Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.
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PMID:[A case of painless myocardial injury probably caused by coronary artery spasm]. 143 52

For several years, cerebral blood flow (CBF) studies have been fueling the controversy surrounding the pathophysiology of migraine headache. The earliest studies focused mainly on migraine with aura (MA+) and provided evidence in support of the classical hemodynamic theory: a decrease in blood flow during the aura is followed by reactive vasodilation during the headache phase. Studies in migraine without aura (MA-), although less numerous, consistently demonstrated an increase in CBF during the attack. Olesen et al., gave rise to a heated debate by suggesting that hemodynamic manifestations are different in MA+ and MA-; in their view, CBF remains unchanged in MA-, whereas MA+ is associated with a wave of posterior blood flow deficiency which slowly spreads forwards in a manner reminiscent of experimental spreading depression; they interpret this hemodynamic pattern as evidence that the attack is mainly caused by a neural mechanism rather than a vascular spasm. This concept of MA- with no hemodynamic changes suggests that the pathophysiology of MA- may be completely different from that of MA+. However, most studies using stationary detectors or single photon emission computerized tomography (SPECT) with Xenon 133 or HMPAO as the tracer have demonstrated increased CBF during migraine attacks. The increase was not correlated with the side of the pain suggesting that vasodilatation is not the only cause of the pain. Current data do not seem to support the view that MA- and MA+ are different pathophysiologic entities; whether the mechanism of the attack is neural or vascular cannot be determined on the basis of CBF data.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral blood flow in migraine without aura]. 149 16

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
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PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

Myocardial perfusion scintigraphy with thallium-201 was performed in 33 subjects (mean age 45 years, range 28-61) with exercise-induced, rate-dependent left bundle branch block (LBBB) in order to assess both the value of Thallium-201 myocardial imaging for the diagnosis of coronary artery disease (CAD) and the pathogenesis (ischaemic or not) of the conduction defect. Of the 33 patients evaluated, 16 had chest pain suggestive of CAD and 17 were asymptomatic. None had a history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 b.min-1. Eighteen patients showed repolarization abnormalities (ST segment depression with deep inverted T waves) compatible with ischaemia, after QRS normalization. Thallium-201 myocardial uptake was normal in 12 subjects; in the remaining 21, reversible Thallium-201 defects were demonstrated in the septum (18 patients), septum and apex (2), and septum and infero-apical wall (1). No patient had irreversible defects and all had normal coronary angiography, with negative ergonovine tests for coronary artery spasm. The patients were followed up for a mean of 43 months (range 16-80). One patient died from sudden death, but no cardiac event occurred in the other patients. In conclusion, exercise Thallium-201 myocardial scintigraphy showed a high prevalence (64%) of reversible perfusion defects in a group of patients with exercise-induced LBBB without any evidence of CAD at angiography or coronary spasm at ergonovine test. Moreover, follow-up showed a relatively low rate of major cardiac events.
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PMID:Assessment of myocardial perfusion with thallium-201 scintigraphy in exercise-induced left bundle branch block: diagnostic value and clinical significance. 164 85

The aim of the regional administration of opioids is to provide an efficient and prolonged analgesia. Then, opiates can be useful for postoperative analgesia and for the treatment of chronic pain of malignant origin. Analgesia is correlated with several adverse effects of which the most frequent are nausea and itching and the most severe is respiratory depression. Beside the adverse effects, other properties of opiates could be responsible of favourable effects which can be taken in advantage in specific indications. In the postoperative period, epidurally administered opioid can attenuate the neuroendocrine and metabolic responses to surgery and pain. This effect is responsible of a reduction of the resistance to insulin and of a better nutritional balance, especially after major abdominal surgical procedures. Opioids also act by a reduction of the motor functions of the bowel, which perhaps could reduce the incidence of anastomotic breakdowns. Finally, other effects have been reported, as anecdotes, such as the treatment of spasm after bilateral replantation of the ureters, neurologic bladder dysfunctions and enuresis. Spinal administration of opioids has also been used as a treatment of premature ejaculation.
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PMID:[Non-analgesic effects of opioids]. 167 72

To assess the difference between cardiovascular responses to treadmill exercise (TM) and those to bicycle ergometer exercise (EM) in provoking coronary spasm, we compared the ST segment shifts (elevation or depression) during TM and EM in 67 patients with vasospastic angina. Coronary artery spasm was demonstrated on angiography. Both TM and EM were performed on the same day during a medication-free period. For both tests, multistage, symptom-limited exercise protocols were used; EM in the morning and TM in the afternoon. The results obtained were as follows: 1. Rate-pressure products at peak exercise during TM and EM were similar. Systolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.01). The patients' heart rates at peak exercise were higher during TM than during EM (p < 0.01). Diastolic blood pressure levels at peak exercise were higher during EM than during TM (p < 0.05). 2. Exercise-induced ST elevation occurred more frequently with TM than with EM (19% vs 9%, p < 0.05). 3. Exercise-induced ST depression was provided in 27 patients during TM and in 13 during EM (40% vs 19%, p < 0.01). Among 45 patients without significant lesions, ST depression occurred in 19 during TM, but in only 7 during EM (42% vs 16%, p < 0.01). In conclusion, coronary spasm seemed to occur more frequently with TM than with EM. The mechanism causing such difference remains to be elucidated, however, we speculate that the difference between TM and EM as to enhanced autonomous nervous system activity and coronary perfusion exercise may be related to the difference in the incidence of coronary spasm.
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PMID:[Exercise-induced ST segment shift in vasospastic angina with special reference to comparisons between treadmill and bicycle ergometer exercise testings]. 184 8

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p less than 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p less than 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during spacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p less than 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p less than 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.
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PMID:Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress. 203 78

Neurological deficits following human subarachnoid hemorrhage (SAH) have been related to the cerebral arterial spasm and the increase in intracranial pressure (ICP) secondary to the development of hydrocephalus. Metabolic depression in experiment study was thought as resulting from brain stem dysfunction. On the other hand, some reports have shown no relationship between vasospasm and neurological abnormalities. The mechanism of cerebral metabolism depression after SAH remains unclear. The effect of blood in the cortical subarachnoid space on the cerebral metabolism has not been known well. To investigate this effect, a new cortical SAH model was developed using rat and local cerebral glucose utilization (LCGU) after production of SAH was measured. A cortical SAH model: a small burr hole was made on the left parietal bone and the arachnoid membrane was pierced with a tapered glass-needle 60 mu tip in diameter. Fresh autologous non-heparinized arterial blood 0.04 ml was injected into subarachnoid space within 60 seconds through that needle. The blood extended over the left cerebral cortical surface with thin subarachnoid hematoma on the parietal cortex, but did not extend on the right hemisphere and the basal cistern. The increase in ICP during production of SAH was minimal, mean value of 7.2 mmHg and ICP slowly returned to the basal level within 30 minutes. Rats were divided into 3 groups; rats 2 hours (SAH-2h, n = 7) and 48 hours (SAH-48h, n = 7) after production of SAH and rats 2hours after 0.04 ml saline injection for control (Control, n = 7). LCGU was studied according to the methods developed by Sokoloff.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of the cortical subarachnoid hemorrhage on cerebral glucose metabolism]. 205 20

A case of exercise induced ST segment depression preceding ST segment elevation in precordial leads and persistent ST segment depression in inferior leads is reported. Such an exercise response should suggest significant fixed coronary stenosis in addition to coronary spasm.
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PMID:Exercise induced ST segment depression preceding ST segment elevation. 208 11

The significance of U-wave inversion during coronary arterial spasm was investigated in 188 consecutive ergometric tests performed in 69 patients. All patients had previously undergone coronary arteriography which had clearly shown coronary spasm either at rest or after a single 0.4 mg injection of ergometrine. The ergometrine tests were then performed at the patient's bedside using a standard protocol with injection of incremental doses of ergometrine: 0.05, 0.1, 0.2 and 0.4 mg every 5 minutes with 12-lead ECG recordings every minute. Fifty of the 59 patients with positive tests had classical signs of spasms: ST elevation or depression and/or T wave inversion; the other 9 patients had inversion of the U wave alone (2 cases) or associated with classical ST segment changes in the remaining cases. The 10 other patients had no ECG changes although 2 of them suffered typical anginal pain. Negative U waves were observed in 4 of the 12 patients with spasm of the left anterior descending artery, accompanied by ST elevation in the anterior wall leads. A negative U wave would appear to be a sign of less ischaemia than the classical ECG changes because anginal pain is less common: 4 out of 9 cases in which U wave inversion was a very early change, 8 out of 9 cases in which it was the first or only abnormality. The recognition of a negative U wave increases the sensitivity of the electrocardiogram during resting angina and allows earlier treatment of coronary spasm with nitrate derivatives after an ergometrine test.
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PMID:[Value of negative U waves in coronary artery spasm]. 210 54


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