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At least 271 records · Page 15Linked to original sources
PubMed1990

[Hemodynamic studies on the vertebral artery system during the vertebral arterial surgery].

Few hemodynamic studies on the vertebral artery system in the human can be seen. The authors measured the vertebral arterial blood flow (VAF) with an electromagnetic flow meter in 45 patients who obtained vertebral arterial surgeries. The patients showing vertebrobasilar insufficiency such as vertigo and drop attack had serious kinking and stenosis at the first portion of the vertebral artery. The effects of induced hypotension by trimethaphan camsilate, induced hypertension by phenylephrine, cervical epidural anesthesia and induced hypertension under epidural anesthesia on the VAF were investigated. During the control state, mean systemic arterial blood pressure (SABP), mean VAF were 97 mmHg and 54 ml/min, respectively. The effects of varied SPBP were analyzed by (delta mean VAF/mean VAF)/(delta mean SABP/mean SABP), (delta V/delta S). The delta mean VAF and delta mean SABP indicated varied mean values of VAF and SABP, respectively. Mean SABP was varied significantly by about 25% in each method. The delta V/delta S in induced hypotension, induced hypertension, epidural anesthesia and induced hypertension under epidural anesthesia were -0.05, 0.07, 0.90 and 0.61, respectively, on the average. Induced hypotension by epidural anesthesia and induced hypertension under epidural anesthesia presented significant changes in mean VAF.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1977

Pharmacology and clinical use of drugs in hypertensive emergencies.

The clinical pharmacology and appropriate choice of antihypertensive agents useful in the treatment of hypertensive emergencies are reviewed. The antihypertensive agents discussed are diazoxide, sodium nitroprusside, hydralazine hydrochloride, trimethaphan camsylate, methyldopa, reserpine and phentolamine mesylate.

Adrenal Gland Neoplasms↗
PubMed1977

Menetrier's disease. Effect of medical and surgical vagotomy.

A 62-year-old woman with incapacitating atherosclerotic vascular occlusive disease was found to have severe hypoproteinemia as a result of Menetrier's disease. That diagnosis was suspected on roentgenographic and gastroscopic examinations and confirmed by examination of full-thickness surgical gastric biopsy specimens. The protein loss from the stomach was significantly decreased by treatment with trimethaphan and atropine and led us to perform proximal gastric vagotomy at the time of endarterectomy. Subsequent protein turnover studies suggest that there has been a significant decrease in protein loss by the stomach. Further evaluation of the possible role of medical and surgical vagotomy in this disease seems warranted.

Atropine↗
PubMed1983

A canine model of acute coronary artery stenosis: effects of deliberate hypotension.

Coronary artery disease is considered a contraindication to inducing hypotension during surgery because the combined effects of stenosis and hypotension in reducing distal coronary artery perfusion pressure might produce myocardial ischemia. To study the effect of deliberate hypotension (mean systemic pressure, 50 mmHg) on regional myocardial perfusion, oxygenation, and lactate extraction, we constricted the left-anterior descending coronary artery (LADCA) in dogs. Two degrees of stenosis were studied: "critical" stenosis, which reduced resting coronary blood flow from 34.4 to 31.2 ml/min and abolished reactive hyperemia of the LADCA in response to 10 s of total coronary artery occlusion; and a more "severe" stenosis, which reduced resting coronary blood flow by 40%. LADCA pressure was measured distal to the stenosis, and LADCA perfusion pressure was obtained by subtracting the left ventricular end-diastolic pressure from the coronary artery diastolic pressure measured past the stenosis. Hypotension was induced by administering sodium nitroprusside, halothane at a high concentration, or trimethaphan. Lactate extraction and oxygen consumption were measured across the myocardium distal to the stenosis (from the coronary artery to the great cardiac vein) and across the whole heart (from the coronary artery to the coronary sinus). Regional myocardial blood flow was measured using radioactive microspheres. A transmural electrocardiogram was obtained from electrodes implanted in the subendocardium and the subepicardium in the distribution of the LADCA distal to the stenosis. Although the combination of critical stenosis and hypotension reduced regional myocardial blood flow and lowered LADCA perfusion pressure to 27 +/- 3 (SE) mmHg, myocardial ischemia did not occur, as evidenced by continued lactate extraction and no redistribution of transmural blood flow or change in ST segment. On the other hand, the combination of severe stenosis and hypotension reduced LADCA perfusion pressure to 17 +/- 2 (SE) mmHG and produced evidence of ischemia by regional lactate production, reduction of the subendocardial/subepicardial flow ratio, and depression of the ST segment.

Animals↗
PubMed1978

Arterial hypertension induced by femoral lengthening. A canine model.

In a canine experimental model, femora were lengthened 2.5 to 3.0 centimeters over a one-minute period. Systolic blood-pressure elevation averaged forty millimeters of mercury and diastolic blood-pressure elevation, twenty-two millimeters of mercury. The average peak arterial pressure was 193/115 millimeters of mercury. The effects of sympatholytic agents on the experimental model were tested. Alpha-adrenergic blockade by phenoxybenzamine, total-body catecholamine depletion by reserpine, and sympathetic ganglionic blockade by trimethaphan camphorsulfonate all inhibited the rise in arterial pressure, but beta-adrenergic blockade by propranolol did not. A differential spinal anesthetic with Xylocaine solution dramatically decreased the elevation in arterial pressure.

Anesthesia, Spinal↗
PubMedDate not supplied

Intravenous drugs used in treating hypertensive emergencies.

Drugs used to treat hypertensive emergencies should have the characteristics of rapid action, short duration, high potency, reversibility, a low toxic/therapeutic ratio, no association tachyphylaxis, and a specific action on the cardiovascular system. Of the three mentioned only SNP fulfills all of the requirements. SNP is used, with few exceptions, to treat hypertensive crisis. Trimethaphan camsylate is useful in preventing hemorrhage secondary to a dissecting aneurysm; the other drugs may worsen the tear. Diazoxide is good when no prolonged monitoring is available, since the drug is administered as a bolus rather than an infusion. Side effects, contraindications, and drug interactions are important points to remember during administration of these medications. Care is directed toward limiting or avoiding side effects by titrating the drug and by close observation of the patient. Concurrent maintenance therapy must be initiated to prevent a recurrence of hypertension upon discontinuance of the acute drug protocol.

Acute Disease↗
PubMed1995

Interactions between sodium balance, intrarenal dopamine synthesis, and sympathetic activity in HLA-identical kidney donors and recipients.

Intrarenal dopamine (DA) synthesis, sympathetic activity and sodium homeostasis were studied in eight HLA-identical kidney recipient and donor pairs at 50, 150, and 300 mmol sodium intake. Trimethaphan was given intravenously (i.v.), to mimic acute denervation, tyramine i.v. to induce noradrenaline (NE) release, and the DA precursor DOPA i.v. to study DOPA to DA conversion. Blood pressure was higher in the recipients (P < 0.05) and was not influenced by sodium intake. Cumulative sodium balances were not different between the groups. Sodium intake did not affect DA excretion in either group. The recipients had higher DA (P < 0.05) and DOPA (P < 0.01) excretions and lower urinary DA over DOPA ratio (UDA/DOPA, P < 0.01) and lower NE excretion (P < 0.05) during the whole study. High sodium intake suppressed the UDA/DOPA in both groups (P < 0.05). Trimetaphan decreased renal vascular resistance (RVR) and increased sodium excretion only in the donors (P < 0.05), while GFR increased in both groups. During HiSo tyramine increased RVR in the recipients (P < 0.01) and UDA/DOPA in the donors (P < 0.05). DOPA infusion increased DA excretion four to fivefold but did not change sodium excretion in either group. It is concluded that the recipients maintained sodium homeostasis well but seem to have an impaired functional innervation of the transplanted kidney. NE release seem to stimulate intrarenal DOPA to DA conversion. In both groups a direct relation between DA and sodium excretion was lacking.

Adult↗
PubMed1994

Stimulatory pathways and sites of action of intrathecally administered nicotinic agents.

Intrathecal (i.t.) administration of nicotinic agonists to rats elicits a receptor-mediated pressor response, a heart rate increase and irritation-nociceptive behavior. We examined the stimulatory pathways and sites of action of spinally administered nicotinic agonists. The thoracic region appears more sensitive to nicotine-elicited pressor actions than the lumbar or cervical regions of the spinal cord. Nicotinic receptors evoking a nociceptive response appear to be located over an area extending from the lumbar rostrally to the thoracic region. Similar to the pressor response, the thoracic spinal cord is the most sensitive region to nicotine in producing the heart rate increase. The cervical region is the least responsive to nicotine, suggesting sites of actions caudal to the brain stem. Intravenous infusion of trimethaphan inhibited the nicotine-elicited pressor response and tachycardia without affecting the irritation response. This suggests that the cardiovascular responses to spinal nicotinic agonists result from enhanced sympathetic outflow. Intrathecal morphine and MK-801 block spinal nicotine-elicited irritation and tachycardia but not the pressor response, indicating that pressor and irritation responses involve independent receptor-mediated pathways. Tachycardia may be associated with the irritation response. In contrast to nicotine, both pressor and irritation responses to cytisine were blocked by morphine with no effect on heart rate. Spinal transection at the T1-2 level eliminated the nociceptive response to nicotine but not the pressor response. Cytisine responses were similar to nicotine; however, cytisine was significantly less potent as a pressor agent in the transected compared with intact animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗
PubMed1994

Cardiovascular and behavioral responses to nicotinic agents administered intrathecally.

We have examined the role of the spinal nicotinic receptors in mediating cardiovascular and behavioral responses in conscious rats. Intrathecal administration of nicotinic agonists to the lumbosacral region of the spinal cord caused a dose-dependent increase in systolic blood pressure, heart rate and a nociceptive (behavioral) response. The order of potencies for the pressor response was l-nicotine > or = cytisine > N-methylcarbamylcholine > or = dimethylphenylpiperazinium > d-nicotine. However, cytisine was the most potent in producing the heart rate increase and nociceptive response. Unlike the other agonists, cytisine also exhibited marked desensitization of the three responses upon repeated administration. The effects of nicotine were antagonized in a dose-dependent fashion by mecamylamine, hexamethonium, alpha-lobeline, dihydro-beta-erythroidine and methyllycaconitine. By contrast, cytisine-induced responses were blocked effectively by mecamylamine and methyllycaconitine, but not by alpha-lobeline or dihydro-beta-erythroidine. However, when alpha-lobeline or dihydro-beta-erythroidine antagonism of the pressor response to cytisine was monitored during the initial minute following intrathecal administration, both antagonists significantly inhibited the response. The competitive ganglionic blocker, trimethaphan, or the elapid alpha-toxin, alpha-bungarotoxin, when administered intrathecally, had no effect on nicotine- or cytisine-elicited responses. The cardiovascular responses to intrathecal nicotine and cytisine have two components. The first is likely mediated through direct sympathetic output and desensitizes rapidly to cytisine, the second is coupled indirectly to the nociceptive response and shows a diminished capacity for rapid desensitization. Agonist and antagonist specificities indicate that the spinal nicotinic receptor differs from those in ganglia and those characterized in brain to date. Although antagonist specificity of the blockade of nicotine and cytisine elicited responses differ, this may be due to the unique desensitization capacity of cytisine rather than an action mediated by distinct receptor subtypes.

Aconitine↗
PubMed1993

[Effects of induced hypotension on perioperative renal and hepatic functions].

Hypotensive anesthesia induced by trimethaphan was maintained at 70-79 mmHg of the systolic radial artery pressure for two hours in 35 patients undergoing spherical acetabul osteotomy. The creatinine clearance, free water clearance, fractional sodium excretion, urine volume, urinary excretion of NAG and levels of gamma-GTP, serum GOT and GPT were measured perioperatively. The creatinine clearance, free water clearance and urine volume decreased by 50% during surgery but recovered to normal values on the third day after surgery. The fractional sodium excretion remained unchanged during and after surgery. The urinary NAG activity increased from 3 +/- a (SD) to 10 +/- 5 U.g-1 and gamma-GTP activity increased from 23 +/- 7 to 33 +/- 13 U.g-1 during surgery, and these remained at high levels for three days after surgery. The serum GOT and GPT levels were within normal ranges for 21 postoperative days. The increase in urinary enzyme activities during and after surgery indicates that mild damage of renal tubular cells has occurred during hypotensive anesthesia.

Adolescent↗
PubMed1997

Desmethyl tirilazad reduces brain nitric oxide synthase activity and cyclic guanosine monophosphate during cerebral global transient ischemia in rats.

Experiments were conducted to evaluate the effects of desmethyl tirilazad (10 mg/kg, i.p.), a 21-aminosteroid, on constitutive nitric oxide synthase (cNOS) activity and cyclic guanosine monophosphate (cGMP) levels in brain homogenates of rats subjected to cerebral global transient ischemia induced by bilateral clamping of the carotids for 30 minutes and reduction of arterial pressure (to 50-60 mmHg) by intravenous infusion of 1.5 ml of a solution of trimethaphan (5 mg/ml). Our results show that ischemia induces a rise in cNOS activity (from 62.0 +/- 6.1 to 133.3 +/- 13.3 pmol/min/mg protein) and cGMP levels (from 459.3 +/- 49.6 to 1074.1 +/- 132.1 fmol/mg protein). Pretreatment with desmethyl tirilazad abolishes these increases. These results are in agreement with the neuroprotective efficacy of desmethyl tirilazad in cerebral ischemia.

Animals↗
PubMed1981

Catecholamine-associated refractory hypertension following acute intracranial hemorrhage: control with propranolol.

Seven patients (4 with subarachnoid hemorrhage, 2 with intracerebral hemorrhage, and 1 with massive cerebral infarction) had acute arterial hypertension refractory to control by several antihypertensive drugs (hydralazine, sodium nitroprusside, alpha-methyldopa, and trimethaphan camsylate) used singly or in combination. In each case, catecholamine excretion--measured by urinary norepinephrine plus epinephrine--was markedly elevated, averaging 218 microgram/day. Patients without the acute refractory hypertension had normal or only slightly elevated urinary catecholamine levels (mean, 72 microgram/day). The beta-adrenergic blocking agent propranolol, in doses between 20 and 40 mg every 6 hours, successfully controlled blood pressure, while other agents failed. The intense sympathetic nervous system discharge resulting in acute refractory hypertension may be due to injury to the diencephalon or brainstem (or both) or to diffuse brain dysfunction from increased intracranial pressure or intracranial blood.

Adult↗
PubMed1988

Aldosterone response to metoclopramide is mediated through the autonomic nervous system in man.

This study primarily examines the role of the autonomic nervous system in the aldosterone response to metoclopramide since there is conflicting evidence as to the involvement of a dopaminergic mechanism in this response. Six normal male volunteers in metabolic balance at 100 mmol sodium/day and 60 mmol potassium/day constant intake received metoclopramide, 10 mg i.v., on five different occasions. The dosing was either metoclopramide alone or combined with ganglionic, muscarinic, beta-adrenergic or calcium-channel blockade. Metoclopramide increased serum aldosterone significantly to 163.3% of basal level at 10 min. Atropine blunted this response and the 10 min level was significantly reduced to 116.03% of the basal value. The highest aldosterone levels were attained when metoclopramide was administered during a trimethaphan infusion and a peak of 292.8% of basal level occurred at 90 min. In the presence of atenolol, with or without nifedipine, the metoclopramide-induced aldosterone response was significantly greater at 15 min than with metoclopramide alone. The results of this investigation suggest that the aldosterone response to metoclopramide is mediated by acetylcholine released from post-ganglionic cholinergic nerve terminals, and that an adrenergic mechanism exerts a tonic inhibitory influence on aldosterone secretion in man.

Adult↗
PubMed1991

Effect of ketanserin on cerebral blood flow autoregulation in healthy volunteers.

The effect of a clinically relevant dose of ketanserin (10 mg as a bolus followed by an infusion of 6 mg/h) on cerebral blood flow (CBF) and CBF autoregulation was examined in 12 healthy volunteers. Changes in CBF were estimated by the cerebral arteriovenous-oxygen saturation difference method, while mean arterial blood pressure (MABP) was increased by norepinephrine and decreased by ganglionic blockade (trimethaphan camphosulphonate) combined with lower body negative pressure one hour after the infusion of ketanserin. During ketanserin infusion, MABP fell insignificantly by 2.5 mmHg (6 to -2), while CBF rose insignificantly by 5 ml/100 g/min. Autoregulation was preserved in all volunteers. CO2-correction factors from 0 to 4.6% CBF/0.1 kPa were used. The lower limit of CBF autoregulation was 82 mmHg (80-86) with an SE of 3 mmHg (1-5) similar to a previous control group of healthy volunteers. Aside from a major decrease in MABP in one subject, no adverse side effects were observed. The present study shows that CBF autoregulation is maintained during ketanserin infusion.

Blood Flow Velocity↗
PubMed1993

Electroencephalogram spectral edge frequency, lower esophageal contractility, and autonomic responsiveness during general anesthesia.

Both the electroencephalogram (EEG) spectral edge frequency (SEF) and lower esophageal contractility (LEC) indices have been reported to be useful indicators of anesthetic depth. We designed a prospective study to evaluate the relationship between changes in these two variables and objective measurements of physiologic responsiveness to surgical stress (i.e., changes in hemodynamic variables and plasma levels of norepinephrine, epinephrine, total catecholamines, and vasopressin). Eighty-nine consenting adult males undergoing radical prostatectomy procedures under a standardized general anesthetic technique were studied according to a randomized, single-blinded protocol. General anesthesia was induced with 30 micrograms/kg intravenous (i.v.) alfentanil, 2.5 mg/kg i.v. thiopental, and 0.1 mg/kg i.v. vecuronium, and subsequently maintained with 0.5 microgram/kg/min alfentanil, nitrous oxide (N2O) 67% in oxygen, and 0.8 microgram/kg/min vecuronium. Following retropubic dissection, 81 patients (92%) manifested acute hypertensive responses, with mean arterial pressure increasing from 90 +/- 14 to 122 +/- 14 mm Hg (mean +/- SD). This acute hypertensive response was treated with one of three different treatment modalities (20 to 60 micrograms/kg i.v. alfentanil, 0.5 to 2.0% inspired isoflurane, or 0.05 to 0.15 mg/kg i.v. trimethaphan) to return the mean arterial pressure to within 10% of the preincisional (baseline) value within 5 to 10 minutes. Although the mean arterial pressure, heart rate, and plasma levels of catecholamines and vasopressin significantly increased following the surgical stimulus, and decreased after adjunctive therapy, the EEG-SEF and LEC index (LECI) values did not significantly change during these study intervals. Furthermore, using a logistic regression analysis, we observed that preincision EEG-SEF and LECI values could not predict whether patients would manifest a hypertensive response. Therefore, the EEG-SEF and LECI were unreliable indicators of anesthetic depth.

Aged↗
PubMed1976

Cardiac effects of succinyldicholine and succinylmonocholine.

The present study evaluated possible contribution of succinylmonocholine in producing serious cardiovascular effects with or without succinyldicholine, using albino rabbits as the experimental animal. Forty-eight experiments were performed, 22 in vivo and 26 in vitro (Langendort heart). Succinyldicholine and succinylmonocholine administered separately or together produced an immediate bradycardia in vivo as well as in vitro. The combination of these drugs had a direct arhythmogenic effect as well as an indirect reflux mediated cardiac effect. When succinyldicholine was given within five minutes following a dose of succinylmonocholine there was significant nodal and ventricular ectopic beats, but no bradycardia. Dysrhythmias in in vivo hearts were abolished by cord trans-section, trimethaphan and reserpine pretreatment. There was no evidence in vivo that succinylmonocholine produced more serious bradycardia, dysrhythmias or hypotension than succinyldicholine,

Animals↗
PubMed1990

The effects of prolonged controlled hypotension induced by prostaglandin E1 on renal tubular function.

The effects of the prolonged 3-hour and 6-hour controlled hypotension induced by prostaglandin E(1) (PGE(1)) on renal tubular function have been comparatively studied with trimethaphan (TMP; 3-hour hypotensive anesthesia) and enflurane deep anesthesia (6-hour hypotensive anesthesia), using the urine N-acetyl-Beta-D-glucosaminidase (NAG index) and the serum and urine Beta(2)-microglobulin (fractional clearance of Beta(2)-m; Fc-Beta(2)-m) as markers. During 3-hour and 6-hour controlled hypotension PGE(1), NAG index and Fc-Beta(2)-m and urine volume could be maintained without remarkable changes. In the group with TPM, NAG index and Fc-Beta(2)-m significantly increased. The increasing trend was also noted over time in deep anesthesia with enflurane. On 1st postoperative day, Fc-Beta(2)-m significantly increased in PGE(1) group in both 3-hour and 6-hour hypotensive anesthesia, whereas it restored to normal on 2nd postoperative day. Also, in TMP and enflurane deep anesthesia, Fc-Beta(2)-m significantly increased on 1st postoperative day. With the latter, significant increase was also observed on 2nd postoperative day. These results suggest that, in 3-hour and 6-hour controlled hypotension induced by PGE(1), renal tubular function is normally maintained and that it is useful for prolonged controlled hypotensive anesthesia. However, further study is necessary because tubular dysfunction might appear on 1st postoperative day.

Journal Article↗
PubMed1975

Current therapy of hypertension. A pharmacologic approach.

Adequate treatment of hypertension requires that the physician understand the pharmacologic actions of antihypertensive agents. Although no drug is without adverse reactions, it should be possible to choose an agent or combination of agents which can effectively lower blood pressure and be tolerated by the patient. The indications, proposed mechanisms of actions and adverse effects of the following antihypertensive drugs are discussed: thiazide diuretics, spironolactone, triamterene, trimethaphan, Rauwolfia alkaloids. guanethidine, bethanidine, methyldopa, clonidine, pargyline, propranolol, hydrazaline, minoxidil, guancydine, diazoxide and sodium nitroprusside.

Adrenergic alpha-Antagonists↗