Sodium Nitroprusside-induced Hypotension Research Articles

Anaphylaxis stimulates afferent vagal nerve activity and efferent sympathetic nerve activity in the stomach of anesthetized rats.

Systemic anaphylaxis is a life-threatening and allergic reaction that affects various organs. We previously reported that, in the stomach, gastric vasoconstriction occurring at the late phase (15-55 min after injection of ovalbumin antigen) was observed in anesthetized rats sensitized with ovalbumin. In addition, anaphylaxis enhances gastric motility and delays emptying. However, the role of extrinsic autonomic nervous system on antigen-induced gastric alterations was not known. Thus, using the same rat anaphylaxis model, we aimed to determine the changes in the efferent and afferent autonomic nerve activities in the stomach during anaphylactic hypotension. The findings showed that injection of ovalbumin antigen caused substantial systemic hypotension in all sensitized rats. The efferent gastric sympathetic nerve activity (ef-GSNA), but not the efferent vagal nerve activity, increased only at the early phase (1-10 min after injection of ovalbumin antigen) and showed baroreceptor reflex, as evidenced by a stimulatory response to sodium nitroprusside-induced hypotension. In general, excitation of ef-GSNA could induce pylorus sphincter contraction and gastric vasoconstriction. In the present study, we found that sympathectomy attenuated the anaphylaxis-induced decrease in gastric flux but not the increase in gastric vascular resistance. Thus, the increase in ef-GSNA may cause anaphylactic pylorus sphincter contraction but not anaphylactic gastric vasoconstriction. On the other hand, the afferent gastric vagal nerve activity, but not the afferent sympathetic nerve activity, increased during the early phase of anaphylactic hypotension. However, vagotomy produced no effects on the anaphylactic gastric dysfunction. In conclusion, the gastric sympathetic nerves partly modulate stomach function during systemic anaphylaxis.

Effect of glutamate on the vestibulo-solitary projection after sodium nitroprusside-induced hypotension in conscious rats.

Orthostatic hypotension is most common in elderly people, and its prevalence increases with age. Attenuation of the vestibulo-sympathetic reflex (VSR) is commonly associated with orthostatic hypotension. In this study, we investigated the role of glutamate on the vestibulo-solitary projection of the VSR pathway to clarify the pathophysiology of orthostatic hypotension. Blood pressure and expression of both pERK and c-Fos protein were evaluated in the nucleus tractus solitarius (NTS) after microinjection of glutamate into the medial vestibular nucleus (MVN) in conscious rats with sodium nitroprusside (SNP)-induced hypotension that received baroreceptor unloading via sinoaortic denervation (SAD). SNP-induced hypotension increased the expression of both pERK and c-Fos protein in the NTS, which was abolished by pretreatment with glutamate receptor antagonists (MK801 or CNQX) in the MVN. Microinjection of glutamate receptor agonists (NMDA or AMPA) into the MVN increased the expression of both pERK and c-Fos protein in the NTS without causing changes in blood pressure. These results indicate that both NMDA and AMPA receptors play a significant role in the vestibulo-solitary projection of the VSR pathway for maintaining blood pressure, and that glutamatergic transmission in this projection might play a key role in the pathophysiology of orthostatic hypotension.

Effects of sodium nitroprusside-induced controlled hypotension on pancreatic function assessed by pancreatitis-associated protein in patients undergoing radical prostatectomy: Retraction

Effects of sodium nitroprusside-induced controlled hypotension on pancreatic function assessed by pancreatitis-associated protein in patients undergoing radical prostatectomy: Retraction

The Effects of Sodium Nitroprusside-Induced Hypotension on Splanchnic Perfusion and Hepatocellular Integrity

The Effects of Sodium Nitroprusside-Induced Hypotension on Splanchnic Perfusion and Hepatocellular Integrity

Overexpression of eNOS prevents the development of renovascular hypertension in mice

Gene therapy has become an important tool for understanding several cardiovascular diseases. In the present study we investigated the effects of endothelial nitric oxide synthase (eNOS) overexpression on renovascular hypertension. Experiments were carried out in C57BL/6 mice randomly assigned to either a two-kidney one-clip (2K1C) hypertension group or a sham-operated group. At the same time surgery was carried out, both 2K1C and sham mice received an intravenous injection of recombinant adenovirus expressing the functional gene eNOS or the reporter gene beta-galactosidase (beta-gal). Fourteen days later, arterial pressure, baroreflex sensitivity, and cardiac sympathetic and parasympathetic tone were evaluated in conscious mice. Measurement of mean arterial pressure showed arterial hypertension in 2K1C-betagal mice compared with sham-betagal mice (121 +/- 3 vs. 96 +/- 2 mm Hg, p < 0.01), which was prevented by eNOS overexpression (2K1C-eNOS 100 +/- 4 vs. sham-eNOS 99 +/- 3 mm Hg). Linear regression analysis of the reflex tachycardia response to sodium nitroprusside-induced hypotension showed that baroreflex sensitivity was significantly attenuated in 2K1C-betagal mice (5.8 +/- 0.5 vs. sham-betagal 8.0 +/- 0.8 beats.min-1 x mm Hg-1, p < 0.05), but this decrease was not prevented by eNOS overexpression (2K1C-eNOS 7.2 +/- 0.5 vs. sham-eNOS 8.8 +/- 0.7 beats x min-1 x mm Hg-1, p < 0.05). The cardiac sympathetic tone was augmented and the vagal tone was reduced in 2K1C-betagal (152 +/- 17 and 45 +/- 12 beats.min-1, respectively) compared with sham-betagal mice (112 +/- 6 and 89 +/- 7 beats.min-1, respectively), and similar results were observed in 2K1C-eNOS mice compared with sham-eNOS. The data indicate that eNOS overexpression was able to prevent the development of 2K1C renovascular hypertension in mice, without affecting other characteristic cardiovascular dysfunctions.

Esmolol attenuates hepatic blood flow responses during sodium nitroprusside-induced hypotension in dogs.

The hemodynamic responses secondary to sympathetic suppression by esmolol may alter blood flow to splanchnic organs. We investigated whether esmolol might modify splanchnic organ blood flow responses during sodium nitroprusside (SNP)-induced hypotension in dogs anesthetized with sevoflurane. The control group (n = 10) received SNP (SNP group). The ES25 and ES100 groups (n = 10, each) received SNP combined with esmolol infused at a constant rate of 25 and 100 micro g*kg(-1)*min(-1) during the hypotensive period after a mean arterial pressure (MAP) of 60 mmHg was attained by the infusion of a 0.03% SNP solution, respectively. The renal, hepatic, and pancreatic blood flows (RBF, HBF, and PBF) were measured by using the hydrogen clearance method. Cardiac index in the SNP group increased (P < 0.01), but in the ES groups it decreased (P < 0.01). Left ventricular dP/dtmax in the SNP group remained unchanged, but in the ES groups it decreased (P < 0.01, each) during the hypotensive period. Except for HBF in the SNP group, the splanchnic blood flow in all groups decreased (P < 0.01, each). The HBF in the ES groups was lower than that in the SNP group (SNP vs ES25, ES100; 70 +/- 1 vs 64 +/- 5, 6 3 +/- 3 mL*min(-1)*100 g(-1)). This study shows that the differences in HBF between SNP-induced hypotension with or without esmolol may be due to the changes in cardiac output caused by alterations of cardiac contractility. These findings suggest that a small dose of esmolol may impair the maintenance of HBF during SNP-induced hypotension.

Retracted: Cerebral effects and blood sparing efficiency of sodium nitroprusside-induced hypotension alone and in combination with acute normovolaemic haemodilution

The combined reduction of oxygen-carrying capacity and perfusion pressure during the combination of acute normovolaemic haemodilution (ANH) and controlled hypotension (CH) raises concerns of hypoperfusion and ischaemic injury to the brain. Forty-two patients undergoing radical prostatectomy were prospectively allocated to receive CH induced by sodium nitroprusside (mean arterial pressure (MAP) 50 mm Hg), a combination of CH+ANH (post-ANH haematocrit 29%; intraoperative MAP 50 mm Hg), or standard anaesthesia (control). Serum levels of the brain-originated proteins neuron-specific enolase (NSE) and protein S-100, blood loss, transfusion requirements, adverse effects, and postoperative recovery profile were compared among the three groups. Intraoperative blood loss in the CH group (mean (SD)) (788 (193) ml) and CH+ANH group (861 (184) ml) was significantly less than in the control group (1335 (460) ml). Significantly fewer total units of allogeneic packed red blood cells (PRBC) were transfused in the patients receiving hypotensive anaesthesia (CH, 3 units; CH+ANH, 2 units; control, 17 units). There was no difference in immediate postoperative recovery profile among the three groups as determined by the emergence from anaesthesia and time to discharge from the postanaesthesia care unit. Serum S-100 protein concentrations increased significantly in all groups from baseline to peak concentrations 2 h postoperatively (CH 0.25 (0.11) microg litre(-1); CH+ANH 0.31 (0.12) microg litre(-1); control 0.31 (0.10) microg litre(-1)). A return to baseline values was seen within 24 h postoperatively in all patients. No changes in NSE concentrations were seen. Our observations suggest that CH and CH+ANH were effective in reducing blood loss and transfusion requirements in patients undergoing radical prostatectomy. Increased serum S-100 protein concentrations imply a disturbance in astroglial cell membrane integrity and an increased endothelial permeability of the blood-brain barrier. There were no associations between serum S-100 protein or NSE and adverse cognitive effects. Further work needs to be done to determine the prognostic importance of S-100 protein and NSE as surrogate variables of postoperative cerebral complications.

Local 42 degrees C hyperthermia improves vascular conductance of the R3230Ac rat mammary adenocarcinoma during sodium nitroprusside infusion.

The effect of sodium nitroprusside-induced hypotension on the perfusion of the R3230 adenocarcinoma during local 42 degrees C hyperthermia was studied using a combination of intravital microscopy and laser Doppler flowmetry. Fischer 344 rats were implanted with dorsal skin flap window chambers containing the R3230Ac tumor and allocated to three treatment groups (34 degrees C with nitroprusside, 42 degrees C with nitroprusside, and 42 degrees C with 0.9% saline). After baseline observation at 34 degrees C, tumors were locally heated to 42 degrees C using a water bath and either 0.9% saline or nitroprusside sufficient to reduce blood pressure 20% below pretreatment baseline was infused. Nitroprusside at 34 degrees C decreased tumor vascular conductance 40% with no effect on the diameter of arterioles entering the tumor. The diameter of arterioles entering 42 degrees C heated tumors increased 35% independent of blood pressure change. Saline at 42 degrees C had no effect on tumor vascular conductance; however, nitroprusside at 42 degrees C increased tumor vascular conductance 55%. Local 42 degrees C tumor heating, combined with a moderate reduction in blood pressure with nitroprusside, overrides the vascular steal effect associated with reduced perfusion pressure alone and results in improved tumor perfusion. Observations of the effect of vasodilator substances on normothermic tumor perfusion cannot be extrapolated to situations where moderate hyperthermia is used.

The Effects of Sodium Nitroprusside-Induced Hypotension on Splanchnic Perfusion and Hepatocellular Integrity: Retracted

The Effects of Sodium Nitroprusside-Induced Hypotension on Splanchnic Perfusion and Hepatocellular Integrity: Retracted

Altered airway and cardiac responses in mice lacking G protein-coupled receptor kinase 3.

Contraction and relaxation of airway smooth muscles is mediated, in part, by G protein-coupled receptors (GPCRs) and dysfunction of these receptors has been implicated in asthma. Phosphorylation of GPCRs, by G protein-coupled receptor kinase (GRK), is an important mechanism involved in the dampening of GPCR signaling. To determine whether this mechanism might play a role in airway smooth muscle physiology, we examined the airway pressure time index and heart rate (HR) responses to intravenous administration of the cholinergic agonist methacholine (MCh) in genetically altered mice lacking one copy of GRK2 (GRK2 +/-), homozygous GRK3 knockout (GRK3 -/-), and wild-type littermates. (GRK2 -/- mice die in utero.) GRK3 -/- mice demonstrated a significant enhancement in the airway response to 100 and 250 microgram/kg doses of MCh compared with wild-type and GRK2 +/- mice. GRK3 -/- mice also displayed an enhanced sensitivity of the airway smooth muscle response to MCh. In addition, GRK3 -/- mice displayed an altered HR recovery from MCh-induced bradycardia. Although direct stimulation of cardiac muscarinic receptors measured as vagal stimulation-induced bradycardia was similar in GRK3 -/- and wild-type mice, the baroreflex increase in HR associated with sodium nitroprusside-induced hypotension was significantly greater in GRK3 -/- than wild-type mice. Therefore, these data demonstrate that in the mouse, GRK3 may be involved in modulating the cholinergic response of airway smooth muscle and in regulating the chronotropic component of the baroreceptor reflex.

Effects of Sodium Nitroprusside-induced Hypotension under Acute Normovolemic Hemodilution on the Cardiovascular System and Systemic Oxygen Balance in Dogs

Effects of Sodium Nitroprusside-induced Hypotension under Acute Normovolemic Hemodilution on the Cardiovascular System and Systemic Oxygen Balance in Dogs

The role of angiotensin in arterial blood pressure regulation in the toad Bufo marinus.

Little is known about the role of the renin-angiotensin system in anuran amphibians, although they appear to possess the functional components of such a system. We investigated the role of angiotensin (ANG) in arterial blood pressure regulation in the conscious toad Bufo marinus using the angiotensin-converting enzyme blocker captopril. We found that conversion of endogenous ANG I to ANG II made a significant contribution to mean arterial pressure in undisturbed animals. The vascular tone contributed by ANG II was not mediated via &agr ; adrenergic mechanisms because increases in pressure in response to ANG infusion were unaffected by the presence of the &agr ; antagonist phentolamine. Angiotensin-induced vasoconstriction was shown to be an important mechanism in arterial blood pressure regulation in the face of an acute hypotensive perturbation of pressure brought about by sodium nitroprusside. Blockade of the conversion of ANG I to ANG II significantly delayed the recovery of mean arterial pressure after sodium nitroprusside-induced hypotension. This suggests that the renin-angiotensin system may play an important role in the initial responses to hypotension in anurans, whether brought about by haemorrhage or dehydration.

Modulation of ovine fetal adrenocorticotropin secretion by androstenedione and 17beta-estradiol.

Parturition in sheep is initiated by increases in activity of the fetal hypothalamic-pituitary-adrenal axis. We have previously reported that cortisol negative feedback efficacy is decreased at the end of gestation. The present study was designed to test the hypothesis that increasing plasma estrogen and/or androgen concentrations in the fetus might increase plasma adrenocorticotropic hormone (ACTH) concentration, either by stimulating ACTH secretion or by altering the negative feedback effect of cortisol on ACTH. Fetal sheep were chronically catheterized and treated with no steroid (control), 17beta-estradiol, or androstenedione (each approximately 0.24 mg/day). After catheterization and implantation of steroid pellet, fetuses were subjected to two short (10 min) periods of sodium nitroprusside-induced hypotension with or without pretreatment with intravenous infusion of hydrocortisone sodium succinate (0.5 microg/min) to test fetal ACTH responsiveness to stress and cortisol negative feedback efficacy. Estradiol treatment significantly increased basal plasma ACTH and cortisol concentrations relative to control fetuses but did not interfere with the inhibition of ACTH secretion by cortisol. Fetal plasma ACTH responses to hypotension were significantly suppressed approximately 60% in both control and estradiol-treated groups. Androstenedione treatment significantly increased basal fetal plasma ACTH and decreased basal fetal plasma cortisol concentration. Androstenedione did not alter stimulated levels of fetal ACTH but did block the inhibition of stimulated ACTH by cortisol. We conclude that increased fetal cortisol and ACTH secretion at the end of gestation may be due to the combined effects of the gonadal steroids in that estradiol increases basal plasma ACTH secretion while androstenedione reduces cortisol negative feedback efficacy.

Effect of sodium nitroprusside-induced hypotension on the blood flow in subcutaneous and intramuscular BT 4An tumors and normal tissues in rats

To examine the effect of infusion of the vasodilator sodium nitroprusside (SNP) on the blood flow in normal tissues and BT4An tumors growing subcutaneously or intramuscularly in BD IX rats. Sodium nitroprusside was given as a continuous intravenous infusion to keep the mean arterial pressure stable at 60 mmHg. The cardiac output, organ blood flow, and perfusion of the BT4An tumors were measured by injection of radiolabelled microspheres at control conditions and after 20 min SNP infusion in each animal. Two series of experiments were performed with two anesthetics with different mechanisms of action, Inactin and the midazolam-fentanyl-fluanisone combination (MFF), to secure reliable conclusions. Cardiac output, heart rate, and blood flow to the skeletal muscles, heart, and liver increased during SNP infusion in either anesthetic group. In the kidneys and particularly the skin, decreased blood flow by SNP was observed. When located subcutaneously on the foot, the blood flow in the tumor fell to 23.4% and 21.4% of the control values in the MFF- and Inactin-anesthetized animals, respectively. This was accompanied by a similar fall in the blood flow in the foot (tumor bed) itself. In the intramuscular tumor, the blood flow fell to 24.8% of the control value in the MFF group, whereas the corresponding figure was 36.2% in the Inactin group. In the surrounding muscle (tumor bed) the blood flow increased significantly, most pronounced in the MFF experiment, where it was tripled. The fall in the tumor perfusion by SNP may be exploited therapeutically to increase the tumor temperature during hyperthermia. Predominant heating of the tumor compared to the tumor bed can be expected if the tumor is growing in or near skeletal muscles.

Effect of Esmolol upon Sodium Nitroprusside-Induced Hypotension under Halothane Anesthesia in Dog : Impact on the Hemodynamic Parameters and the Sodium Nitroprusside Dose Requirement

Effect of Esmolol upon Sodium Nitroprusside-Induced Hypotension under Halothane Anesthesia in Dog : Impact on the Hemodynamic Parameters and the Sodium Nitroprusside Dose Requirement

Effect of N ω-nitro-L-arginine methyl ester on arterial pressure and on vasodilator and vasoconstrictor responses: influence of initial vascular tone

Intravenous N ω-nitro-L-arginine methyl ester (L-NAME) 0.3, 3 and 30 mg/kg produced a dose-dependent increase of blood pressure in urethane-anesthetized rats. Similar pressure responses occured in rats after ganglionic or adrenergic blockade, hemorrhage or acetylcholine infusion. L-NAME potentiated the pressor response to phenylephrine in pentolinium-treated rats. L-NAME increased the depressor effect of acetylcholine and sodium nitroprusside and shortened the acetylcholine response. Phenylephrine potentiated the magnitude but not the duration of the acetylcholine response and had no effect on the duration or magnitude of sodium nitroprusside-induced hypotension. L-NAME potentiated the initial fall of blood pressure induced by a 5 min acetylcholine infusion but had no effect on the pressure drop at the end of infusion. These results suggest that basal production of nitric oxide (NO) is not related to vascular tone and do not support the view that acetylcholine releases NO from resistance vessels in vivo.

Changes in Plasma Concentration of Catechloamine during Sodium Nitroprusside-induced Hypotension

Changes in Plasma Concentration of Catechloamine during Sodium Nitroprusside-induced Hypotension

Cryosurgical denervation of the heart: Acute and chronic effects

A newly developed procedure for total cardiac denervation employing cryosurgical techniques is described. Thirty-three dogs underwent cryosurgical cardiac denervation. Twenty-seven survived the procedure and were divided into three groups. Completeness of denervation was evaluated by recording hemodynamic responses to sodium nitroprusside-induced hypotension, phenylephrine-induced hypertension, and direct cardiac autonomic nerve stimulations acutely (group I, n = 11) and 2 weeks after denervation (group II, n = 5). Serial drug infusion studies were performed during an 8-month period in group III animals (n = 11). Myocardial biopsies for catecholamine content were done in groups II and III. Both direct and reflex hemodynamic responses to autonomic neural stimulation were abolished in the acutely denervated hearts. Furthermore, at 2 weeks, direct neural stimulation was without effect, and myocardial catecholamine content was 95% depleted (p less than 0.001). Serial drug infusion studies revealed a changing spectrum of responses, suggesting the onset of reinnervation by 8 months following the procedure. Myocardial catecholamine content was 85% depleted at that time (p less than 0.001). Cryosurgical cardiac denervation is an effective technique offering the advantages of safety, simplicity, and completeness.

Preservation of renal blood flow during hypotension induced with fenoldopam in dogs

The introduction of drugs that could induce hypotension with different pharmacological actions would be advantageous because side effects unique to a specific drug could be minimized by selecting appropriate therapy. Specific dopamine-1, (DA1) and dopamine-2 (DA2) receptor agonists are now under clinical investigation. Fenoldopam mesylate is a specific DA1 receptor agonist that lowers blood pressure by vasodilatation. The hypothesis that fenoldopam could be used to induce hypotension and preserve blood flow to the kidney was tested. Systemic aortic blood pressure and renal blood flow were measured continuously with a carotid arterial catheter and an electromagnetic flow probe respectively, in order to compare the cardiovascular and renal vascular effects of fenoldopam and sodium nitroprusside in ten dogs under halothane general anaesthesia. Mean arterial pressure was decreased 30 +/- 8 per cent from control with infusion of fenoldopam (3.4 +/- 2.0 micrograms.kg-1.min-1) and 34 +/- 4 per cent with infusion of sodium nitroprusside (5.9 micrograms.kg-1.min-1) (NS). Renal blood flow (RBF) increased during fenoldopam-induced hypotension 11 +/- 7 per cent and decreased 21 +/- 8 per cent during sodium nitroprusside-induced hypotension (P less than 0.01). Sodium nitroprusside is a non-selective arteriolar and venous vasodilator that can produce redistribution of blood flow away from the kidney during induced hypotension. Fenoldopam is a selective dopamine-1 (DA1) receptor agonist that causes vasodilatation to the kidney and other organs with DA1 receptors and preserves blood flow to the kidney during induced hypotension.

The Effects of Captopril on the Renin—Angiotensin System and the Sympathetic Nervous System During Sodium Nitroprusside-Induced Hypotension in the Halothane-Anesthetized Rabbit

Three groups of New Zealand white rabbits were used to study the effects of captopril on the renin-angiotensin system and sympathetic nervous system during sodium nitroprusside (SNP)-induced hypotension and halothane anesthesia. Two groups of rabbits (C and CH) were treated with captopril 2 mg/kg i.v. One captopril-treated group (CH) and the third, untreated group (H) received SNP to induce hypotension. In these two groups, the mean arterial blood pressure (MAP) was reduced by 40% for 150 min. Group C did not undergo SNP-induced hypotension and served to document the effects of captopril alone during the 150-min study period. Arterial blood samples for norepinephrine (NE), epinephrine (EPI), and plasma renin activity (PRA) were drawn prior to, during hypotension, and in the recovery period. The SNP dose required to maintain the hypotension was continuously recorded. NE, EPI, and PRA all increased in group H, indicating activation of both the renin-angiotensin system and the sympathetic system during hypotension. This was accompanied by a dramatic increase in SNP dose requirement. In the CH group, PRA levels rose sharply and remained elevated. Plasma NE levels increased, while EPI levels remained unchanged with a decline in the SNP dose requirement. The C group demonstrated a rise in PRA levels, accompanied by unchanged NE and EPI levels and MAP during the study period. Captopril administration decreased the SNP dose requirement and significantly decreased the sympathetic response (measured by NE and EPI levels) in group CH as compared to the H group.(ABSTRACT TRUNCATED AT 250 WORDS)