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Biomedical subjects

J N Bates

Publications and source records attributed to J N Bates.

At least 37 records · Page 2Linked to original sources
PubMed1995

An evaluation of the effect of anesthetic technique on reproductive success after laparoscopic pronuclear stage transfer. Propofol/nitrous oxide versus isoflurane/nitrous oxide.

BACKGROUND: Laparoscopic pronuclear stage transfer (PROST) is the preferred method of embryo transfer after in vitro fertilization in many infertility programs. There are scant data to recommend the use or avoidance of any particular anesthetic agent for use in women undergoing this procedure. The authors hypothesized that propofol would be an ideal anesthetic for laparoscopic PROST because of its characteristic favorable recovery profile that includes minimal sedation and a low incidence of postoperative nausea and vomiting. The purpose of the study was to compare propofol and isoflurance with respect to postanesthetic recovery and pregnancy outcomes after laparoscopic PROST. METHODS: One hundred twelve women scheduled for laparoscopic PROST were randomized to receive either propofol/nitrous oxide or isoflurane/nitrous oxide for maintenance of anesthesia. RESULTS: Visual analog scale scores for sedation were lower in the propofol group than in the isoflurance group at all measurements between 30 min and 3 h after surgery. More women experienced emesis and were given an antiemetic during recovery in the isoflurance group than in the propofol group. However, the percentage of pregnancies with evidence of fetal cardiac activity was 54% in the isoflurane group compared with only 30% in the propofol group (P = 0.023). Also, the ongoing pregnancy rate was greater in the isoflurane group than in the propofol group (54% vs. 29%, P = 0.014). CONCLUSIONS: Propofol/nitrous oxide anesthesia was associated with lower clinical and ongoing pregnancy rates compared with isoflurane/nitrous oxide anesthesia.

Adult↗
PubMed1995

Treatment of respiratory failure in an infant with bronchopulmonary dysplasia infected with respiratory syncytial virus using inhaled nitric oxide and high frequency ventilation.

A 2-month-old, former 28-week premature infant with bronchopulmonary dysplasia infected with respiratory syncytial virus was treated with nitric oxide and high frequency oscillatory ventilation after conventional therapy failed. Nitric oxide and high frequency oscillatory ventilation rapidly improved oxygenation allowing recovery without the need for extracorporeal membrane oxygenation. This treatment regimen should be considered as an option in high-risk infants with respiratory syncytial virus infection who meet extracorporeal membrane oxygenation criteria.

Administration, Inhalation↗
PubMed1995

Modulation of baroreceptor activity by nitric oxide and S-nitrosocysteine.

The goal of this study was to determine whether nitric oxide (NO) and the NO donor, S-nitrosocysteine (cysNO), modulate the activity of carotid sinus baroreceptors. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in anesthetized rabbits. Baroreceptor activity decreased in a dose-dependent manner after injection of either NO or cysNO as constant pressure was maintained, and activity recovered spontaneously over time, within seconds to minutes. The baroreceptor pressure-activity relation was shifted significantly to the right by cysNO, with a profound suppression of activity at high pressure. Baroreceptor activity at 160 mm Hg averaged 76 +/- 8%, 60 +/- 6%, and 36 +/- 5% of the control maximum during exposure to 10(-4), 2 to 3 x 10(-4), and 10(-3) mol/L cysNO, respectively. The inhibition of activity by the L and D isomers of cysNO was equivalent and was blocked by reduced hemoglobin, suggesting that the effect was mediated by NO. The suppression of baroreceptor activity by cysNO was not related to vascular relaxation as measured by videomicrometer. Inhibition of soluble guanylate cyclase with methylene blue or 6-anilinoquinoline-5,8-quinone (LY83583, 10(-5) mol/L) did not attenuate and dibutyryl cGMP (10(-3) mol/L) did not mimic the suppression of baroreceptor activity by cysNO, suggesting a cGMP-independent mechanism. Activation of endogenous NO formation with thimerosal (10(-5) to 10(-4) mol/L) reduced maximum baroreceptor activity in five of eight experiments to 59 +/- 7% of the control maximum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Nerve-mediated nitric oxide production by opossum lower esophageal sphincter.

Antagonists of nitric oxide synthesis inhibit nerve-induced hyperpolarization and relaxation of muscle from the opossum lower esophageal sphincter. These studies test the hypothesis that nitric oxide is released during stimulation of intrinsic esophageal nerves. The intrinsic nerves were stimulated with an electrical field (10-sec trains of 1-msec, 30-V pulses delivered at 10 Hz). Nitric oxide production was measured with a DASIBI model 2108 Chemiluminescence NO Analyzer. NG-Nitro-L-arginine, an inhibitor of NO synthase, antagonized nerve-induced relaxation the lower esophageal sphincter. Nerve stimulation increased NO production from 0.50 +/- 0.04 nmol/min/100 mg tissue to 0.87 +/- 0.07 nmol/min/100 mg tissue (P < 0.01). NG-nitro-L-arginine inhibited both basal (0.030 +/- 0.09 nmol/min/100 mg tissue, P < 0.05 vs baseline) and stimulated (0.38 +/- 0.10 nmol/min/100 mg tissue, P < 0.01 vs stimulated). These studies support the hypothesis that nerve stimulation releases nitric oxide from the lower esophageal sphincter.

Amino Acid Oxidoreductases↗
PubMed1994

Does early administration of epidural analgesia affect obstetric outcome in nulliparous women who are receiving intravenous oxytocin?

BACKGROUND: Some studies suggest that epidural analgesia prolongs labor and increases the incidence of cesarean section, especially if it is administered before 5 cm cervical dilation. The purpose of the current study was to determine whether early administration of epidural analgesia affects obstetric outcome in nulliparous women who are receiving intravenous oxytocin. METHODS: Informed consent was obtained from healthy nulliparous women with a singleton fetus in a vertex presentation, who requested epidural analgesia while receiving intravenous oxytocin at at least 36 weeks' gestation. Each patient was randomized to receive either early or late epidural analgesia. Randomization occurred only after the following conditions were met: (1) the patient requested pain relief at that moment, (2) a lumbar epidural catheter had been placed, and (3) the cervix was at least 3 but less than 5 cm dilated. Patients in the early group immediately received epidural bupivacaine analgesia. Patients in the late group received 10 mg nalbuphine intravenously. Late-group patients did not receive epidural analgesia until they achieved a cervical dilation of at least 5 cm or until at least 1 h had elapsed after a second dose of nalbuphine. RESULTS: Early administration of epidural analgesia did not prolong the interval between randomization and the diagnosis of complete cervical dilation, and it did not increase the incidence of malposition of the vertex at delivery. Also, early administration of epidural analgesia did not result in an increased incidence of cesarean section or instrumental vaginal delivery. Thirteen (18%) of 74 women in the early group and 14 (19%) of 75 women in the late group underwent cesarean section (relative risk for the early group 0.94; 95% confidence interval 0.48-1.84). Patients in the early group had lower pain scores between 30 and 120 min after randomization, and were more likely to experience transient hypotension. Infants in the late group had lower umbilical arterial and venous blood pH and higher umbilical arterial and venous blood carbon dioxide tension measurements at delivery. CONCLUSIONS: Early administration of epidural analgesia did not prolong labor or increase the incidence of operative delivery, when compared with intravenous nalbuphine followed by late administration of epidural analgesia, in nulliparous women who were receiving intravenous oxytocin.

Adult↗
PubMed1994

Does early administration of epidural analgesia affect obstetric outcome in nulliparous women who are in spontaneous labor?

BACKGROUND: Some studies suggest that epidural analgesia prolongs labor and increases the incidence of cesarean section, especially if it is administered before 5 cm cervical dilation. The purpose of the current study was to determine whether early administration of epidural analgesia affects obstetric outcome in nulliparous women who are in spontaneous labor. METHODS: Informed consent was obtained from 344 healthy nulliparous women with a singleton fetus in a vertex presentation, who requested epidural analgesia during spontaneous labor at at least 36 weeks' gestation. Each patient was randomized to receive either early or late epidural analgesia. Randomization occurred only after the following conditions were met: (1) the patient requested pain relief at that moment, (2) a lumbar epidural catheter had been placed, and (3) the cervix was at least 3 cm but less than 5 cm dilated. Patients in the early group immediately received epidural bupivacaine analgesia. Patients in the late group received 10 mg nalbuphine intravenously. Late-group patients did not receive epidural analgesia until they achieved a cervical dilation of at least 5 cm or until at least 1 h had elapsed after a second dose of nalbuphine. Ten of the 344 patients were excluded because of a protocol violation or voluntary withdrawal from the study. RESULTS: Early administration of epidural analgesia did not increase the incidence of oxytocin augmentation, prolong the interval between randomization and the diagnosis of complete cervical dilation, or increase the incidence of malposition of the vertex at delivery. Also, early administration of epidural analgesia did not result in an increased incidence of cesarean section or instrumental vaginal delivery. Seventeen (10%) of 172 women in the early group and 13 (8%) of 162 women in the late group underwent cesarean section (relative risk for the early group 1.22; 95% confidence interval 0.62-2.40). Patients in the early group had lower pain scores between 30 and 150 min after randomization. Infants in the late group had lower umbilical arterial and venous blood pH and higher umbilical venous blood carbon dioxide tension measurements at delivery. CONCLUSIONS: Early administration of epidural analgesia did not prolong labor, increase the incidence of oxytocin augmentation, or increase the incidence of operative delivery, when compared with intravenous nalbuphine followed by late administration of epidural analgesia, in nulliparous women who were in spontaneous labor at term.

Adult↗
PubMed1993

Characterization and mediation of inhibitory junction potentials from opossum lower esophageal sphincter.

BACKGROUND: Activating nonadrenergic, noncholinergic (NANC) nerves of the lower esophageal sphincter (LES) hyperpolarizes and relaxes its circular smooth muscle. This relaxation is mediated by nitric oxide (NO) or an NO-containing compound. These studies were undertaken to compare the electrophysiological responses of circular smooth muscle from the LES and esophagus in response to NANC nerve stimulation and to test the hypothesis that NO mediates LES hyperpolarization. METHODS: The transmembrane potential difference was recorded with glass microelectrodes. Nerve-mediated membrane responses were evoked by electrical pulses of 0.5 msec duration and 50 V amplitude. RESULTS: Responses of LES muscle differed from those of the esophageal muscle. The duration of hyperpolarization was much longer in sphincteric muscle. The depolarization that followed hyperpolarization of esophageal muscle was not observed in sphincteric muscle. NG-nitro-L-arginine, an inhibitor of NO synthase, attenuated the nerve-induced hyperpolarization. L-arginine, the substrate for NO synthase, antagonized the effect of NG-nitro-L-arginine. Exogenous NO hyperpolarized of the smooth muscle membrane. CONCLUSIONS: These data support the hypothesis that NO or an NO-like compound may mediate nerve-induced hyperpolarization of the opossum LES.

Animals↗
PubMed1993

The nitrovasodilators. New ideas about old drugs.

The nitrovasodilators are a diverse group of pharmacological agents that produce vascular relaxation by releasing nitric oxide. The mechanisms by which these compounds release nitric oxide vary, depending on their chemical structure. Compounds with lower oxidation states of nitrogen such as nitroprusside, nitrosamines, and nitrosothiols release nitric oxide nonenzymatically. In the case of nitroprusside, this involves a one-electron reduction that may occur upon exposure to a variety of reducing agents and tissues such as vascular smooth muscle membranes. In the case of the organic nitrates, which have higher oxidation states of nitrogen, the release of nitric oxide in vascular tissue occurs predominantly by a poorly understood enzymatic process. This interesting property of nitroglycerin is important because it "targets" its effect to vascular tissues that are capable of this enzymatic process. In the case of the coronary circulation, nitroglycerin predominantly dilates the larger coronary arteries while having a minimal effect on coronary resistance vessels < 100 microns in diameter. This prevents the development of coronary steal, which is often encountered with agents that produce intense vasodilation of the coronary resistance vessels. In this review, the mechanisms by which the nitrovasodilators (particularly nitroglycerin) release nitric oxide will be considered, and recent studies of nitroglycerin bioconversion in various-sized coronary vessels will be discussed in detail.

Animals↗
PubMed1993

Nitric oxide and S-nitroso-L-cysteine as endothelium-derived relaxing factors from acetylcholine in cerebral vessels in cats.

BACKGROUND AND PURPOSE: The predominant view is that the endothelium-derived relaxing factor generated by acetylcholine from blood vessels is nitric oxide. However, there is evidence suggesting that certain nitric oxide-containing compounds such as nitrosothiols resemble the endothelium-derived relaxing factor generated by acetylcholine more closely than does nitric oxide itself. Accordingly, we compared the effects of nitric oxide and S-nitroso-L-cysteine on cerebral arteriolar caliber in relation to the associated increments in nitrite concentration in the effluent. METHODS: Acetylcholine, nitric oxide, and S-nitroso-L-cysteine were administered by continuous superfusion in oxygen-free solution through the space under a cranial window in anesthetized cats. Nitrite concentration was measured in the effluent. The degree of vasodilation induced was evaluated in relation to the increment in nitrite concentration. RESULTS: All agents induced dose-dependent vasodilation and dose-dependent increments in nitrite concentration in the effluent. For any given degree of vasodilation, the increments in nitrite concentration were equivalent during acetylcholine or S-nitroso-L-cysteine infusion, whereas the nitrite concentrations were 10 times higher during nitric oxide infusion. After administration of nitroarginine, a competitive inhibitor of nitric oxide synthesis from arginine, there was depression in the vasodilation as well as the increment in nitrite concentration induced by acetylcholine. CONCLUSIONS: S-Nitroso-L-cysteine resembles endothelium-derived relaxing factor from acetylcholine more closely than does nitric oxide.

Acetylcholine↗
PubMed1992

Does epidural fentanyl decrease the efficacy of epidural morphine after cesarean delivery?

Earlier studies have suggested that epidural fentanyl improves intraoperative analgesia during cesarean section, but others have suggested that it worsens postoperative analgesia from epidural morphine. The purpose of this study was to determine whether epidural fentanyl given before epidural morphine improves the quality of intraoperative epidural anesthesia without worsening postoperative analgesia provided by epidural morphine. Sixty patients having epidural anesthesia for cesarean delivery were studied. Epidural anesthesia was established using 2% lidocaine with epinephrine 5 micrograms/mL. After delivery, either fentanyl 100 micrograms/10 mL or normal saline-control 10 mL was injected through the epidural catheter in a randomized, double-blind manner. All patients received 3.5 mg of morphine epidurally after uterine repair. After administration of the epidural study drug, there were no significant differences in the pain responses during surgery between the two groups. Patients in the fentanyl group experienced significantly less nausea and vomiting between delivery and the end of surgery than did patients in the normal saline-control group (P = 0.013). Postoperatively, visual analogue scale scores for pain, pruritus, nausea, and sedation were similar at 1, 2, 4, and 8 h in the two groups. We conclude that fentanyl 100 micrograms administered epidurally during cesarean delivery did not improve intraoperative analgesia, but significantly reduced intraoperative nausea and vomiting without diminishing the efficacy of postoperative analgesia provided by epidural morphine.

Adult↗
PubMed1991

Nitric oxide generation from nitroprusside by vascular tissue. Evidence that reduction of the nitroprusside anion and cyanide loss are required.

Nitric oxide (NO) was produced from sodium nitroprusside in the presence of vascular tissue but was not released spontaneously from the nitroprusside anion. In the absence of tissue in the dark nitroprusside did not release NO. When solutions of nitroprusside alone were irradiated with visible light, nitric oxide was released at rates linearly proportional to nitroprusside concentration and light intensity. Nitric oxide was produced from solutions of nitroprusside in the dark after the addition of vascular tissue, including lengths of rabbit aorta, subcellular fractions of aorta, and human plasma. NO was also released from nitroprusside after reaction with various reducing agents including cysteine and other thiols, ascorbic acid, sodium dithionite, ferrous chloride, hemoglobin, myoglobin, and partially purified cytochrome P450 with an NADPH-regenerating system. HCN was simultaneously produced in these solutions, and addition of KCN blocked NO release. Iodine oxidized intermediate cyanoferrates and blocked nitric oxide release. KCN or iodine also blocked NO production by tissue, but had no effect upon photochemical NO release. These results show that, apart from photolysis which makes no physiological contribution, release of nitric oxide from nitroprusside, in simple solutions and in biological tissue, occurs after nitroprusside has undergone reduction and lost cyanide.

Animals↗
PubMed1991

Effects of nitric oxide on platelet-activating factor- and alpha-adrenergic-stimulated vasoconstriction and glycogenolysis in the perfused rat liver.

Effects of nitric oxide (NO) on hemodynamic and glycogenolytic responses to platelet-activating factor (PAF) and phenylephrine were investigated in perfused livers derived from fed rats. Infusion of NO (34 microM) into perfused livers inhibited PAF (0.22 nM)-induced increases in hepatic glucose output and portal pressure approximately 90 and 85%, respectively, and abolished effects of PAF on hepatic oxygen consumption. NO attenuated PAF-stimulated increases in glucose output and portal pressure, the latter indicative of hepatic vasoconstriction, with a similar dose dependence with an IC50 of approximately 8 microM. In contrast to its effects on PAF-induced responses in the perfused liver, NO inhibited increases in hepatic portal pressure in response to phenylephrine (10 microM) approximately 75% without altering phenylephrine-stimulated glucose output and oxygen consumption. Similarly, infusion of NO into perfused livers significantly inhibited increases in hepatic portal pressure but not in glucose output in response to a submaximal concentration of phenylephrine (0.4 microM). Like NO, sodium nitroprusside (83 microM) significantly inhibited hemodynamic but not glycogenolytic responses to phenylephrine in perfused livers. However, PAF (0.22 nM)-stimulated alterations in hepatic portal pressure, glucose output, and oxygen consumption were unaffected by infusion of sodium nitroprusside (83 microM) into perfused livers. These results provide the first evidence for regulatory effects of NO in the perfused liver and support the contention that PAF, unlike phenylephrine, stimulates glycogenolysis by mechanisms secondary to hepatic vasoconstriction. These observations raise the intriguing possibility that NO may act in liver to regulate hemodynamic responses to vasoactive mediators.

Adrenergic alpha-Antagonists↗
PubMed1991

EDRF: nitrosylated compound or authentic nitric oxide.

Endothelium-derived factor (EDRF) from bovine aortic endothelial cells was compared to solutions of authentic nitric oxide (NO) and to solutions of the nitrosothiol S-nitroso-L-cysteine. EDRF was produced from endothelial cells by basal release or by stimulation with the calcium ionophore A23187. Biological activity was measured as relaxation of porcine coronary arteries preconstricted with prostaglandin F2 alpha, and chemical analysis was made of the nitrosyl content by measurement of NO released after chemical reduction with 1% sodium iodide in glacial acetic acid. EDRF, NO, and nitrosocysteine had identical half-lives, were all inactivated by hemoglobin and methylene blue, and were all augmented in their biological activity by superoxide dismutase. When solutions were analyzed for their biological activity as a function of the NO content (after NaI/acetic acid reduction), nitrosocysteine showed more vasodilation per amount of contained NO than did authentic NO. Solutions containing EDRF (basal release or by stimulation with A23187) subjected to the same analysis appeared similar to nitrosocysteine, and were distinct from solutions of NO. These experiments show that nitrosyl compounds other than NO can have properties very similar or identical to EDRF, and that in this system EDRF appears more similar to nitrosocysteine than to NO.

Animals↗
PubMed1991

Nitric oxide: mediator of nonadrenergic noncholinergic responses of opossum esophageal muscle.

Nonadrenergic noncholinergic (NANC) nerves of the opossum esophagus mediate relaxation of circular muscle from the lower esophageal sphincter (LES) and the off contraction of circular esophageal muscle. The latencies between the end of the stimulus and the off contraction describe a gradient so that the latency is longest in muscle from the caudad esophagus. NG-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthase, and NO were used to test the hypothesis whether NO is a mediator of these nerve-induced responses. Both electrical field stimulation (EFS) of intrinsic esophageal nerves and exogenous NO relaxed LES muscle. Only EFS-induced relaxation was inhibited by L-NNA [half-maximal response (EC50) = 60.0 +/- 20.0 microM]. L-Arginine, the substrate for NO synthase, reversed the inhibitory effect of L-NNA. Exogenous NO did not contact circular esophageal muscle. Both the amplitude (EC50 = 14.7 +/- 4.0 microM) and the latency of the off contraction (EC50 = 41.1 +/- 5.6 microM) were diminished by L-NNA. L-Arginine prevented the action of L-NNA. NG-nitro-L-arginine also attenuated the gradient in the latency of the off response by shortening latencies in muscle from the caudad esophagus. It had no effect on cholinergic nerve-induced contraction of longitudinal esophageal muscle. These data support the hypothesis that NO or an NO-containing compound may be a mediator of NANC nerve-induced responses of the esophagus and LES.

Animals↗
PubMed1991

Nitric oxide: mediator of NANC hyperpolarization of opossum esophageal smooth muscle.

Activation of intrinsic nonadrenergic noncholinergic (NANC) esophageal nerves during peristalsis or by electrical field stimulation (EFS) in vitro produces a hyperpolarization followed by a depolarization of the circular smooth muscle of the opossum esophagus. N omega-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase, and nitric oxide (NO) were used to test the hypothesis that NO or a NO-containing compound is a mediator of this NANC nerve-induced hyperpolarization of circular esophageal smooth muscle. The transmembrane potential difference of esophageal circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated membrane responses were evoked by single electrical pulses of 0.5 ms duration and 50 V amplitude. L-NNA abolished the initial hyperpolarization and reduced the amplitude of and the time to maximal depolarization. L-Arginine (1 mM), the substrate for NO synthase, antagonized the effect of L-NNA. Exogenous NO produced hyperpolarization of the smooth muscle membrane potential and attenuated the amplitudes of EFS-induced hyperpolarization and depolarization. The effect of NO was blocked neither by L-NNA nor by tetrodotoxin (1 microM). The data support the hypothesis that NO or a NO-containing compound mediates NANC nerve-induced responses of the esophageal smooth muscle membrane.

Amino Acid Oxidoreductases↗
PubMed1991

Mechanisms responsible for the heterogeneous coronary microvascular response to nitroglycerin.

Nitroglycerin dilates large (greater than or equal to 100 microns) but not small coronary arterial microvessels, and a putative metabolite of nitroglycerin, S-nitroso-L-cysteine, has been shown in vitro to dilate both large and small coronary microvessels. Based on this evidence, we tested the hypothesis that the lack of response of small coronary microvessels was due to an inability of small coronary microvessels to convert nitroglycerin into its vasoactive metabolite and examined possible explanations for this phenomenon. We studied left ventricular epicardial microvessels in vivo using video microscopy and stroboscopic epi-illumination in anesthetized, open-chest dogs. Diameters were determined while the epicardium was suffused with nitroglycerin, S-nitroso-L-cysteine, or S-nitroso-D-cysteine (all 10 microM) and nitroglycerin in the presence of L- or D-cysteine (100 microM). None of the agents affected systemic hemodynamics. Nitroglycerin dilated large arterioles (20 +/- 2%) but not small arterioles (1 +/- 1%). Both S-nitroso-L-cysteine and S-nitroso-D-cysteine were potent dilators of all size classes of microvessels. Concomitant application of L-cysteine and nitroglycerin evoked dilation in small microvessels (22 +/- 4%, p less than 0.5 versus nitroglycerin alone) and larger microvessels (27 +/- 6%, p = NS versus nitroglycerin alone). D-Cysteine did not alter the microvascular response to nitroglycerin in either small (7 +/- 4%, p = NS versus nitroglycerin alone) or large (18 +/- 3%, p = NS versus nitroglycerin alone) microvessels. Neither L-cysteine nor D-cysteine had a direct effect on microvascular diameter. These findings suggest that 1) sulfhydryl groups are required for the conversion of nitroglycerin to its vasoactive metabolite; 2) the interaction between nitroglycerin and sulfhydryl residues is a stereospecific process, indicating either an intracellular mechanism or a membrane-associated enzymatic reaction; and 3) a lack of available sulfhydryl groups may be responsible for the lack of response of small coronary arterioles to nitroglycerin.

Analysis of Variance↗
PubMed1990

Is there a role for an endothelium-derived relaxing factor in nociception?

Many of the circulating algesic agents released in response to ischemia produce a profound vasodilatation possibly through the release of an endothelium-derived relaxing factor (EDRF) as well as pain. We report here that intravenously administered S-nitrosocysteine, a putative EDRF, and not the nitric oxide liberating compound sodium nitroprusside produces significant alterations in nociceptive behavior that are abolished by bilateral vagotomy. These results are consistent with a role for EDRF in peripheral nociceptive mechanisms.

Analysis of Variance↗