Transient Decrease In Mean Arterial Pressure Research Articles

Cardiovascular function, pulmonary gas exchange and tissue oxygenation in isoflurane-anesthetized, mechanically ventilated Beagle dogs with four levels of positive end-expiratory pressure

ObjectivesTo compare pulmonary gas exchange, tissue oxygenation and cardiovascular effects of four levels of end-expiratory pressure: no positive end-expiratory pressure (ZEEP), positive end-expiratory pressure (PEEP) of maximal respiratory system compliance (PEEPmaxCrs), PEEPmaxCrs + 2 cmH2O (PEEPmaxCrs+2), PEEPmaxCrs + 4 cmH2O (PEEPmaxCrs+4), in isoflurane-anesthetized dogs. Study designProspective randomized crossover study. AnimalsA total of seven healthy male Beagle dogs, aged 1 year and weighing 10.2 ± 0.7 kg (mean ± standard deviation). MethodsThe dogs were administered acepromazine and anesthesia was induced with propofol and maintained with isoflurane. Ventilation was controlled for 4 hours with ZEEP, PEEPmaxCrs, PEEPmaxCrs+2 or PEEPmaxCrs+4. Cardiovascular, pulmonary gas exchange and tissue oxygenation data were evaluated at 5, 60, 120, 180 and 240 minutes of ventilation and compared using a mixed-model anova followed by Bonferroni test. p < 0.05 was considered significant. ResultsCardiac index (CI) and mean arterial pressure (MAP) were lower in all PEEP treatments at 5 minutes when compared with ZEEP. CI persisted lower throughout the 4 hours only in PEEPmaxCrs+4 with the lowest CI at 5 minutes (2.15 ± 0.70 versus 3.45 ± 0.94 L minute–1 m–2). At 180 and 240 minutes, MAP was lower in PEEPmaxCrs+4 than in PEEPmaxCrs, with the lowest value at 180 minutes (58 ± 7 versus 67 ± 7 mmHg). Oxygen delivery index (DO2I) was lower in PEEPmaxCrs+4 than in ZEEP at 5, 60, 120 and 180 minutes. Venous admixture was not different among treatments. Conclusion and clinical relevanceThe use of PEEP caused a transient decrease in MAP and CI in lung-healthy dogs anesthetized with isoflurane, which improved after 60 minutes of ventilation in all levels of PEEP except PEEPmaxCrs+4. A clinically significant improvement in arterial oxygenation and DO2I was not observed with PEEPmaxCrs and PEEPmaxCrs+2 in comparison with ZEEP, whereas PEEPmaxCrs+4 decreased DO2I.

Dose-Dependent Acute Circulatory Fates Elicited by Cadmium Are Mediated by Differential Engagements of Cardiovascular Regulatory Mechanisms in Brain.

Whereas cadmium is a toxicant that has been shown to cause cardiovascular toxicity and mortality in mammals, few mechanistic studies address its acute circulatory actions. The present study assessed the hypothesis that cadmium effects dose-dependent acute circulatory fates via differential participation of the cardiovascular regulatory mechanisms in brain. In Sprague-Dawley rats maintained under propofol anesthesia, cadmium acetate (8 mg/kg, iv) induced significantly high mortality rate within 10 min, concomitant with progressive decline toward zero level of mean arterial pressure (MAP), heart rate (HR), baroreflex-mediated sympathetic vasomotor tone, and carotid blood flow (CBF). There were concurrent tissue anoxia, cessation of microvascular perfusion, reduction of mitochondrial membrane potential and ATP production, and necrotic cell death in the rostral ventrolateral medulla (RVLM), the brain stem site that maintains blood pressure and sympathetic vasomotor tone. On the other hand, a lower-dose of cadmium (4 mg/kg, iv) resulted in only a transient decrease in MAP that was mirrored by an increase in CBF and baroreflex-mediated sympathetic vasomotor tone, minor changes in HR, along with transient hypoxia, and apoptotic cell death in RVLM. We conclude that cadmium elicits dose-dependent acute cardiovascular effects with differential underlying biochemical and neural mechanisms. At a higher-dose, cadmium induces high mortality by effecting acute cardiovascular collapse via anoxia, diminished tissue perfusion, mitochondrial dysfunction and bioenergetics failure that echo failure of cerebral autoregulation, leading to necrosis, and loss of functionality in RVLM. On the other hand, a lower-dose of cadmium elicits low mortality, transient decrease in arterial pressure, and hypoxia and apoptosis in RVLM that reflect sustained cerebral autoregulation.

Haemodynamic Tolerance of Cardiac Surgical Patients Receiving Vasoactive Therapy in Upright Positioning

Introduction: There is a lack of consensus regarding when it is safe to commence exercise with cardiac surgical patients in the Intensive Care Unit (ICU) receiving vasoactive therapy. Patients receiving vasoactive therapy may therefore be subject to unnecessary bed rest. Objectives: The aims were to measure the effect of exercise in upright positioning on haemodynamic parameters of cardiac surgical patients receiving vasoactive therapy, to clarify what level of vasoactive medication may allow safe exercise, and determine the incidence of adverse events. Methods: This was a prospective, single-centre, cohort study conducted in the ICU of a cardiothoracic tertiary, university-affiliated hospital in Australia. Eligible participants were recruited from August 2017 to May 2018. The Flotrac-Vigileo system was utilized to obtain haemodynamic measurements. Subjects were progressively positioned from supine, standing and marching on spot and returned to supine. A between-within repeated measures ANOVA was conducted to compare haemodynamic variables over various positions and interactions with positions and dose of low vs medium to high levels of vasoactive medication. Results: 20 participants; 16 (80%) male; mean age of 65.9 (10.6) years; were studied, with 6 (30%) receiving low dose vasoactive medication and 14 (70%) receiving a moderate to high dose. There were significant increases in mean arterial pressure (MAP) (p = 0.018), heart rate (HR) (p = 0.050) and respiratory rate (RR) (p = 0.049) with upright positioning. There was no significant interaction between position and dose. There were no significant changes in cardiac output, stroke volume or cardiac index during upright positioning. One minor adverse event occurred in a participant on low dose Dopamine. This was a transient decrease in MAP. Conclusions: Exercise caused an increase in MAP, HR and RR, and led to no significant increases in other hemodynamic parameters. Our findings suggest that vasoactive therapy alone should not be considered a contraindication to exercise post-cardiac surgery.

Activation of the central melanocortin system contributes to the increased arterial pressure in obese Zucker rats

We have previously demonstrated that leptin-mediated activation of the central nervous system (CNS) melanocortin system reduces appetite and increases sympathetic activity and blood pressure (BP). In the present study we examined whether endogenous melanocortin system activation, independent of leptin's actions, contributes to the regulation of BP and metabolic functions in obese Zucker rats, which have mutated leptin receptors. The long-term cardiovascular and metabolic effects of central melanocortin-3/4 receptor (MC3/4R) antagonism with SHU-9119 were assessed in lean (n = 6) and obese (n = 8) Zucker rats. BP and heart rate (HR) were measured 24-h/day by telemetry and an intracerebroventricular cannula was placed in the brain lateral ventricle. After stable control measurements, SHU-9119 was infused intracerebroventricularlly (1 nmol/h) for 10 days followed by a 10-day recovery period. Chronic CNS MC3/4R antagonism significantly increased food intake and body weight in lean (20 ± 1 to 45 ± 2 g and 373 ± 11 to 432 ± 14 g) and obese (25 ± 2 to 35 ± 2 g and 547 ± 10 to 604 ± 11 g) rats. No significant changes were observed in plasma glucose levels in lean or obese rats, whereas plasma leptin and insulin levels markedly increased in lean Zucker rats during CNS MC3/4R antagonism. Chronic SHU-9119 infusion in obese Zucker rats reduced mean arterial pressure (MAP) and HR by 6 ± 1 mmHg and 24 ± 5 beats/min, whereas in lean rats SHU-9119 infusion reduced HR by 31 ± 9 beats/min while causing only a transient decrease in MAP. These results suggest that in obese Zucker rats the CNS melanocortin system contributes to elevated BP independent of leptin receptor activation.

Ranolazine, a Novel Anti‐Anginal Agent, Does Not Alter Isosorbide Dinitrate‐ or Sildenafil‐Induced Changes in Blood Pressure in Conscious Dogs

Ranolazine is under clinical development for the treatment of chronic angina. Our goal was to determine effects of ranolazine on isosorbide dinitrate (ISDN)- or sildenafil-induced changes in mean arterial pressure (MAP) and heart rate (HR) in conscious dogs. Dogs (n=7) were chronically instrumented for measurements of MAP and HR. ISDN (0.2 mg/kg, IV) and, 2.5 hr later, sildenafil (0.5 mg/kg, IV) were given in the absence and presence of ranolazine. Bolus IV injections of ISDN or sildenafil caused a transient (~20 sec) decrease in MAP and an increase in HR followed by a prolonged (10-15 min) decrease in MAP by 11±1.6 and 11±2.2mmHg for ISDN and sildenafil, respectively, without significant changes in HR. Infusion of ranolazine alone (plasma level=4-5 or 8-10 μM) for 10 min did not significantly affect MAP and HR. During ranolazine infusion, ISDN and sildenafil still caused a prolonged decrease in MAP by 10±1.7 to 16±2.5 mmHg, respectively. The transient hypotension and tachycardia caused by ISDN were not altered by ranolazine. The sildenafil-induced transient tachycardia ( HR: 114±10) was significantly (P<0.05) blunted by 4-5 ( HR: 71±8 bpm) or 8-10 (( HR: 66±9 bpm) μM ranolazine. However, the sildenafil-induced transient decrease in MAP was not altered by ranolazine. The results indicate that except for a blunting of the 20-sec transient tachycardia caused by sildenafil, ranolazine at concentrations up to 10 μM (i.e., within the therapeutic range) does not alter changes in MAP and HR induced by ISDN or sildenafil.

Mechanisms of the cerebrovascular response to apnoea in humans

We measured ventilation, arterial O2 saturation, end‐tidal CO2 (PET,CO2), blood pressure (intra‐arterial catheter or photoelectric plethysmograph), and flow velocity in the middle cerebral artery (CFV) (pulsed Doppler ultrasound) in 17 healthy awake subjects while they performed 20 s breath holds under control conditions and during ganglionic blockade (intravenous trimethaphan, 4.4 ± 1.1 mg min−1 (mean ±s.d.)). Under control conditions, breath holding caused increases in PET,CO2 (7 ± 1 mmHg) and in mean arterial pressure (MAP) (15 ± 2 mmHg). A transient hyperventilation (PET,CO2−7 ± 1 mmHg vs. baseline) occurred post‐apnoea. CFV increased during apnoeas (by 42 ± 3 %) and decreased below baseline (by 20 ± 2 %) during post‐apnoea hyperventilation. In the post‐apnoea recovery period, CFV returned to baseline in 45 ± 4 s. The post‐apnoea decrease in CFV did not occur when hyperventilation was prevented. During ganglionic blockade, which abolished the increase in MAP, apnoea‐induced increases in CFV were partially attenuated (by 26 ± 2 %). Increases in PET,CO2 and decreases in oxyhaemoglobin saturation (Sa,O2) (by 2 ± 1 %) during breath holds were identical in the intact and blocked conditions. Ganglionic blockade had no effect on the slope of the CFV response to hypocapnia but it reduced the CFV response to hypercapnia (by 17 ± 5 %). We attribute this effect to abolition of the hypercapnia‐induced increase in MAP. Peak increases in CFV during 20 s Mueller manoeuvres (40 ± 3 %) were the same as control breath holds, despite a 15 mmHg initial, transient decrease in MAP. Hyperoxia also had no effect on the apnoea‐induced increase in CFV (40 ± 4 %). We conclude that apnoea‐induced fluctuations in CFV were caused primarily by increases and decreases in arterial partial pressure of CO2 (Pa,CO2) and that sympathetic nervous system activity was not required for either the initiation or the maintenance of the cerebrovascular response to hyper‐ and hypocapnia. Increased MAP or other unknown influences of autonomic activation on the cerebral circulation played a smaller but significant role in the apnoea‐induced increase in CFV; however, negative intrathoracic pressure and the small amount of oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.

Endothelin-1-induced elevation in blood pressure is independent of increases in sympathetic nerve activity in normotensive rats.

This study was performed to determine if endothelin-1 (ET-1)-induced pressor responses in urethane-anesthetized, normotensive rats are due to increased sympathetic nerve activity. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic nerve activity. ET-1 (30- 1000 pmol/kg) or sarafotoxin (S6c, ET B receptor agonist, 10-3,000 nmol/kg) given by bolus injection produced transient decreases in mean arterial pressure (MAP) and increases in RSNA and heart rate (HR). ET-1 caused a delayed but sustained increase in MAP that was not inhibited by acute sinoaortic denervation or alpha 1 -adrenergic receptor blockade. ET-1 never caused a sustained change in HR or RSNA. A-192621 (ET B receptor antagonist, 12 mg/kg) increased MAP (10-20 mm Hg) and decreased HR and RSNA. A-192621 blocked the transient decrease in MAP and increase in RSNA and HR caused by ET-1 and S6c. In A-192621-treated rats, ET-1, but not S6c, caused a sustained increase in MAP and decrease in HR and RSNA. After A-192621 treatment, ET-1 infusion caused a sustained elevation in MAP; HR and RSNA decreased only after the highest ET-1 dose. These results indicate that the initial increase in RSNA after ET-1 or S6c is secondary to ET B receptor-mediated vasodilation. Increased RSNA does not contribute to ET-1-induced pressor responses; these responses are likely due to vasoconstriction in normotensive, anesthetized rats. Finally, baroreceptor reflexes function after ET-1 or S6c treatment.

Acute cardiovascular effects of the alpha2-adrenoceptor antagonist, idazoxan, in rats: influence of the basal sympathetic tone.

Intravenous administration of the alpha2-adrenoceptor antagonist, idazoxan, elicits variable cardiovascular effects, depending on experimental conditions. In this study, the effects of idazoxan were investigated in rats with high, low, or no basal sympathetic tone. In a group of conscious Sprague-Dawley rats (n = 9), mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nervous activity (RSNA) were recorded. Idazoxan (250 microg/kg, i.v.) induced a transient decrease in MAP (-12+/-3 mm Hg) that was accompanied by increases in HR (49+/-14 beats/min) and RSNA (53+/-14%). In six of nine rats, a light pentobarbitone anesthesia was given. Basal RSNA was decreased (6.0+/-1.3 microV from 12.8+/-4.1 microV; p<0.05), and the depressor effect of idazoxan was reversed to a pressor effect (21+/-6 mm Hg) associated with bradycardia (-16+/-8 beats/min) and sympathoinhibition (-56+/-15%). In eight conscious intact rats, idazoxan (250 microg/kg, i.v.) attenuated by approximately 40% the pressor response to the selective alpha1-adrenoceptor agonist, cirazoline (0.5 microg/kg, i.v.). In three groups of six to seven ganglion-blocked (chlorisondamine, 2.5 mg/kg, i.v.) conscious rats, idazoxan dose-dependently increased mean arterial pressure (MAP: 39+/-2, 55+/-3, and 69+/-4 mm Hg at 125, 250, and 500 microg/kg, i.v., respectively) with minimal changes in HR. In contrast, the noradrenaline-releasing agent, tyramine (62.5, 125, and 250 microg/kg, i.v.), dose-dependently increased both MAP and HR. The alpha1-adrenoceptor antagonist, prazosin (1 mg/kg, i.v.; n = 8) blunted by approximately 70% (p<0.01) the pressor effect of 250 microg/kg idazoxan. It is concluded that in rats with high sympathetic tone, idazoxan has depressor effects, most likely related to its peripheral alpha-adrenoceptor antagonist properties. In rats with low or no sympathetic tone, idazoxan induced pressor responses mainly secondary to its partial agonist activity at vascular postjunctional alpha1-adrenoceptors.

Subtypes of metabotropic glutamate receptors in the nucleus of the solitary tract of rats

We have determined the role of subgroups of metabotropic glutamate receptors (mGluRs) in the nucleus of the solitary tract (NTS) of normotensive Wistar rats. Unilateral microinjection of ( S)-3,5-dihydroxyphenylglycine (3,5-DHPG), an agonist of group I mGluRs, into the NTS significantly decreased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) (−19.4±2.6 mmHg, −16.4±5.1 beats/min, and −30.6±5.7% by 1 nmol). Microinjection of ( R, S)-1-aminoindan-1,5-dicarboxylic acid (AIDA; 1 nmol), a putative antagonist of group I mGluRs, into the NTS caused transient decreases in MAP and RSNA, followed by sustained increases in MAP (+8.3±2.4 mmHg) and RSNA (+27.7±10.8%). Pretreatment with AIDA failed to prevent the cardiovascular and RSNA responses to microinjection of 3,5-DHPG. Unilateral microinjection of ( S)-4-carboxy-3-hydroxyphenylglycine (4C3HPG), an agonist of group II mGluRs, into the NTS also significantly decreased MAP, HR, and RSNA, whose responses were not inhibited by pre-microinjection of (2 S)-α-ethylglutamic acid (EGLU; 2 nmol), a putative antagonist of group II mGluRs. On the other hand, unilateral microinjection of l(+)-2-amino-4-phosphonobutyric acid ( l-AP4), an agonist of group III mGluRs, into the NTS caused dose-related decreases in MAP (−8.3±1.5 mmHg by 0.1 nmol and −45.1±3.4 mmHg by 0.3 nmol), HR, and RSNA (−21.3±3.9% by 0.1 nmol and −77.2±6.5% by 0.3 nmol), whose responses were suppressed by pre-microinjection of ( R, S)-α-cyclopropyl-4-phosphonophenylglycine (CPPG; 0.3 nmol), an antagonist of group III mGluRs. These results suggest that all subgroups of mGluRs participate in cardiovascular and sympathetic regulations in the NTS of rats, and that endogenous group I mGluRs in the NTS may contribute to tonic cardiovascular and sympathetic regulations.

Role of angiotensin in renal sympathetic activation in cirrhotic rats.

Central nervous system (CNS) renin-angiotensin activity influences the basal level of renal sympathetic nerve activity (RSNA) and its reflex regulation. The effect of type 1 angiotensin II (ANG II)-receptor antagonist treatment (losartan) on cardiac baroreflex regulation of RSNA and renal sodium handling was examined in rats with cirrhosis due to common bile duct ligation (CBDL). Basal levels of heart rate, mean arterial pressure (MAP), RSNA, and urinary sodium excretion were not affected by intracerebroventricular administration of either losartan or vehicle to CBDL rats. After acute intravenous isotonic saline loading (10% body wt) in vehicle-treated CBDL rats, MAP was unchanged and the decrease in RSNA seen in normal rats did not occur. However, in losartan-treated CBDL rats, there were significant concurrent but transient decreases in MAP (-20 +/- 2 mmHg) and RSNA (-25 +/- 3%). The natriuretic response to acute volume loading in losartan-treated CBDL rats was significantly less than that in vehicle-treated CBDL rats only at those time points where there were significant decreases in MAP. Antagonism of CNS ANG II type 1 receptors augments the renal sympathoinhibitory response to acute volume loading in CBDL. However, the natriuretic response to the acute volume loading is not improved, likely due to the strong antinatriuretic influence of the concomitant marked decrease in MAP (renal perfusion pressure) mediated by widespread sympathetic withdrawal from the systemic vasculature.

The effects of hyperoxic and hypercarbic gases on tumour blood flow.

Carbogen (95% O2 and 5% CO2) has been used in preference to 100% oxygen (O2) as a radiosensitizer, because it is believed that CO2 blocks O2-induced vasoconstriction. However, recent work suggests that both normal and tumour arterioles of dorsal flap window chambers exhibit the opposite: no vasoconstriction vs constriction for O2 vs carbogen breathing respectively. We hypothesized that CO2 content might cause vasoconstriction and investigated the effects of three O2–CO2 breathing mixtures on tumour arteriolar diameter (TAD) and blood flow (TBF). Fischer 344 rats with R3230Ac tumours transplanted into window chambers breathed either 1%, 5%, or 10% CO2 + O2. Intravital microscopy and laser Doppler flowmetry were used to measure TAD and TBF respectively. Animals breathing 1% CO2 had increased mean arterial pressure (MAP), no change in heart rate (HR), transient reduction in TAD and no change in TBF. Rats breathing 5% CO2 (carbogen) had transiently increased MAP, decreased HR, reduced TAD and a sustained 25% TBF decrease. Animals exposed to 10% CO2 experienced a transient decrease in MAP, no HR change, reduced TAD and a 30–40% transient TBF decrease. The effects on MAP, HR, TAD and TBF were not CO2 dose-dependent, suggesting that complex physiologic mechanisms are involved. Nevertheless, when ≥ 5% CO2 was breathed, there was clear vasoconstriction and TBF reduction in this model. This suggests that the effects of hypercarbic gases on TBF are site-dependent and that use of carbogen as a radiosensitizer may be counterproductive in certain situations. © 1999 Cancer Research Campaign

Endothelin ET B receptors counteract venoconstrictor effects of endothelin-1 in anesthetized rats

The inhibitory effects of BQ 788 (3 mg/kg, i.v., ET B-receptor antagonist) on endothelin-1 (ET-1)- or IRL 1620 (ET B-receptor agonist)-induced changes in mean arterial pressure (MAP), mean circulatory filling pressure (MCFP, driving force of venous return), arterial resistance (R A), venous resistance (R V) and cardiac output (CO) were characterized in 6 groups of pentobarbital-anesthetized rats. ET-1 or IRL 1620 (0.5, 1 and 2 nmol/kg, i.v.) dose-dependently increased MAP, R A, R V and MCFP and decreased CO. Maximum changes in R A, R V and CO elicited by ET-1 were greater than those by IRL 1620. Equimolar doses of ET-1 and IRL 1620 also caused similar initial transient decreases in MAP. BQ 788 alone slightly elevated MCFP, but did not alter other variables. The ET B-blocker abolished all changes elicited by IRL 1620, but only partially inhibited its responses on MCFP, showing the presence of BQ 788-insensitive receptors. BQ 788 also abolished ET-1's depressor response, partially inhibited its effect on MCFP, and markedly augmented its effects on R A, R V and CO. Thus, ET B-receptors counteract the sustained constrictor effects of ET-1 on arterial and venous resistance vessels. Our results indicate a substantial arterial and venous dilator role for ET B receptors.

Endothelium-derived nitric oxide partially mediates salbutamol-induced vasodilatations

This study examined the ability of salbutamol (selective β 2-adrenoceptor agonist) to cause endothelium-dependent relaxation in rat aortic rings and depressor response in conscious rats. Salbutamol (0.01–100 μM) concentration dependently relaxed preconstricted aortic rings. The relaxant response was partially attenuated by either mechanical removal of the endothelium or treatment with N G-nitro- l-arginine methyl ester (L-NAME, 100 μM). In conscious rats, either i.v. infused phenylephrine (5 μg/kg per min) or i.v. bolus injected L-NAME (12.8 mg/kg), but not the vehicle, caused similar sustained increases in mean arterial pressure (MAP). I.v. infused salbutamol (2–128 μg/kg per min, each dose for 5 min) dose dependently decreased MAP in vehicle-treated rats; the depressor responses were potentiated by hypertension induced by phenylephrine. In contrast, the magnitudes of the depressor response to salbutamol in L-NAME-treated rats were less than those in rats pretreated with phenylephrine or the vehicle. I.v. bolus injections of salbutamol (0.25–16 μg/kg) also caused dose-dependent and transient decreases in MAP in vehicle-treated rats. The magnitude but not the duration of the depressor response to salbutamol was less in rats treated with L-NAME, compared to those in rats given phenylephrine or the vehicle. These results suggest that endothelium-derived nitric oxide is partially involved in β 2-adrenoceptor-mediated vasodilatation.

Thoracic epidural anaesthesia decreases the incidence of ventricular arrhythmias during acute myocardial ischaemia in the anaesthetized rat.

The aim of the present investigation was to study the effect of high thoracic epidural anaesthesia (TEA) on the incidence of ventricular arrhythmias after ligation of the left coronary artery in chloralose-anaesthetized rats. Forty animals were randomly assigned to receive either 40-50 microliter of bupivacaine (5 mg/ml) or saline in implanted thoracic epidural catheters. TEA decreased mean arterial pressure (MAP) from 118 +/- 5 mmHg to 72 +/- 4 mmHg and heart rate (HR) from 450 +/- 9 to 387 +/- 8 beats/min, while epidural saline did not affect MAP and HR. In both groups coronary artery ligation induced a transient decrease in MAP within the first 5-10 min after ligation. In the control group HR increased, during the 30-min post-ligation period, from 453 +/- 9 to 474 +/- 10 beats/min (P less than 0.05) while no significant change was seen in the TEA group. In both groups the mortality rate was 10%. In the TEA group 30% and in the control group 0% had normal sinus rhythm during the recording period (P less than 0.001). The incidence of ventricular fibrillation and/or tachycardia was significantly lower (P less than 0.05) in the TEA group (20%) compared to the control group (53%). The incidence of ventricular extrasystoles did not differ between the two groups. We conclude that TEA-induced blockade of sympathetic afferents and efferents may offer protection against malignant ventricular arrhythmias in the early phase of acute myocardial infarction.