Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of antihypertensive drugs, such as nifedipine, chlorpromazine, reserpine and thiopental on mean arterial blood pressure (ABP), mean intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were studied in 43 patients with systemic hypertension and intracranial hypertension due to hemorrhagic cerebrovascular diseases and other causes. These drugs are commonly used in neurosurgical practice for the treatment of systemic hypertension. Nifedipine, chlorpromazine and reserpine reduced the mean ABP, raised the mean ICP and decreased the CPP. The effects of these drugs on mean ICP and CPP were more pronounced in patients with severely increased ICP (more than 40 mmHg) than in patients with moderately increased ICP (20-40 mmHg). Thiopental reduced both mean ABP and ICP, whereas the CPP was unchanged from the preadministration level. During thiopental administration, however, respiratory depression was observed, and hence, intubation and ventilation were required. We suggest that, in the treatment of systemic hypertension in patients with increased ICP, barbiturates are more desirable than agents with calcium channel or alpha-adrenergic blocking actions, despite the problem of respiratory control.
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PMID:Effects of antihypertensive drugs on intracranial hypertension. 195 Feb 24

The goal of this study was to examine the hypothesis that intravenous anesthetic induction agents alter neuroregulation of the cardiovascular system. Additional goals were to investigate this in an animal model devoid of other drug effects. Healthy mongrel dogs had arterial catheters inserted and pneumatic occluders positioned around the thoracic aorta and inferior vena cava. After 10 to 14 days of recovery, neurocirculatory control mechanisms were assessed in the absence of anesthesia by recording changes in the RR interval of the electrocardiogram in response to alterations in systolic arterial pressure. Systolic pressure was manipulated over a range of 65 to 200 mm Hg by random occlusion of either the inferior vena cava (hypotension) or aortic (hypertension) occluders. The animals were then given bolus doses of either thiopental (20 mg/kg), diazepam (2 mg/kg), ketamine (5 mg/kg), or etomidate (1.2 mg/kg) on separate days and in random order. The arterial pressure alterations were repeated 3, 10, and 20 minutes after the drugs were given. Regression curves were calculated expressing the slope relation between RR interval and systolic pressure at awake control and each time point after drug administration. The responses were compared with control by repeat measures analysis of variance. Thiopental significantly decreased this slope relation for 10 minutes. Diazepam decreased this slope at 3 minutes only. Ketamine, like thiopental, decreased this slope for 10 minutes. Following etomidate, the slopes were similar to control. We conclude that thiopental, diazepam, and ketamine impair neurocirculatory control capabilities. The effect of diazepam is only transient, whereas that of thiopental and ketamine is longer, and etomidate does not affect these reflexes.
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PMID:Effect of anesthetic induction agents on cardiovascular neuroregulation in dogs. 249 6

It is estimated that between 1971 and 1987 the number of carotid endarterectomies has increased from 15,000 to over 85,000 per year. Unless the procedure can be performed safely with a combined morbidity and mortality which is below the yearly risk of stroke (5%) for patients with symptomatic carotid artery disease, one should reconsider this operation as a therapeutic option. We review our experience with 891 carotid endarterectomies performed between January 1979 and June 1987. There were 579 (65%) men and 312 (35%) women of ages from 34 to 82 (median 65); risk factors included diabetes mellitus 213 (14%), hypertension 603 (68%), and smoking 630 (70%). Clinical presentation consisted of transient ischemic attacks 506 (57%), cerebral infarction with minimal neurological residual 252 (28%), stroke in evolution 3 (0.3%) and, asymptomatic stenosis 130 (15%). All patients were operated on under endotracheal anesthesia with transoperative monitoring of intra-arterial pressure, central venous pressure and arterial blood gases. Thiopental (3-5 mg/kg) and lidocaine (1 mg/kg) were given for induction and at 15 minute intervals during carotid cross-clamping. Intraluminal shunts were used in 13 (2%). A conventional (open) endarterectomy was performed in 561 (63%) and a limited endarterectomy (closed) in 330 (37%). Complications included 11 (1%) deaths, 26 (3%) developed a major neurological deficit that persisted, 30 (3%) had perioperative TIA's which resolved completely. Of the patients with preoperative neurological deficits, 33 (4%) recovered. Therefore, at one month after surgery, 854 (96%) were either as well or better than preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pitfalls during carotid endarterectomy. 284 25

We studied the effects of nifedipine, chlorpromazine, reserpine, furosemide, and thiopental on the mean arterial blood pressure, mean intracranial pressure, and cerebral perfusion pressure in 38 patients with increased intracranial pressure resulting from either hemorrhagic cerebrovascular disease or systemic hypertension. These agents are widely used in neurosurgical practice for the treatment of systemic hypertension. Patients were assigned to two groups on the basis of their mean intracranial pressure. Group I comprised 20 patients with a mean intracranial pressure of 20-40 mm Hg (moderately increased ICP group), and Group II consisted of 18 patients with a mean intracranial pressure of greater than 40 mm Hg (severely increased ICP group). Nifedipine, chlorpromazine, and reserpine reduced mean arterial blood pressure by 18-20% in both groups (p less than 0.05 in each). In Group I these agents raised mean intracranial pressure by 10-35% and decreased cerebral perfusion pressure by 20-32% (p less than 0.05 for both), but in Group II these changes were more marked: mean intracranial pressure increased 38-64% and cerebral perfusion pressure decreased 40-54% (p less than 0.01 for both). Furosemide did not significantly reduce mean arterial blood pressure but slightly reduced mean intracranial pressure in each group. Thiopental reduced both mean arterial blood pressure and intracranial pressure in both groups. The effect on intracranial pressure was pronounced in Group II, in which mean arterial blood pressure fell by 18% (p less than 0.05) and mean intracranial pressure decreased 50% (p less than 0.01), whereas in Group I mean arterial blood pressure was reduced by 16% and mean intracranial pressure dropped 23% (p less than 0.05 in each).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of systemic hypertension and intracranial hypertension in cases of brain hemorrhage. 335 14

We report the effect of 250 mg of sodium thiopental on vascular tone at constant blood flow in 26 patients undergoing cardiopulmonary bypass while the ascending aorta was cross-clamped. Light anaesthesia was effected with fentanyl and enflurane, muscle relaxation with pancuronium. After a latent period of 10.5 +/- 0.7 s there was a hypertensive response of 9.8 +/- 0.5 s duration and of 21.4 +/- 1.7 mmHg (2.8 +/- 0.2 kPa) magnitude; this was followed by hypotension of 39.6 +/- 4.2 s duration and of 18.4 +/- 1.9 mmHg (2.4 +/- 0.3 kPa) magnitude. There was a statistically significant inverse correlation between the hypertension and body temperature (P = 0.005); the time to onset of hypertension correlated directly with pump volume (P = 0.001), weight of the patient (P = 0.03), and cross-clamp time before the drug was given (P = 0.002), and correlated inversely with the serum sodium concentration (P = 0.001). The duration of hypertension was inversely related to the plasma bicarbonate (P = 0.01) and body temperature (P = 0.04). The duration of hypotension was significantly longer in women (P = 0.0001) and was directly related to the duration of cross-clamping (P = 0.0007), to pH (P = 0.0016), and to PCO2 (P = 0.04). We speculate that thiopental induced the hypertensive response due to a potentiation of the vasoconstrictive (local) effect of norepinephrine, and induced the hypotensive response by a central nervous system effect. Thiopental had no apparent effect on venous tone.
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PMID:Hypertensive response to thiopental in man during cardiopulmonary bypass. 381

Barbiturate therapy is a controversial mode of therapy instituted in patients with acute head injuries after conventional means of treatment to decrease intracranial hypertension have been unsuccessful. Thiopental is a fast-acting central nervous system depressant and is one of the agents used for barbiturate therapy. Baseline laboratory values and access to four IV sites, including a Swan-Ganz catheterization site, should be obtained prior to institution of barbiturate therapy. While a patient is on barbiturate therapy, it is difficult to assess his clinical status. Nursing care for a patient on barbiturate therapy is an exciting challenge. It is the nurse's responsibility to continuously assess the patient's pressure readings, laboratory values, fluid balance, and pulmonary status to accurately interpret his clinical status.
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PMID:Nursing management for barbiturate therapy in acute head injuries. 654 36

The cardiopulmonary effects and tendencies to produce ventricular arrhythmias were evaluated in 13 dogs given a surgical plane of anesthesia by thiopental (IV) or a combination of thiopental and lidocaine (IV). Thiopental (22 mg/kg of body weight) was compared with a combination of thiopental (11 mg/kg) and lidocaine (8.8 mg/kg). Preanesthetic agents were not given. Both methods for IV anesthesia provided a smooth induction suitable for easy intubation. The thiopental/lidocaine combination had a shorter duration, produced no arrhythmias, and resulted in less cardiopulmonary depression than did thiopental alone. Bigeminy developed after intubation during 19 of 20 thiopental inductions as compared with that in 0 of 22 thiopental/lidocaine inductions. The bigeminies were preceded by systemic hypertension and tachycardia which developed as the trachea was being intubated. The increase in aortic pressure and heart rate was minimal after intubation during the thiopental/lidocaine inductions. Five minutes after administration of thiopental alone, increases in heart rate, aortic pressure, total peripheral vascular resistance, and left ventricular systolic and end-diastolic pressures were observed. When these increases in rate, preload, and afterload were considered in relation to a stabile maximum positive first derivative of left ventricular pressure, left ventricular contractility was considered to be decreased. Mild respiratory acidosis and hypoxemia were present at 5 and 10 minutes after thiopental induction. Because the combination of thiopental/lidocaine had less cardiopulmonary depressive effects and protected against arrhythmias, it would appear to be a good method for anesthetic induction of the patient with cardiopulmonary disease. In the patient with normal cardiopulmonary function, thiopental produces only a moderate and reversible depression.
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PMID:Cardiopulmonary effects of thiopental/lidocaine combination during anesthetic induction in the dog. 682 18

Using two infusion anaesthesiamethods for laryngomicroscopy in 187 non-selected patients we studied the recovery phase with the aid of a special questionnaire filled in by the recovery room nurse. Premedication was with Thalamonal and atropine. Muscle relaxation was achieved by a succinylcholine drip. Induction doses: fentanyl 0.05-0.1 mg and thiopental 3-5 mg/kg bodyweight (Th-group) or diazepam 10-20 mg and ketamine 1 mg/kg bodyweight (K-group). Infusion doses: Thiopental 11.7 mg/min. (Th-group) or diazepam 0.2 mg/min. and ketamine 2 mg/min (K-group). Anaesthesia lasted for 20-30 min. We observed and noted during recovery: Breathing, cough-frequency and -quality, alertness, reaction to speech and stimulation, orientation, motor behaviour and well-being. Anaesthesia was sufficient in both groups. The patients of the K-group woke up earlier and their laryngeal reflexes seemed to stabilize quicker than in the Th-group. Because of the elevation of blood pressure caused by the stimulation of the laryngoscopy both methods are not recommended for patients at risk from high blood pressure.
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PMID:[Recovery after ketamine-diazepam and thiopental-fentanyl-infusion anesthesia with jet-ventilation for laryngomicroscopy]. 685 95

Since 1970 we have investigated postischemic anoxic encephalopathy and potential treatments for cerebral resuscitation after cardiac arrest by cardiopulmonary-cerebral resuscitation (CPCR). The post-resuscitation syndrome has been studied at the levels of cell, organ, organism and community. Short-term and long-term models in rats, dogs, and monkeys have been developed, and an international multicenter randomized clinical trial mechanism was established. Clinical studies disproved the 5-min limit of reversible cardiac arrest and yielded other valuable data on treatments and prognostication. Thiopental loading or calcium entry blocker therapy (lidoflazine) gave no significant improvement in patients. Free radical scavengers are under investigation in the laboratory. We hypothesize that post-arrest perfusion failure and necrotizing cascades require etiology-specific combination treatments. Standard (control) therapy in a current dog model of cardiac arrest (no flow) of 12.5-20 min, reperfusion with cardiopulmonary bypass, and intensive care for 72-96 h has consistently resulted in survival with brain damage. After ventricular-fibrillation (VF) arrest of 17 min, moderate hypothermia (28-32 degrees C) inconsistently improved cerebral outcome. After VF arrest of 12.5 min, hypertension plus hemodilution normalized the local (multifocal) cerebral hypoperfusion post-arrest and, again, inconsistently improved cerebral outcome. Additional mild hypothermia (34-36 degrees C), however, consistently improved cerebral outcome, whether induced before or during and after arrest.
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PMID:Systematic development of cerebral resuscitation after cardiac arrest. Three promising treatments: cardiopulmonary bypass, hypertensive hemodilution, and mild hypothermia. 842 45

This study was conducted on 10 pediatric patients in whom intracranial hypertension stemming from head injury was reduced by high-dose thiopental administered for a prolonged period. All children showed a favorable recovery of their neurological functions. The total dose normalized to body weight averaged 335 +/- 135 mg/kg, and the mean treatment duration was 93.0 +/- 37.1 h. Data analysis was modeled for each patient to cover all the doses on the whole plasma thiopental concentration-time curve, according to a one-compartment open model. A better fit was obtained using a linear model rather than a Michaelis-Menten elimination model. Model selection was guided by evaluation of the minimum objective function, the weighted residuals, and the Akaike criterion. Thiopental pharmacokinetic parameters in pediatric patients were compared with those determined in an adult control group with similar total doses and durations of treatment. No significant difference was found between the two groups in spite of a 33% decrease of the elimination half-life in children (11.7 +/- 5.7 h) compared with adults (17.5 +/- 9.03 h). The mean values obtained were 2.42 and 2.19 ml/min/kg for total clearance and 2.18 and 2.90 L/kg for Vd in pediatric and adult groups, respectively. The linear regression of pharmacokinetic parameters in terms of age was not significant. When high doses of thiopental were administered over a prolonged period, the pharmacokinetic parameters computed for pediatric patients did not differ from those obtained in adults.
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PMID:Pharmacokinetics of high-dose thiopental in pediatric patients with increased intracranial pressure. 902 49


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