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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The energy metabolism of cardiac hypertrophy in spontaneously hypertensive rats (SHR) was studied chronologically by histochemical and in part chemical methods. The activities of various enzymes, such as glucose-6-phosphate dehydrogenase (G6PDH), lactate dehydrogenase (LDH), isocitrate dehydrogenase, succinate dehydrogenase, beta-hydroxybutylate dehydrogenase (beta-HBDH) and monoamine oxidase (MAO) in the cardiac muscle were determined histochemically. beta-HBDH activity was greatly increased in the stage of developing hypertension in SHR. LDH activity increased simultaneously with the rise of beta-HBDH activity. Moreover, MAO activity increased markedly in later stages when the blood pressure was already elevated in SHR. To confirm the histochemical findings of beta-HBDH activity, the mitochondrial fraction of cardiac muscle was subjected to chemical assay. The chemical findings of myocardial beta-HBDH in SHR corresponded well with the histochemical findings. The myocardial beta-HBDH activity in SHR increased markedly at the age of 5 to 9 weeks, while no or minimal activity was found in controls of the same age. No significant difference of beta-HBDH activity was observed between SHR and controls in the mitochondrial fraction from the diaphragm and liver. The increase of beta-HBDH activity in the cardiac muscle of SHR prior to the development of cardiac hypertrophy suggests that the metabolism of ketone bodies may play an important role in providing the energy necessary for the development of cardiac hypertrophy in SHR.
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PMID:Cardiac hypertrophy in spontaneously hypertensive rats. 12 86

Contractile responses to field stimulation of intramural nerves of arteries and veins taken from rabbits made hypertensive by partial constriction of the abdominal aorta have been related to the carotid artery pressure. The increase in contraction of cephalic and short saphenous veins with rise in carotid artery pressure can be accounted for by an increase in sensitivity of the alpha-adrenergic receptor. The neurogenic contraction of the ear artery increased with carotid artery pressure rise. Changes in some of the extraneuronal factors that influence transmitter distribution and disposition in the tunica media were examined. In hypertensive animals, the percentage of released adrenergic transmitter entering the vessel wall might be expected to decrease due to an increase in medial thickness. However, this percentage was not significantly altered in the ear artery probably due, in part, to a concomitant increase in medial permeability to the transmitter. Extraneuronal transmitter disposition factors, i.e. extraneuronal uptake, monoamine oxidase, and catechol-O-methyltransferase activity are directly related to the wet weight of the vessel wall. Thus, their contribution to transmitter disposition would be expected to increase with increase in vessel wall thickness and tend to reduce the response to sympathetic activity. As the contractile response increased in the hypertensive vessels despite such changes, the increase in effector cell mass and density of neuronal terminal plexus, shown previously to increase with hypertension, are more important than these other considerations.
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PMID:Changes in the contractile response of arteires and veins from hypertensive rabbits to sympathetic nerve activity: assessment of some postsynaptic influences. 18 Nov 4

Tranylcypromine (TCP) is a monoamine oxidase inhibitor used extensively in the treatment of patients with reactive depression. Hypertensive crisis can complicate drug therapy, but the mechanism through which TCP causes high blood pressure is unknown. The present study was undertaken because recent investigations have shown that TCP can inhibit production of a potent vasodilator hormone, prostacyclin (PGI2), by blood vessels, possibly explaining the mechanism of pressor effects by the drug. Heart rate, left atrial, pulmonary artery and aortic pressures were monitored in dogs under control conditions and continuously following the IV infusion of TCP at the rate of 1 mg/kg over a period of one minute. Right femoral and the left internal mammary arteries were obtained during the control period and the left femoral and right internal mammary arteries resected between 6 and 30 minutes following drug infusion for PGI2 studies. Concentrations of the drug that caused significant elevation of the mean systemic pressure to 203 +/- 8 mmHg had no inhibitory effect on PGI2 production. Therefore, the influence of TCP on the hemodynamic parameters does not appear to be mediated through the inhibition of vascular PGI2 synthesis.
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PMID:Tranylcypromine induced hypertension is not mediated by the inhibition of prostacyclin synthesis. 39 90

1 The role of monoamine oxidase (MAO) in the maintenance of deoxycorticosterone-sodium chloride (DOCA-salt) hypertension was investigated by assaying the MAO activity both in central as well as peripheral blood vessels and in brain tissue. 2 The results suggest that the activity of MAO in the DOCA-salt hypertensive rat is similar to the activity present in the normotensive rat.
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PMID:Brain and vascular monoamine oxidase activity in the deoxycorticosterone-salt hypertensive rat. 84 81

A review of the anesthesia literature outlines safe limits for use of epinephrine with halothane anesthesia and adequate ventilation. Excluded from the safe category are patients with previous cardiac disease, hypertension, patients taking monoamine oxidase inhibitors and reserpine. Considered as safe is 10 milliliters of 1:100,000 epinephrine in 10 minutes and not more than 30 milliliters of 1:100,000 epinephrine per hour.
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PMID:Safe use of epinephrine with halothane anesthesia. 88 20

A defect in the level of monoamine oxidase activity of platelets was observed in essential arterial hypertension. This defect seems dependent upon a lower rate of synthesis of the enzyme and not to the presence of an isoenzyme, as the net rate of return of the enzymatic activity after pargyline inhibition does not significantly differ between hypertensive and normotensive subjects.
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PMID:Monoamine oxidase defect in essential arterial hypertension. A single dose pargyline test. 97 92

Due to the rapid evolution of vascular lesions it is not surprising that most causes of sudden death of cerebral origin are due to vascular pathology. Of the traumatic causes extradural haemorrhage is a fairly common clinical entity but as a cause of death declining in its frequency. Sources of diagnostic error can be attributed to the fact that not all patients with extradural haematomas have marked external evidence of trauma and a significant number, particularly children and adolescents, show no radiological, clinical or for that matter, post-mortem evidence of a fracture. Subdural haematomas of a chronic variety are usually produced by minor trauma and occur predominantly in the older person. Acute subdural haematomas are most frequently the result of trauma and may be rapidly fatal due to the associated massive cerebral damage. That intracranial aneurysm or angioma may rupture into the subdural space and cause an acute or chronic subdural haematoma, is less widely appreciated. The acute spontaneous arterial subdural haematoma due to the rupture of a cortical vessel, usually one affected by atheroma, into the subdural space is an uncommon entity. It should be looked for specifically in patients with minimal trauma and the clinical picture of an acute subdural haematoma. Subarachnoid haemorrhage due to aneurysmal rupture is still the common cause of unexpected rapid demise in young adults. There is very little evidence that antecedent trauma or exertion play a part as precipitating factors. Centrally placed aneurysms situated at the anterior communicating artery origin or terminal carotid seem to be particularly malignant in their effects. Cause of death is usually massive extrusion of blood into the intracranial cavity with increasing intracranial pressure, compressive haematoma formation and widespread arterial spasm with ischaemic consequences. Whether aneurysmal rupture can be caused by trauma cannot really be satisfactorily resolved. Intracerebral haemorrhage is most commonly due to hypertension but, as in the case of other haematomas, bleeding disorders may also be a cause. Intracerebral haematoma may, however, also result from rupture of micro-angiomata and the brain should be carefully examined for them in the young patient without evidence of hypertension. Hypertensive crises occurring in people on monoamine oxidase inhibitors should also be remembered as a cause of intracerebral haemorrhage.
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PMID:Unexpected natural death of cerebral origin in medicolegal practice. 113 58

A case of orthostatic hypotension with autonomic failure is presented, and the patient's clinical response to the combined regime of a monoamine oxidase inhibitor and 9-alpha-fluorohydrocortisone is discussed. This therapy provided a relatively convenient means of alleviating the patient's symptoms and appears to be of considerable value in the management of orthostatic hypotension. However, close patient supervision is essential when these drugs are used as they cause hypertension in the supine position in subjects with poor baroreceptor function.
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PMID:Idiopathic orthostatic hypotension controlled with a monoamine oxidase inhibitor and 9-alpha-fluorohydrocortisone. 122 Dec 78

This study was performed in 60 women aged between 47-55 years (mean age 50.46 +/- 1.7), divided into two groups: premenopausal and postmenopausal. Each group was subdivided according to arterial pressure: with normal pressure and arterial hypertension. Daily urinary excretion of catecholamines was determined according to method of Euler and Lishajko, the activity of dopamine--beta-hydroxylase in serum according to Nagatsu et al. The activity of catechol-O-methyltransferase in erythrocytes according to Axelrod et al., the activity monoamineoxidase in serum according to Wurtman et al. Daily urinary excretion of vanilmandelic acid determined according to Pisano et al. It was found that women with menopausal arterial hypertension have significantly greater urinary excretion of adrenaline and noradrenaline (p < 0.001) in the premenopausal period, and adrenaline (p < 0.01) in the postmenopausal period. The activity of dopamine-beta-hydroxylase did not differ from the control group. The activity of COMT in erythrocytes of women and MAO in serum of women with menopausal arterial hypertension was significantly lower. Daily urinary excretion of vanillinmandelic acid in women with menopausal arterial hypertension was significantly lower.
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PMID:[Excretion of free catecholamines in urine and activity of some enzymes involved in catecholamine metabolism with arterial hypertension during menopause]. 130 16

The mechanisms of action of monoamine oxidase inhibitors (MAOIs) suggest that patients taking them may respond with hyper- or hypotension when undergoing coronary artery surgery. We describe a case where MAOIs were present and fentanyl and midazolam were the anaesthetic agents used. The anaesthesia and surgery were performed without incident. Postoperative ICU care was complicated by hypertension, hyperthermia, and severe shivering followed by hypotension resistant to therapy and finally death. Diagnoses of pulmonary embolism and sepsis were unproven and may have played a role. The MAOIs may also have played a role. Reactions in patients while taking both meperidine and MAOIs are unusual and animals react differently from humans to a combination of MAOIs and narcotics. There are only five reported cases where fentanyl was given to patients on MAOIs. We conclude that, until there is more information, MAOIs should be discontinued, if possible, before surgery in which catecholamines may be needed.
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PMID:MAO inhibitors and coronary artery surgery: a patient death. 146 33


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