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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous clinical studies establishing the efficacy of midazolam maleate (RO 21-3981), a new water-soluble benzodiazepine for induction of anesthesia, have not critically evaluated the effects of this agent on the cardiovascular system. The present study compares the cardiovascular effects of midazolam maleate and diazepam in conscious dogs. Systemic arterial, pulmonary arterial and central venous pressures, cardiac output, LVmax dP/dt, heart rate and regional coronary blood flow were measured 3 min following intravenous administration of diazepam (0.5, 1.0, and 2.5 mg/kg) or midazolam maleate (0.25, 1.0, and 10.0 mg/kg). Midazolam maleate increased heart rate 10--20 per cent with all three doses and decreased mean arterial blood pressure approximately 10--20 per cent at 1.0 and 10 mg/kg. Cardiac output was increased 10--12 per cent with all three doses of midazolam maleate, and LVmax dP/dt was decreased 13--16 per cent at the two higher doses. Diazepam at all three doses did not alter heart rate or mean arterial blood pressure. Diazepam, 1.0 and 2.5 mg/kg, produced significant (17 per cent) decreases in LVmax dP/dt, and 2.5 mg/kg produced a significant (10 per cent) increase in cardiac output. Neither drug in any dosage altered regional coronary blood flow, systemic or coronary vascular resistance, stroke volume, or stroke work. Maximum alterations in cardiovascular variables occurred with doses of midazolam maleate that are 10--15 times the recommended clinical induction dosage. It is concluded that in concentrations necessary for induction of anesthesia midazolam maleate has minimal effects on cardiovascular function.
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PMID:Cardiovascular responses to diazepam and midazolam maleate in the dog. 49 58

The effect of racemic mephobarbital and its optical isomers on survival time of mice exposed to 5% O2 was studied. There was an increase in survival time from 4.2 minutes to 12.6 minutes for 100 mg/kg of the anesthetically active (-) isomer and the racemic form, but no increase for 100 mg/kg of the inactive (+) isomer. Since it has been shown that there is no difference in brain concentrations between the isomers, we conclude that the barbiturate protective effect is bound to the anesthetic effect. All mice convulsed, and since the non-anesthetized animals convulsed earlier and stronger than the anesthetized, it was possible that barbiturate protection was accounted for by its anticonvulsant effects. Diazepam 7.5 mg/kg, while reducing convulsions to the same degree as barbiturates without producing anesthesia, only increased survival time to 6.2 minutes. Thus, the barbiturate protective effect is distinct from the anticonvulsant effect. It seems to be bound to a stereospecific receptor for both protection and anesthesia.
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PMID:Cerebral protection with barbiturates: relation to anesthetic effect. 64 7

In 30 patients with congenital or acquired heart disease the haemodynamic effects of diazepam (Valium) 0.3 mg/kg were investigated during surgical procedures under neuroleptanalgesia. The following parameters were measured or calculated: Heart rate (HR), arterial pressure (-Part, Psyst, Pdiast), pulmonary artery pressure (-PAP), right (-PRA) and left atrial pressure (-PLA), left ventricular pressure (PLV), left ventricular enddiastolic pressure (PLVED), left ventricular peak dp/dt (dp/dtmax), cardiac output (CO), cardiac index (CI), stroke volume (SV), stroke index (SI), total systemic resistance (TSR), total pulmonary resistance (TPR), work index of the right (RVWI) and left ventricle (LVWI). In comparison with a control group (n = 36) diazepam caused a decrease in arterial pressure cardiac index, stroke index, right and left atrial pressure and dp/dtmax. This, however, was mainly attributable to vasodilatation and not to a negative inotropic effect, which is of only minor importance with diazepam. These haemodynamic changes resulted in a reduction in myocardial oxygen consumption. Diazepam is a valuable drug in neuroleptanalgesia, when an increase in blood pressure can not be controlled by fentanyl or droperidol.
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PMID:[Diazepam (valium). Changes in haemodynamics, myocardial oxygen consumption and vascular tone (author's transl)]. 69 81

Diazepam was administered to ten patients with heart disease during diagnostic cardiac catheterization, in order to determine whether or not this drug's circulatory actions could alter results obtained during the procedure. Diazepam produced no change in baroreceptor sensitivity; however, there was a significant rise in heart rate and a significant fall in aortic systolic and left ventricular end-diastolic pressures. Cardiac index was unchanged, whereas stroke volume fell significantly. Systemic vascular resistance and peak left ventricular dp/dt did not change throughout the study. Clinical response in terms of sedation was judged to be satisfactory in eight patients, and no adverse effect on respiration was noted. Diazepam has little effect on basal circulatory and respiratory parameters when changes in these parameters are averaged for our ten patients. However, substantial changes in hemodynamic parameters did occur in several individuals, and such alteration in circulatory function must be considered when this agent is used routinely in patients having diagnostic cardiac catheterization.
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PMID:Circulatory effects of diazepam in heart disease. 99 59

Diazepam (0.1 mg. per kilogram) was given intravenously to 12 patients with hemodynamic left ventricular failure at the time of cardiac catheterization. Anxiety was effectively relieved in 10 patients. Systemic and coronary hemodynamic parameters were assessed before and 5 and 15 minutes after diazepam. Heart rate, cardiac index, and left ventricular stroke-work index did not change significantly. Mean aortic pressure decreased in all patients (average of 10 mm. Hg) and left ventricular end-diastolic pressure (LVEDP) decreased from a mean +/- S.E.M. of 24.3 +/- 3 mm. Hg at rest to 16 +/- 2.1 at 5 minutes (p less than 0.001) and 15.8 +/- 2.1 at 5 minutes (p less than 0.002). Left ventricular angiography performed 30 minutes after diazepam did not increase LVEDP above the pre-diazepam control value. Systolic ejection period and tension-time index also decreased significantly after diazepam. Coronary hemodynamics and myocardial metabolism were unaltered by diazepam. The fall in LVEDP induced by diazepam is probably secondary to a decrease in arterial pressure (afterload) possibly associated with a decrease in venous return (preload). Our data therefore suggest that diazepam exerts a beneficial action on depressed left ventricular function and, thus, may be a sedative agent of choice in patients with myocardial infarction and heart failure.
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PMID:Therapeutic implications of diazepam in patients with elevated left ventricular filling pressure. 127 25

Sixteen men with previously untreated diastolic blood pressure of 100-120 mm Hg were studied hemodynamically at rest supine and sitting and during a 100 W bicycle exercise. Blood pressure (BP) was recorded intra-arterially, and cardiac output (CO) by the dye-dilution method. After initial study, patients were treated with tiapamil in increasing doses (300-600 mg b.i.d., with a mean daily dose of 980 mg). The patients were restudied and then changed to felodipine (5-10 mg b.i.d., with a mean daily dose of 15 mg). Casual (cuff) BP at rest sitting was as follows: end placebo, 166/105 mm Hg; 1 year of tiapamil, 148/92 mm Hg; 1 year of felodipine, 139/86 mm Hg. Pretreatment hemodynamic results at rest sitting were as follows: BP, 169/105 mm Hg; MAP, 129 mm Hg; cardiac index (CI), 2.43 L/min/m2; total peripheral resistance index (TPRI), 4,305 dyn s/cm-5/m2. Both drugs reduced systolic (SAP), diastolic (DAP), and mean (MAP) arterial pressure significantly in all situations. BP reduction seemed to be more pronounced on felodipine than on tiapamil. Felodipine reduced MAP by 15% at rest supine, 14% at rest sitting, and 11% during exercise. The BP reduction was entirely due to reduction in TPRI (15, 16, and 13%, respectively). CI as well as stroke index (SI) and heart rate (HR) were unchanged. Tiapamil did not reduce TPRI significantly and the fall in BP was due to a combination fall in TPRI and CI.
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PMID:Chronic hemodynamic effects of tiapamil and felodipine in essential hypertension at rest and during exercise. 169 26

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

Propofol, in both its new oil-in-water emulsion and the former cremophor-EL solution, is known to produce significant decreases in arterial blood pressure. The aim of this study was to obtain a precise hemodynamic profile of anesthesia induction with propofol under conditions of daily routine (additional 70% nitrous oxide) and to evaluate the influence of (1) premedication with lormetazepam and (2) additional i.v. injection of fentanyl. Forty patients (ASA classes I and II) were randomly assigned to one of four groups (A, B, C, and D). Anesthesia was induced with a sleep dose of propofol (mean: 2.4 mg/kg) and the patient was ventilated with 30% O2 and 70% N2O via a face mask. In groups B and D, 3 micrograms/kg fentanyl were injected immediately prior to propofol injection. Patients in groups A and B received no premedication. Patients in groups C and D received 2 mg lormetazepam on the evening prior to the anesthetic and 1 mg 2 h prior to the anesthetic orally. The following parameters were determined immediately prior to induction of anesthesia and 1, 3, 5, 8, and 10 min after the start of the propofol injection: heart rate (HR), mean arterial blood pressure (MAP), mean pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary occlusion pressure (POP), cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR). In all four groups a slight decrease in HR and SVR occurred while a marked decrease in arterial blood pressure (SAP, MAP, DAP) and cardiac output was seen. PAP and preload pressures showed no significant changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics under propofol-nitrous oxide anesthesia: effects of premedication with lormetazepam and of additional fentanyl]. 289 30

In connection with a mass screening of the Bergen population 93 patients with essential hypertension and 48 normotensive controls were studied in 1965-66. Blood pressure (BP) was recorded intraarterially, cardiac output (CO), by dilution method, heart rate (HR) by ECG and oxygen consumption (VO2) by Douglas bag/Scholander technique. Studies were performed during rest and 50, 100 and 150 watt steady state exercise. The most important initial findings were: Although CO and HR were higher in the youngest hypertensive group (17-29 yrs) than in normotensive age matched controls VO2 was also increased and no true luxury perfusion was demonstrated. Exercise stroke index (SI) did not increase to the same level as in normotensives and total peripheral resistance index (TPRI) during exercise was increased. Cross-sectional data showed a reduction in SI and CI and an increase in TPRI with increasing age - at rest as well as during exercise. 10-year follow-up: 28 subjects initially below 40 years were completely untreated. During the first 10 years there was a fall in CI and SI of approximately 15% and TPRI increased by 20%. The same changes were seen at rest as well as during exercise. Resting blood pressure was practically unchanged. Nearly all patients greater than 40 yrs were treated. 20-year follow-up: Between the 10 year and 20 year follow-up DAP rose to 100 mmHg or more in most of the subjects less than 40 yrs and treatment had to be started. Generally diuretics, betablockers or a combination of the 2 were used. Before the 20 year follow-up, treatment was withdrawn for 2 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamics in essential hypertension at rest and during exercise--a 20-year follow-up study. 325 Mar 16

Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg.kg-1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP = 40 mm Hg increased from 60.0 +/- 4.8 mm Hg to 64.8 +/- 4.1 mm Hg (N = 4, p less than 0.02) and LVETI at LBNP = 20 mm Hg increased from 384.4 +/- 5.2 ms to 396.8 +/- 6.2 ms (N = 6, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human cardiovascular reactions to simulated hypovolaemia, modified by the opiate antagonist naloxone. 339 65


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