AVP (except at the lowest concentration used here) induced concentration-dependent vasoconstriction of pial arterioles in anesthetized rabbits. The vasoconstrictor effect of 10(-7) M AVP was reduced after transient (5-min) cerebral ischemia.