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

In the past few years, echocardiography has emerged as a useful noninvasive clinical tool in cardiac diagnosis. Conventional methods for analyzing echocardiographic data involve time consuming and tedious manual techniques for measuring various distances and computing cardiac parameters of interest. This paper describes a useful method for automating the analysis of M scan echocardiograms both for routine clinical work as well as for special research oriented ultrasonic cardiac studies. Using a GRAF/PEN digitizer interfaced to a PDP-11 minicomputer system, relevant points of the ventricular and mitral valve interfaces, R-R intervals, and time and distance calibration points are entered from hard copies of M scan echocardiograms. The computer then determines all the parameters of interest such as left ventricular (LV) diameters, LV volumes, LV mass, ejection fraction, stroke volume, cardiac output, septal and posterior wall dynamics, as well as such mitral valve (MV) parameters as opening/closing velocities, excursions, and areas subtended by both MV leaflets. The data and results are stored on disc or tape and a report of the results is immediately available from a printer for incorporation into the patient's record file.
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PMID:Digital computer analysis of M-scan echocardiograms. 81 16

Cervical spinal cord stimulation (cSCS) has been employed as a treatment for intractable pain for the past 20 years. Recently, we reported that cSCS increased regional cerebral blood flow (rCBF) in cats and humans. The present study was designed to examine the effects of cSCS on experimental cerebral strokes, using a cat middle cerebral artery occlusion model (MCAO). A total of 31 cats were randomly assigned to three groups; Group 1: control, Group 2: sham operation, Group 3: cSCS. Mortality of the control group was 92% as long as 4 days after MCAO. Groups 2 and 3 showed a prolongation of survival rate (44% and 56%, respectively). CSCS reduced the rate of death within 24 hours after MCAO. There was no alteration of infarct size, which was estimated by the TTC method and measured by computer technique (PDP-11/23), was found in dead cats of all groups. In cats that survived in Group 3, however, drastic prevention of an infarct progression was found, compared to Group 2. The results provide a clinical application of cSCS for stroke patients, although no evident mechanism was obtained.
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PMID:The effects of cervical spinal cord stimulation (cSCS) on experimental stroke. 247 58

Studies were made of the effects of two doses of minoxidil (3 mg/kg), given 24 hours apart, on cardiovascular hemodynamics, regional myocardial blood flow, and cardiac morphology in beagle dogs. Minoxidil caused increases in mean right atrial and left ventricular end-diastolic pressure. Systemic and pulmonary vascular resistance were reduced; cardiac output was increased. Left ventricular stroke work and the systolic pressure time index were unchanged by monoxidil administration. The diastolic pressure time index and ratio of diastolic/systolic pressure time index were decreased by minoxidil. Regional myocardial blood flow, measured with radioactive microspheres, increased in all regions of the heart except to the left ventricular papillary muscles. Minoxidil increased blood flow to left ventricular subendocardial tissue; however, this increase was significantly less than that observed in corresponding areas of subepicardial tissue, thus reducing the subendocardial/subepicardial tissue blood flow ratio. These results suggest that minoxidil is an effective peripheral vasodilator but may result in inadequate subendocardial perfusion. Morphologic studies disclosed two types of minoxidil-induced cardiac lesions: left ventricular papillary muscle necroses, and hemorrhagic lesions which were most prominent in right atrium and were associated with inflammation, intramural hemorrhage, and fibrinoid necrosis of small arteries. The papillary muscle necrosis were attributed to hypoxia. The atrial lesions were not of ischemic or hypoxic origin, because minoxidil did not decrease blood flow to atrial tissue. It is suggested that the atrial lesions are related to excessive vasodilation.
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PMID:Influence of minoxidil on myocardial hemodynamics, regional blood flow, and morphology in beagle dogs. 315 33

Minoxidil in combination with propranolol and diuretics was used in the treatment of 41 patients with severe refractory hypertension due to a spectrum of causes. These etiologies included essential hypertension, advanced renal failure, renovascular hypertension, and kidney transplant rejection. All patients had evidence of renal and cardiac damage prior to therapy and had failed to respond to all standard medications. The study included patients treated for periods of 3--42 months. Forty of the 41 patients responded most impressively to this therapy. Minoxidil was given in a dose of 7.5--40 mg daily. No tolerance to minoxidil was observed. Side effects were minimal. Three myocardial infarcts were observed. Two of these patients had had previous infarcts. One patient suffered a fatal cerebrovascular accident after he had deliberately stopped all medications. Nine patients showed sodium retention, which was easily controlled in 8 cases. Mild hirsutism was occasionally seen. Mean serum creatinine levels showed a slight decrease in the essential hypertension group after treatment. Best long-term results were seen in the essential hypertension and renovascular groups, although several cases with advanced renal disease and with kidney transplant rejection hypertension showed very impressive and encouraging outcomes.
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PMID:Minoxidil in the treatment of refractory hypertension due to a spectrum of causes. 615 48

A method of determining the regional cerebral blood flow with the use of gamma-chamber is described, and the results of using this method for examining the changes of the flow in two patients with cerebral hemorrhage of various intervals after surgical elimination of hematoma are presented. The mean regional cerebral flow in a whole hemisphere, and the regional cerebral flow in 10 zones with projections to particular anatomic structures are determined. The isotope clearance curves were processed on a PDP/8E mini-computer. The magnitudes of the cerebral blood flow were calculated by the stochastic two-component and the initial inclination methods. The cerebral flow examinations revealed substantial changes in the patients' cerebral hemodynamics. The results obtained may be of importance for developing pathogeneticaly substantiated therapy of patients who have a cerebral stroke.
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PMID:[Quantitative determination of regional cerebral blood flow using a gamma camera]. 743 48

We used echocardiography to investigate the changes in the cardiac function of dogs treated with minoxidil (a vasodilator, administered at doses which can produce mild lesions in the myocardium of the left ventricle) and quinidine (an antiarrhythmic at doses up to 8 times the upper limit of the therapeutic range in dogs). Groups of three beagles received a single administration of minoxidil at doses of 0.5 or 2 mg/kg. Two groups of two dogs received a single administration of quinidine at doses of 80 or 160 mg/kg. Two groups of three control dogs were treated concurrently with the vehicle alone. M-mode echocardiography was performed under two-dimensional echocardiography guidance on three occasions the day before treatment, immediately before dosing and 1, 3 and 24 h after dosing. We measured or calculated end diastolic, end systolic, and stroke volumes (EDV, ESV and SV), fractional shortening (FS), ejection fraction (EF), the percentage of thickening of the septum and of the left ventricle posterior wall (PST and PWT), and the mean and maximal velocities of the left ventricle posterior wall (PWVm and PWVM). At the same time as echocardiography recording, heart rate was measured by cardiac auscultation. Minoxidil produced a marked tachycardia. Less marked increases in heart rate occurred after quinidine. Both compounds were associated with a decrease in ESV and with marked increases in FS, EF, PWVm and PWVM which, in comparison with data for controls, are indicative of an increase in the amplitude and velocity of cardiac contraction. Both drugs also produced a decrease in EDV and consequently there was no increase in SV despite the increased amplitude of ventricular contraction. Cardiac output increased in proportion to the increase in heart rate. Overall, the effects were dose-related and are consistent with the pharmacological properties of the compounds. However, to date these effects have been demonstrated only by invasive methods. To conclude, we have shown that echocardiography allows a non-invasive investigation of the cardiac effects of suprapharmacological doses of antiarrhythmics and of the changes in heart function induced by vasodilators known to cause left ventricular lesions in dogs.
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PMID:Echocardiography, a non-invasive method for the investigation of heart morphology and function in laboratory dogs: 2. Effects of minoxidil and quinidine on the left ventricle function. 958 1

Doppler and M-mode echocardiography (EC) were used to investigate the effects of minoxidil on the cardiac function of the dog and potentially to clarify the pathogenesis of cardiac lesions, in particular the necrotic lesion in the left ventricle and the haemorrhagic lesion in the right atrium. Groups of three dogs were treated with a single oral dose of 0.5 or 2 mg/kg minoxidil or control vehicle, and M-mode and Doppler parameters were recorded at different time points before as well as 1, 3 and 24 h after treatment. The treatment produced a number of changes in M-mode parameters that indicate an increase in left ventricle contractility, in particular, increases in the percentage of thickening of the left ventricle wall during systole and in ejection fraction, and decrease of systolic volume. There was also a decrease in diastolic volume, which indicates a decrease in filling of the left ventricle probably due to the tachycardia and subsequent decrease in inter-systolic time. Doppler EC showed an increase in the velocity of the aortic flow, which indicates an increase in cardiac contractility. There was also a mild increase in stroke volume, which together with the tachycardia resulted in a marked increase in cardiac output. Together, Doppler and M-mode recordings gave evidence of an increase in the contractility of the left ventricle. This change is consistent with the generally accepted mechanism for the development of the left ventricle lesion induced by minoxidil. Minoxidil also produced changes in atrio-ventricular flows. The velocity and/or acceleration of E- and A-waves of the mitral and tricuspid flows increased, and the E/A ratio decreased. The changes in the E-wave indicate a faster diastole of the ventricle probably to compensate for the decrease in inter-systolic time. The changes in A wave are characteristic of an increased amplitude and velocity of the atrial contraction. This latter change is much more marked for tricuspid than for mitral flow. For both flows the E/A ratio decreased, which indicates that the contraction of the atria plays an increased role in ventricle filling after minoxidil treatment. This stimulation of atrial contraction that we evaluate with Doppler EC may play a key role in the development of the atrial lesion produced by minoxidil. The fact that the change is more marked in the right than in the left atrium may explain why the lesion occurs only in the right atrium in dogs. This study showed, therefore, that Doppler EC associated with M-mode EC is a useful method for obtaining pertinent information on the pathogenesis of the left ventricle lesion induced by haemodynamic mechanisms. Moreover, Doppler EC allowed the assessment of changes in the function of the right atrium that may be involved in the development of the right atrial lesion.
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PMID:Use of M-mode and Doppler echocardiography to investigate the cardiotoxicity of minoxidil in beagle dogs. 1293 90

Minoxidil is a direct-acting peripheral vasodilator for the treatment of symptomatic hypertension, or refractory hypertension associated with target organ damage, that is not manageable with a diuretic and two other antihypertensive drugs. The most frequent adverse events associated with minoxidil include hypertrichosis and cardiovascular events related to its powerful antihypertensive effect, and less frequently, rashes, bullous eruptions, and Stevens-Johnson syndrome (SJS). Evidence suggests that SJS and toxic epidermal necrolysis (TEN) are variants of a single disease with common causes and mechanisms, but differing severities. Epidermal detachment is mild in SJS, moderate in overlap SJS-TEN, and severe (> 30% of body surface area) in TEN. We describe a case of minoxidil-associated SJS that evolved into fatal TEN. A 69-year-old African-American woman with a history of chronic kidney disease was admitted to the hospital for a cerebrovascular accident and uncontrolled hypertension. On hospital day 12, oral minoxidil was added to her drug regimen. On day 23, she developed a maculopapular rash on her face that gradually diffused to her chest and back. Vesicles and papular lesions extended to her extremities and mucosal membranes; results of a skin biopsy revealed SJS. A positive Nikolsky's sign (blisters spread on application of pressure) was detected. On days 27-31, diffuse bullae developed with rash exacerbation. Skin detachment exceeded 30% and was consistent with TEN. The patient died on day 39. An evaluation of the causality and time course suggested that minoxidil was the most likely culpable drug, with a Naranjo adverse drug reaction probability scale score indicating that the likelihood of the association was possible (score of 3). The mechanism of this reaction has not been well elucidated. It may be related to an impaired clearance of the minoxidil metabolite, or an immune stimulation resulting in apoptosis and epidermis destruction. To our knowledge, this is the first case report of fatal TEN associated with minoxidil. This case report emphasizes the importance of monitoring for serious dermatologic reactions in patients receiving minoxidil therapy.
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PMID:Fatal toxic epidermal necrolysis associated with minoxidil. 1932 21

Minoxidil hair formulation is commonly used for the treatment of male or female androgenic alopecia. Minoxidil is a Health Canada and US FDA-approved medication for hair loss in men and women. The drug is marketed as 2% and 5% topical solutions. This over-the-counter product is considered safe, but should be used with caution. Furthermore, minoxidil is an orally active vasodilator for treatment of severe hypertension. Typical side effects of minoxidil are faster heart rate, augmented heart function and stroke volume (which can be associated with reduced vascular resistance upon baroflex stimulus), retained sodium and water and abnormal hair growth. The most common adverse reactions of the topical formulation are limited to irritant and allergic contact dermatitis on the scalp. Herein, we report a non-arteritic anterior ischemic optic neuropathy caused by topical 5% minoxidil treatment that was resolved after discontinuation of minoxidil.
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PMID:Could Topical Minoxidil Cause Non-Arteritic Anterior Ischemic Optic Neuropathy? 2765 41

Triclosan (TCS) has potentially toxic effects on humans and animals. However, the possible roles and mechanisms of TCS in endothelial cells (ECs) are still unknown. Abnormal damage to ECs and vascular function is a critical process in various cardiovascular diseases, including coronary artery disease (CAD), atherosclerosis, stroke, and hypertension. Hence, we explored the potential toxicological roles of TCS in EC functions. Cell Counting Kit-8, apoptosis, transwell, wound healing, and tube-formation experiments were performed to evaluate the effects of TCS on human umbilical vein endothelial cell (HUVEC) function. Additionally, the levels of PI3K, Akt, and mTOR phosphorylation were measured by Western blot. The results indicated that TCS treatment suppressed HUVECs viability, migration and angiogenesis. TCS treatment increased the expression of inflammatory markers and ROS in cultured HUVECs. Moreover, TCS treatment inhibited PI3K/Akt/mTOR expression. All of these results reveal that TCS induces notable vascular injury and affects the viability, migration and angiogenic capacity of HUVECs, at least in part via the PI3K/Akt/mTOR signaling pathway.
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PMID:Triclosan stimulates human vascular endothelial cell injury via repression of the PI3K/Akt/mTOR axis. 3161 11


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