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)

Using the cannula inserting method, we investigated the responsiveness of isolated skeletal muscle branches of the dog femoral artery to alpha-adrenoceptor agonists and potassium chloride, and the influence of cold storage (3 days and 5-7 days, at 4 degrees C). Epinephrine (EPI) and norepinephrine (NE) induced a marked vasoconstriction in a dose-related manner. A large dose of EPI and NE usually induced an increase in perfusion pressure of more than 100-200 mm Hg. Phenylephrine (PE) and methoxamine (MT) also induced a marked constriction, but clonidine (CLO) and xylazine (XYL) produced only a slight vasoconstriction, even in large doses. Tyramine (TYR) also induced a small vasoconstrictor response. A large dose of KCl induced a marked vasoconstriction. The order of potency of constriction was EPI greater than or equal to NE greater than PE = MT much greater than KCl greater than CLO greater than or equal to TYR greater than or equal to XYL. The vasoconstrictor responses to EPI and NE were significantly suppressed by 3-7 days of cold storage. Vasoconstrictor responses to MT were slightly suppressed by cold storage. However, XYL-, CLO- and TYR-induced vasoconstrictions were not significantly influenced by cold storage. KCl-induced constriction was clearly suppressed by cold storage. These observations suggest that the postjunctional alpha-adrenoceptor in skeletal muscle branches of the femoral artery is of the alpha 1-type. Moreover, it was shown that prolonged cold storage (3-7 days, at 4 degrees C) resulted in a decrease in sensitivity of these vessels to alpha-adrenoceptor agonists and in a marked decrease in sensitivity to KCl, suggesting a depression of the calcium channel by cold storage.
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PMID:Responsiveness of skeletal muscle branches of the dog femoral artery to alpha-adrenoceptor agonists before and after cold storage. 288 40

Patients with coronary artery disease (CAD) have angina pectoris at varying levels of myocardial oxygen demand. Fluctuations in coronary blood supply due to dynamic changes in coronary vasomotor tone are believed to be responsible for this variation in angina threshold. Cutaneous cold application produces an inappropriate increase in coronary vascular resistance in patients with CAD. To assess the effect of a coronary vasoconstrictor stimulus during exercise (when there are competitive stimuli for coronary dilatation), 16 men with documented CAD and angina underwent 2 exercise tolerance tests, 1 performed for control purposes and the other during cold application (hand and forearm immersed in ice). The cold pressor test elicited an increase in systolic blood pressure at rest (134 vs 159 mm Hg, p less than 0.02) at the end of stage I (145 vs 165 mm Hg, p less than 0.02) and at peak exercise (154 vs 166 mm Hg, p less than 0.05). The diastolic pressure was similarly increased during cold pressor exercise test, but the heart rate showed little or no change. Most patients (11 of 16) tolerated equal or greater double products (heart rate X systolic pressure X 10(-3) at angina (17 vs 20, p less than 0.02), 1-mm ST-segment depression (16 vs 18, p less than 0.05) and peak exercise (18 vs 20, p less than 0.08) during cold pressor exercise test as compared with the baseline exercise test, without a reduction in exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Paradoxical elevation of threshold to angina pectoris by cold pressor test in men with significant coronary artery disease. 292 57

Growing evidence indicates that most patients with coronary artery disease frequently have episodes of painless myocardial ischemia. Previous studies from our institution show that the severity and duration of myocardial ischemia are necessary but not sufficient factors to explain the occurrence of anginal pain. The responses to a battery of painful stimuli were studied in 12 patients with predominantly painless (group A) and in 15 patients with predominantly painful (group B) ischemic episodes. The severity of myocardial ischemia as assessed by the measurement of ST-segment depression during exercise stress testing and during ambulatory electrocardiographic monitoring was comparable in the 2 groups. Patients in group A had a significantly higher threshold and tolerance for forearm ischemia (+32%, p less than 0.05; +120%, p less than 0.001), cold (+100%, p less than 0.05; +180%, p less than 0.01) and electrical skin stimulation (+145%, p less than 0.01; +109%, p less than 0.01), but the overlap between the 2 groups was often appreciable. In the 6 patients with the longest tolerance times for forearm ischemic pain (all in group A) and in the 5 having the shortest tolerance times (all in group B), plasma levels of beta endorphin, met-enkephalin, noradrenaline and adrenaline were similar during both the basal state and the induction of forearm ischemic pain. Thus, a generalized defective perception of painful stimuli plays an important role in many patients with predominantly painless myocardial ischemia. Other mechanisms, however, may also be important, particularly in patients whose threshold and tolerance values overlap with those of patients who have predominantly painful myocardial ischemia.
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PMID:Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. 294 17

In each of two trials, plasma corticosterone (B) was measured in Large White turkey tom poults after the following treatments were applied: 1) .9% saline injected; 2) cold water immersion, and 3) adrenocorticotropic hormone (ACTH) injected (10 IU/kg body weight). Poults were treated at 3- to 4-day intervals from the day of hatching to 21 days of age. Plasma samples were obtained at 1, 2, 3, 4, and 6 hr posttreatment. In both trials, there was a depression in B levels within the first 3 hr following ACTH or cold water immersion treatment. Significant increases in plasma B levels of the cold water treatment occurred at 4 hr posttreatment in Trial 1 in 7-day-old poults and in Trial 2 in 21-day-old poults. A significant adrenal cortical response to ACTH injection was observed in 3- and 7-day-old poults at 6 hrs posttreatment in Trial 2. Plasma B concentrations were also measured in three groups of nontreated Large White tom poults on the day of hatching at a commercial hatchery. Plasma samples were obtained from poults in incubators at 1000 hr, immediately following commercial processing procedures at 1030 hr, and at poult placement at 1330 hr. Plasma B levels of poults sampled in the incubator and after processing were similar. However, B levels of poults sampled at placement were increased significantly above the other two groups.
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PMID:Adrenal cortical response of tom poults. 299 46

This study examined the effects of ageing on the cardiopulmonary receptor regulation of vasomotor tone in skeletal muscle and renin release by the kidney. To this end, the changes in forearm vascular resistance (mean arterial pressure divided by plethysmographically measured forearm blood flow), plasma noradrenaline concentration and plasma renin activity were measured in eight young (23 +/- 2 years, mean +/- s.e.m.) and seven elderly healthy subjects (69 +/- 2 years) during manoeuvres which altered cardiopulmonary receptor activity. The cardiopulmonary receptors were stimulated by increasing central venous pressure through passive leg-raising and deactivated by reducing central venous pressure through non-hypotensive (-15 mmHg) and hypotensive (-40 mmHg) levels of lower body negative pressure. During either manoeuvre, central venous pressure changed by the same amount in both groups, but the reflex changes in forearm vascular resistance, plasma noradrenaline and plasma renin activity were significantly less in elderly subjects. Since the increase in forearm vascular resistance induced by a cold pressor test was comparable in young and elderly subjects, a non-specific depression of cardiovascular responsiveness to neural stimuli can be excluded. Thus, healthy normotensive elderly subjects show an impairment of both vascular and neurohumoral influences exerted by cardiopulmonary receptors. This may be involved in the decreased ability of the elderly to cope with gravity challenges.
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PMID:Effects of ageing on the cardiopulmonary receptor reflex in normotensive humans. 307 75

The impulse activity of afferent fibers was studied in n. ethmoidalis. While the room air was being sucked in through the nasal cavity to choanes, marked excitation of cold receptors of the nasal cavity walls occurred. In the air current from the choanes to the nostrils, the activity of the receptors was depressed. Insufflation through the nasal cavity of the mixtures of CO2 (1, 3, 6%) with air also depressed the activity of cold receptors. The degree of the depression depended on the concentration of CO2. The cold receptors of nasal cavity like the lung stretch receptors, have the features of chemoreceptors. Their activity is depressed with physiological concentrations of CO2 in the air.
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PMID:[Suppressive effect of carbon dioxide on excitation of the cold receptors of the nasal cavity of the cat]. 308 95

The in vivo effects of high doses of 1,25(OH)2D3 were studied in condylar cartilage of suckling mice. Seven-day-old animals were treated with 20 ng of the hormone for 7 consecutive days. Biochemical assays on collagen content and synthesis were complemented by structural studies using light and electron microscopy. Indirect immunofluorescent methods were used for the localization of type I and II collagens and for fibronectin. This study revealed that the protein content of the condyle decreased substantially following the administration of the hormone. Protein synthesis increased in hormone-treated animals during the first 4 days but was significantly inhibited thereafter. Collagen synthesis, however, was inhibited instantaneously, followed by a decrease in the percentage of cold hydroxyproline of the total protein. Hormone-treated condyles showed a marked decrease in the distribution of type I collagen, no apparent change in the distribution of type II collagen, but an enhanced reactivity for fibronectin especially around hypertrophic chondrocytes. SDS-gel electrophoresis of collagen chains suggested that the hormone did not induce a significant change in the ratios of type I and II collagen chains, yet additional peaks became evident in 1,25(OH)2D3-treated specimens. The decrease in collagen synthesis was accompanied by ultrastructural changes in the appearance of the extracellular collagen bundles. They later appeared as a dense meshwork of collagen fibrils, a feature that was lacking in control tissues. The changes in collagen fibrillogenesis could be explained by our in vitro studies indicating a marked depression of 35S-sulfate incorporation secondary to treatment with 1,25(OH)2D3. The hormone was also found to suppress the incorporation of 3H-thymidine, hence it may be concluded that 1,25(OH)2D3, when used in high concentrations, possesses an inhibitory effect upon both the proliferative activity of the cartilage progenitor cells as well as upon the metabolic activity of the condylar cells as related to collagen and glycosaminoglycans synthesis.
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PMID:Effects of increased doses of 1,25 dihydroxyvitamin D3 on matrix and DNA synthesis in condylar cartilage of suckling mice. 311 51

The purpose of this study was to investigate the value and to identify any deleterious effects of antishock trouser use during hypothermic cardiovascular depression. Thirteen mongrels were made hypotensive by cooling to a core temperature of approximately 27 degrees C. Eight dogs had antishock trousers inflated for one hour and five dogs served as controls. Metabolic and hemodynamic variables were measured at regular intervals during cooling, during trouser inflation, and after trouser deflation. No study animal experienced ventricular fibrillation. Neither central temperature, pH, or serum potassium nor mean arterial BP or systemic vascular resistance were significantly affected by trouser inflation or deflation. Antishock trouser use during the early phase of hypothermia before rewarming does not appear to result in a central bolus of cold, acidotic, hyperkalemic blood or the precipitation of ventricular fibrillation. There appears to be no significant hemodynamic benefit of antishock trouser use early in the management of hypotension caused by moderate hypothermia.
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PMID:The effects of antishock trouser inflation during hypothermic cardiovascular depression in the canine model. 317 51

To investigate the mechanisms of cold susceptibility in angina pectoris nine male angina patients were studied. All were cold susceptible by history and had developed ischaemic ST changes during a previous exercise test. The patients underwent two additional bicycle exercise tests, one in a cold chamber with an average temperature of -8 degrees C, and the other at room temperature. The ECG was computer analysed and the intra-arterial blood pressure was measured. No significant decrease in work capacity was found during exercise in the cold chamber. In the cold, systolic blood pressure was consistently higher throughout the test and in seven of nine subjects ST depression was more pronounced at corresponding workloads. ST depression was also analysed versus heart work which was assessed as rate pressure product. In the cold, 1 mm ST depression appeared at a somewhat higher rate pressure product when compared to room temperature. It was concluded, therefore, that an augmented heart work, secondary to substantial increases in blood pressure, appears to account for the cold-induced increase in ST depression found in the angina patients in this study.
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PMID:Effects of cold on ST amplitudes and blood pressure during exercise in angina pectoris. 320 73

Postoperative low cardiac output is the most common cause of death in patients undergoing elective repair of tetralogy of Fallot. The incidence is much higher than in elective adult bypass operations for coronary artery disease. To explain this difference, we investigated 16 children having elective repair of tetralogy (mean age 6.3 years). Myocardial biopsy specimens obtained during bypass before arrest, at the end of cold arrest by blood cardioplegia, and after 30 minutes of reperfusion were studied for adenosine triphosphate and lactate levels. Myocardium was submitted for microscopic study shortly after the onset of ischemia. The operation was successful in reducing right ventricular-pulmonary artery gradients from 82 +/- 28 to 9 +/- 1 mm Hg, yet seven patients required significant inotropic support (dopamine, greater than 5 micrograms/kg/min) for more than 24 hours and 12 patients needed prolonged use of digoxin and diuretics for right ventricular failure. Tissue levels of adenosine triphosphate and lactate in the tetralogy groups were compared with those in 20 adults with coronary artery disease having similar myocardial protection techniques. Adenosine triphosphate levels in the tetralogy group decreased during cross-clamping (41 +/- 8 minutes) from 24 +/- 3 to 16 +/- 2 mmol/kg dry weight (mean +/- 1 standard error), with a marked further drop after reperfusion to 9 +/- 2 mmol/kg (p less than 0.01). Adenosine triphosphate levels in the group with coronary disease also decreased from 20 +/- 1 to 16 +/- 1 mmol/kg after a longer cross-clamp time (70 +/- 17 minutes) but remained at 15 +/- 2 mmol/kg after reperfusion. Tissue lactate levels in the tetralogy group rose markedly during ischemia and remained elevated after reperfusion. In contrast, lactate levels in the group with coronary disease rose moderately during ischemia and returned to normal early on reperfusion. Microscopic study revealed focal myocyte necrosis in tetralogy of Fallot. Our findings, which demonstrate inadequate myocardial protection of patients with tetralogy during repair, with depression of adenosine triphosphate and increased lactate during ischemia and reperfusion, suggest a defect in oxidative metabolism. The drop in adenosine triphosphate after reperfusion in the patients with tetralogy implicates reperfusion injury as a mechanism of myocardial damage.
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PMID:Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot. 325 36


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