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PubMed2004

Pacing does not improve hypotension in patients with severe orthostatic hypotension--a prospective randomized cross-over pilot study.

BACKGROUND: Tachypacing has been suggested to compensate for drop in blood pressure as a technique to improve symptoms in patients with severe orthostatic hypotension secondary to autonomic dysfunction. To date, however, no randomized controlled studies have been performed to validate the approach. METHODS AND RESULTS: Six patients with severe orthostatic hypotension and chronotropic incompetence secondary to autonomic dysfunction underwent a prospective randomized cross-over tilt table study with no pacing and with temporary DDD pacing at 90 and 110 bpm. Time to syncope or pre-syncopal symptoms, blood pressure changes, stroke volume and cardiac output were recorded using real time hemodynamic monitoring and echocardiography. All patients, except for one, had a drop in blood pressure and syncope or pre-syncopal symptoms during tilt regardless of whether they were paced or not. There was also no difference in any of the measured hemodynamic and vasomotor parameters with pacing. CONCLUSIONS: Pacing did not produce any benefits in terms of symptoms or in any of the measured hemodynamic variables during tilt for patients with severe orthostatic hypotension secondary to autonomic dysfunction in this limited pilot study.

Aged↗
PubMed2005

Comparison of hypotensive epidural anesthesia and hypotensive total intravenous anesthesia on intraoperative blood loss during total hip replacement.

STUDY OBJECTIVE: To compare hypotensive epidural anesthesia (HEA) and hypotensive total intravenous anesthesia (HTIVA) with propofol and remifentanil on blood loss during primary total hip replacement. DESIGN: Prospective, randomized clinical study. SETTING: University hospital. PATIENTS: Forty ASA physical status I, II, and III patients presenting for primary total hip replacement. INTERVENTIONS: Patients received either HEA with bupivacaine (HEA group, n = 20) or HTIVA with propofol and remifentanil (HTIVA group, n = 20) to maintain mean arterial pressure between 50 and 60 mm Hg. MEASUREMENTS: Duration of hypotension, blood loss, blood transfusions, hemodynamics, and coagulation studies were recorded in both groups. MAIN RESULTS: Intraoperative blood loss, percentage of patients receiving blood substitution, and total packed red blood cells transfused were less in those patients receiving HEA than those receiving HTIVA (P = .001, .04, and .015, respectively). Mean central venous pressure was lower in the HEA group than in the HTIVA group intraoperatively (P = .019). Mean hemoglobin concentrations and coagulation studies were similar between the groups. Neurologic examinations of all patients were intact in the postoperative period. CONCLUSIONS: In spite the similar mean arterial pressure levels noted between groups, HEA results in less intraoperative blood loss than HTIVA during primary total hip replacement. This outcome may be associated with non-positive pressure ventilation, distribution of blood flow, and lower mean intraoperative central venous pressure in the HEA group.

Aged↗
PubMed1979

Labetalol in controlled hypotension: administration of labetalol when adequate hypotension is difficult to achieve.

A study of controlled hypotension was undertaken in 50 major surgical patients using labetalol, a drug with both alpha- and beta-adrenoceptor blocking activity. The patients were such that difficulty in achieving controlled hypotension could be anticipated: the young, the anxious and those for whom halothane was contraindicated. The administration of labetalol quickly induced hypotension which was controlled easily and was rapidly antagonized.

Adolescent↗
PubMed1986

Reflex hypotension due to regional activation of left ventricular mechanoreceptors to explain the hypotension noted in clinical myocardial ischaemia or reperfusion.

To determine if regional increases in myocardial contractility, as may occur clinically in angina pectoris, myocardial infarction, or coronary thrombolysis, can initiate the reflex hypotension that sometimes accompanies these conditions, regional injections of positive inotropic agents were made into 32(3)% of the left ventricular myocardium in seven pneumonectomised dogs on total cardiac bypass. The coronary and systemic circulations were isolated and perfused separately. The systemic circulation was perfused at a constant rate so that changes in systemic pressure reflected changes in resistance. Regional injections of doses from 0.001 to 1.0 micrograms noradrenaline in a 0.1 ml volume appreciably increased regional contractility, detected visually and by strain gauge arches, whereas global contractility (left ventricular peak dP/dt) was increased much less. This caused a fall in the systemic pressure (resistance) of 14(2)% below the control value of 78(5)mm Hg, at the largest dose. The decreases in resistance were abolished by bilateral vagotomy, proving their reflex nature. The smaller (0.0001-0.01 micrograms) doses of noradrenaline and the smallest (0.25 micrograms) dose of veratridine increased regional contractility almost without increasing global contractility, indicating that the increase in regional contractility was the major cause of the reflex decrease in systemic resistance. In one animal a decrease in contractility in a control myocardial region occurred simultaneously with the experimentally produced increase in regional left ventricular contractility. This decrease may be analogous to the increase in contractility in the non-ischaemic left ventricular myocardium that occurs simultaneously with the decrease in contractility in the ischaemic region in clinical or experimental myocardial infarction. Left ventricular mechanoreceptors in the region with increased contractility probably initiate the reflex hypotension that sometimes occurs in both circumstances. Thus in angina pectoris or acute myocardial infarction the reflex hypotension probably originates in the hyperactive non-ischaemic myocardial region, whereas in coronary arterial thrombolysis it probably originates in the newly reperfused, formerly ischaemic, region.

Animals↗
PubMed2003

CSF hypovolemia vs intracranial hypotension in "spontaneous intracranial hypotension syndrome".

OBJECTIVES: To investigate the role of CSF hypovolemia in spontaneous intracranial hypotension (SIH) syndrome because so-called SIH syndrome sometimes lacks intracranial hypotension. METHODS: Ten women (aged from 28 to 49 years) with characteristic orthostatic headache without a previous history of dural tear were investigated. In addition to gadolinium (Gd)-enhanced brain MRI, spinal MRI with and without Gd enhancement was performed. RESULTS: Gd-enhanced brain MRI demonstrated diffuse pachymeningeal enhancement in all patients. Sagittal T2-weighted spinal MRI revealed a variable amount of CSF in the extradural space in all patients. Sagittal T2-weighted MRI or axial Gd-enhanced T1-weighted MRI showed dilated epidural veins located in the high cervical portion in each patient. The intensity of dilatation of the epidural veins correlated significantly with the amount of CSF in the epidural space. This suggested that the Monro-Kellie doctrine was applicable in this circumstance. CONCLUSIONS: Since some patients with SIH syndrome have normal CSF pressure and since a downward displacement of the brain due to a reduction of the buoyant action of CSF may induce symptoms, CSF hypovolemia, not intracranial hypotension, may be the cause. Based on the Monro-Kellie doctrine, detecting leaked CSF and venous engorgement (epidural vein dilatation and pachymeningeal enhancement) is an important clue to diagnose so-called SIH syndrome. Dilatation of epidural veins suggests CSF hypovolemia in appropriate conditions.

Adult↗
PubMed2005

Hypotension associated with prone body position: a possible overlooked postural hypotension.

Conditions related to the dysregulation of blood pressure (BP), such as orthostatic hypotension, have been shown to be significantly associated with cardiovascular disease. Recently, the prone body position has been recognized as a possible postural factor leading to BP dysregulation. We conducted a cross-sectional study to investigate the BP response to a change in body position from supine to prone. The study subjects consisted of 271 middle-aged healthy males, randomly selected from the employees of a large manufacturing enterprise in Ehime Prefecture, Japan. Brachial BP and heart rate were measured in a sitting, supine and prone position, in that order, and each difference was defined as a postural change. The postural changes in aortic hemodynamics were also assessed using a SphygmoCor system. The basal BP measured in the sitting position was significantly decreased in the supine position (132+/-18 to 130+/-17 mmHg, p<0.001). A further reduction was observed after the postural change from supine to prone (130+/-17 to 125+/-16 mmHg, p<0.001). The heart rate was increased with the supine-to-prone postural change (4.1+/-5.8 beats/min, p<0.001), while it showed a significant decrease with the sitting-to-supine postural change (-7.6+/-5.6 beats/ min, p<0.05). The impact of BP reduction was more prominent in the aortic artery (-3.3+/-6.7%) than the brachial artery (-3.0+/-6.3%, p=0.020). Multiple regression analysis showed that basal systolic BP was a solely significant determinant of the prone-hypotension (beta=-0.309, p<0.001). In conclusion, these results indicate that lying in a prone posture could lead to unregulated postural hypotension, which has the possibility of being a novel predictor of cardiovascular frailty.

Adult↗
PubMed1994

[Cause of hypotension during spinal anesthesia--the relation between the level of anesthesia and the hypotension].

A retrospective study was conducted on the cause of hypotension during spinal anesthesia and also on the relation between the level of anesthesia and the hypotension. Two hundred twenty three patients who had received spinal anesthesia for gynecological surgery were divided into two groups. Group I consisted of 87 patients with a significant decrease in blood pressure, while group II consisted of 136 patients with no significant decrease in blood pressure. First, the age, dosage of spinal anesthesia, amount of preoperative transfusion, and level of spinal anesthesia were reviewed and compared between the group I and II. Next, all the patients were classified by the level of spinal anesthesia, and the degree of decrease in blood pressure and the frequency of a significant decrease in blood pressure were examined by each level of spinal anesthesia. Only the level of spinal anesthesia was found to differ significantly between the group I and II. The degree of hypotension was greater at higher levels of spinal anesthesia. More than 50% of the patients with T5 or higher levels of anesthesia had a significant decrease in blood pressure. We conclude that the cause of the significant decrease in blood pressure during high spinal anesthesia is in most part due to the blockade of the cardiac sympathetic nerve.

Adult↗
PubMedDate not supplied

A new trend in the therapy of orthostatic arterial hypotension: prevention by propranolol or metoclopramide of the excessive adrenaline release of brainstem infarct patients with postural hypotension.

The catecholamine (CA) response to upright posture was studied in 30 brainstem infarct patients with orthostatic arterial hypotension; the investigation was made before and after 10 days propranolol therapy (in 15 cases) and before and after 10 days metoclopramide therapy (in other 15 cases). Before treatment almost all patients responded to posture by a rise in adrenaline (A) excretion and by a depression in noradrenaline (NA) excretion. Propranolol therapy prevented the excessive A release produced by standing and normalized their NA response to posture. Metoclopramide administration also prevented the post-orthostatic A discharge but had no significant influence on NA response to posture. Both drugs exerted a favourable influence on postural hypotension of investigated patients. As post-orthostatic A discharge observed in patients with postural hypotension is involved in the pathogeny of this syndrome and both metoclopramide and propranolol are able to correct this disorder one may maintain that the clinical favourable results obtained with these drugs are ascribable at least partly to their blocking effect on A release.

Antiemetics↗
PubMed1989

The hemodynamic and metabolic changes in prostaglandin E1-induced hypotension in dogs--a comparative study with trimetaphan-induced hypotension.

The hemodynamic and metabolic changes in hypotensive state induced with prostaglandin E1 (PGE1) or trimetaphan (TMT) infusion were investigated in dogs. Mean arterial pressure was decreased by about 50% with 1.58 microg/kg/min of PGE1 or 45 microg/kg/min of TMT. Heart rate, pulmonary capillary wedge pressure and central venous pressure remained virtually unchanged in the two groups. Cardiac output was well maintained in PGE1 group, whereas cardiac output showed the tendency to decline in TMT group. Greater reduction in systemic vascular resistance was seen in PGE1 group than in TMT group. Pulmonary vascular resistance showed no significant change in PGE1 group, whereas it increased significantly in TMT group. Gradual decreases in arterial pH, PaO2 and base excess and slight but significant increase in PaCO2 was observed in PGE1 group, and these abnormalities recovered 30 min after hypotension. Abnormalities in blood gases and acid-base balance were considerably more severe and prolonged in TMT group compared with those in PGE1 group. Blood lactate and pyruvate concentrations showed no significant changes in PGE1 group, whereas substantial elevation was seen in L/P ratio especially 30 min after induction of hypotension in TMT group. Oxygen consumption showed minimal changes in PGE1 group, whereas a significant decrease was observed in TMT group. The conclusions derived from these results are as follows; 1) PGE1 maintained cardiac output better than TMT, probably because of its direct inotropic action on the heart, and of its greater reduction of systemic vascular resistance than TMT. 2) PGE1 seemed to provide the better blood perfusion throughout the body than TMT. 3) PGE1 showed less possibility to produce the metabolic derangement compared with TMT.

Journal Article↗
PubMed2001

Calcium channel blockade in vascular smooth muscle cells: major hypotensive mechanism of S-petasin, a hypotensive sesquiterpene from Petasites formosanus.

In vivo and in vitro studies were carried out to examine the putative hypotensive actions of S-petasin, a sesquiterpene extracted from the medicinal plant Petasites formosanus. Intravenous S-petasin (0.1-1.5 mg/kg) in anesthetized rats produced a dose-dependent hypotensive effect. In isolated aortic ring, isometric contraction elicited by KCl or the L-type Ca2+ channel agonist Bay K 8644 was reduced by S-petasin (0.1-100 microM), an action not affected by the cyclooxygenase inhibitor indomethacin, nitric-oxide synthase inhibitor N(omega)-nitro-L-arginine, guanylyl cyclase inhibitor methylene blue, or removal of vascular endothelium. Pretreatment with S-petasin for 10 min shifted the concentration-response curve for KCl (15-90 mM)-induced contraction to the right and reduced the maximal response. In Ca2+-depleted and high K+-depolarized aortic rings preincubation with S-petasin attenuated the Ca2+-induced contraction in a concentration-dependent manner, suggesting that S-petasin reduced Ca2+ influx into vascular smooth muscle cells (VSMCs). Moreover, in cultured VSMCs, whole-cell patch-clamp recording indicated that S-petasin (1-50 microM) inhibited the L-type voltage-dependent Ca2+ channel (VDCC) activities. Intracellular Ca2+ concentration ([Ca2+[(i)) estimation using the fluorescent probe 1-[2-(5-carboxyoxazol-2-yl)-6-aminobenzofuran-5-oxy]-2-(2'-amino-5'-methylphenoxy)-ethane-N,N,N,N-tetraacetic acid pentaacetoxymethyl ester indicated that S-petasin (10, 100 microM) suppressed the KCl-stimulated increase in ([Ca2+[(i)). Taken together, the results suggested that a direct Ca2+ antagonism of L-type VDCC in vascular smooth muscle may account, at least in part, for the hypotensive action of S-petasin.

Animals↗
PubMed1992

[Idiopathic orthostatic hypotension (IOH) and sympathotonic orthostatic hypotension (SOH)].

IOH occurs as progressive autonomic failure (PAF) without any neurologic symptoms indicating multiple system atrophy or Parkinson's disease. The responsible lesion for IOH is yet obscure but has been suggested to be in the peripheral sympathetic nerves, since postganglionic sympathetic neurons in IOH fail to release norepinephrine and there present extensive supersensitivities to exogenous pressors. SOH is characterized as marked tachycardia induced by hypotensive stress like standing, and is less sensitive to the administered catecholamines. Careful examinations by some pharmacological studies are essential to diagnose IOH and SOH in patients with orthostatic hypotension.

Autonomic Nervous System Diseases↗
PubMed2001

[Effect of sanwu hypotensive decoction on blood pressure and lymphokine activated killer cell in patient of primary hypertension and spontaneously hypotensive rats].

OBJECTIVE: To investigate the effect of Sanwu hypotensive decoction (SWHD) on blood pressure (BP) and lymphokine activated killer cell (LAK) and possible mechanism. METHODS: Thirty mild hypertension patients were treated with SWHD for 8 weeks, the levels of BP, proliferative ability and activity of LAK cell, SOD-like substance expressed by LAK cell and its radical scavenger ability before and after treatment were observed using randomized, single blinded, self-control, paralled assay, and compared with other 30 patients treated with captopril for control. In an experimental study, the vasodilatory response of thoracic aortic ring to acetylcholine and nitroglycerine, and effect of LAK cell, standard reagent of SOD, SWHD on the response were observed and compared in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKR). RESULTS: After SWHD treatment, along with lowering of BP, the proliferative ability, activity SOD-like substance expressed by LAK cell and its radical scavenger ability increased significantly. CONCLUSION: SWHD is not only an effective hypotensive agent, but also an immunoregulator.

Animals↗
PubMed1982

[The hypotensive effects and mechanism of SGB-483, a newly-synthesized hypotensive agent].

The effects of SGB-483, a newly-synthesized hypotensive agent, on the blood pressure were studied in unanesthetized and anesthetized rats. SGB-483 produced a significant hypotensive action in the conscious SHR and renal hypertensive (clipping) rats, and it caused reversal of the pressor response to adrenaline in the anesthetized Wistar-Imamichi rats, SHR, and clipping rats. In an isolated guinea pig aorta preparation, SGB-483 competitively inhibited the contractile response to phenylephrine with a pA2 value of 7.64 +/- 0.08. In pithed rats that were pretreated with beta-adrenoceptor blocker, the pressor effect of adrenaline (1 microgram/kg) was not completely blocked by either prazosin (1 mg/kg), an alpha 1-selective blocker, or yohimbine (1 mg/kg), an alpha 2-selective blocker. SGB-483 (1 mg/kg) had no effects on the prazosin-resistant part of the pressor effect of adrenaline, but significantly inhibited the yohimbine-resistant part. Clonidine-induced reversal of the tachycardia induced in the pithed rat by cardiac sympathetic nerve stimulation was unaffected by SGB-483, indicating that SGB-483 is a selective antagonist of the alpha 1-adrenoceptor.

Adrenergic alpha-Antagonists↗
PubMed1993

Hypotension in experimental cirrhosis. Is loss of vascular responsiveness to norepinephrine the cause of hypotension in chronic bile-duct-ligated dogs?

It has been postulated that one of the mechanisms of hypotension associated with cirrhosis is an attenuated responsiveness to catecholamines despite the increased activity of the sympathetic nervous system and the elevated plasma concentrations of the sympathetic neurotransmitter, norepinephrine. This abnormality was studied in a dog model of portal hypertension and cirrhosis. Twelve weeks after bile duct ligation (n = 16), intrasplenic pressure rose significantly from 6.3 +/- 0.4 to 14.6 +/- 1.6 mmHg (p < 0.05), mean arterial pressure had fallen from 106 +/- 4 to 83 +/- 8 mmHg (p < 0.01), cardiac output had risen from 3.1 +/- 0.2 to 3.8 +/- 0.8 l/min (p < 0.05) and plasma norepinephrine concentrations rose from 0.22 +/- 0.12 to 1.17 +/- 0.52 nmol/l (p < 0.05). In 7 sham-operated dogs, the changes in these 4 variables over the same period were non-significant. In vivo pressor responsiveness was tested by studying the effects of intravenous and intra-arterial infusions of norepinephrine and the non-selective beta-adrenoceptor agonist, isoproterenol. In vitro responsiveness was tested by measuring the effects of isoproterenol on the isometric twitch of isolated ventricular strips and the effects of norepinephrine on femoral, mesenteric and renal arterial rings. There was no significant change in the in vivo responses of chronic bile-duct-ligated dogs at 12 weeks compared to the preoperative assessment, or to sham-operated dogs at 12 weeks. Furthermore, there was no significant difference between the in vitro responses of ventricular strips to isoproterenol or arterial rings to norepinephrine prepared from chronic bile-duct-ligated and sham-operated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1980

Hypotension and myocardial metabolism. Drug-induced hypotension and the heart: a comparison between halothane and nitroprusside.

This study investigated the effect of hypotension produced by nitroprusside or halothane on haemodynamics and myocardial metabolism. It is postulated that halothane might influence the balance of supply and demand of oxygen to the heart more favourably than nitroprusside. The results in six open-chested dogs do not support this view. Despite the fact that the two drugs lowered the mean arterial pressure by radically different mechanisms, the reduction in demand for oxygen by the heart seemed to be matched by a similar reduction in supply with both drugs. No evidence of anaerobic metabolism or increased a-v O2 content differences was found. It is concluded that the reduction in mean arterial pressure to these levels by either method is not likely to impair myocardial energetics in healthy hearts with normal coronary anatomy.

Anesthesia, Inhalation↗
PubMed1993

Orthostatic hypotension: with particular reference to experimentally-induced orthostatic hypotension in dogs.

Blood pressure (BP) and heart rate (HR) were measured while standing in a stable position for SPF beagle dogs consisting of 4 females with an average weight of 8.73 +/- 0.58 kg and average age of 7.38 +/- 0.12 months. No anesthetic was used during the procedure. These dogs were subjected to a postural change, a 90 degrees-tilt standing position, and BP and HR were measured one minute and ten minutes later. In addition, 20 mg/kg of tetraethyl-ammonium bromide (TEA) as a gangliolytic drug was administered by i.v. injection within 30 seconds, and then BP and HR were measured in the resting state for 20 minutes. When changing from the resting position to the 90 degrees-tilt standing position after administration of TEA, these were significant decreases in systolic BP, diastolic BP and mean arterial BP one minute and ten minutes later. An experimental model of orthostatic hypotension was considered to have been achieved during these methods.

Animals↗
PubMed2004

Potential hypotensive agents: synthesis and hypotensive activity of oxime ethers derived from 1-naphthoxepines and related compounds.

The synthesis and pharmacological evaluation of substituted oximino-ethers 1 and 2 of naphth[1,2-b]- and naphth[2,1-b]-oxepin-5-ones (4 and 8) were carried out. The hypotensive activity of oximino-ethers 1 and 2 was evaluated on anaesthetized cats. The results indicated that 1c caused a fall of 80 mm/Hg for >100' at a dose of 5mg/kg iv in anaesthetized cats.

Animals↗