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)

Hibernation was induced in hamsters by placing them in a cold room for an extended period of time, after which the hibernating state was confirmed by marked reductions in heart rate, body temperature, and the respiratory rate. The animals were either frozen intact in liquid nitrogen, or aroused and then frozen when body temperature reached 8, 12, 16, 20, 24 or 32 degrees C. A metabolite profile, including glucose-related metabolites, high-energy phosphates, gamma-aminobutyric acid (GABA) and cyclic nucleotides, was determined for both the cerebral cortex and cerebellum. In general, the metabolite changes in the two regions elicited by hypothermia were alike, although some differences were evident. The brains of hibernators were biochemically characterized by (1) a high concentration of energy reserves including glycogen, glucose, adenosine triphosphate, and P-creatine, (2) significantly elevated levels of lactate and GABA, and (3) near depletion of cyclic guanosine monophosphate with only a moderate depression of cyclic adenosine monophosphate. During arousal, the metabolites were restored to near normal values and there was little or no indication that the brain energy metabolism was compromised by the arousal process. The study provides certain insights into the metabolic adaptation of the brain to prolonged periods of profound hypothermia in a hibernating species.
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PMID:Metabolism in the hamster brain during hibernation and arousal. 274 44

Rabbits received twice-a-day doses of verapamil for 8 days and, on day 9 they were sacrificed in order to test contractile responses of the aorta in vitro. Isolated rings of aorta received graded doses of KCl, norepinephrine and norepinephrine along with either phentolamine, phenoxybenzamine or additional (acute) verapamil. Treated rings (those from animals that received verapamil chronically) developed significantly less tension (E) in response to depolarizing doses of KCl, but the degree of developed tension was restored and, in fact, enhanced when the aortic tissue was tested after cold storage 24 hr later (day 10). Responses (E) to norepinephrine in verapamil-pretreated rings were less than in controls by amounts that correlated with the daily verapamil dose and these too were enhanced after cold storage for 24 hr. The equilibrium dissociation constant (KA) of norepinephrine for the alpha 1-adrenoceptor, determined by the method of partial receptor blockade, was increased (reduction in affinity) by amounts that also depended on the daily verapamil dose. In contrast to agonist affinity, phentolamine affinity, determined from Schild-plot analysis, was not different from controls, even for the highest daily dosage of verapamil. Stimulus-effect curves were also the same in control and verapamil-pretreated groups, thus suggesting that the chronic treatment did not affect the basic contractile process distal to the receptor. Further, aortae from pretreated rabbits showed more depression to acute verapamil than was seen in controls and this depression in Emax could not be overcome with even high doses of norepinephrine. In addition to the known alpha-blocking and calcium channel blocking actions of verapamil, these data show that chronic verapamil affects norepinephrine, but not phentolamine-receptor affinity, thus suggesting that the chronic action of this calcium entry blocker may preferentially alter a site on the receptor to which norepinephrine binds.
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PMID:Effects of chronic treatment with verapamil on adrenoceptor-mediated contraction of rabbit aorta. 275 61

The influence of temperature (range 15-37 degrees C) on the isometric contractions of the slow twitch soleus (SOL) and the fast twitch extensor digitorum longus (EDL) muscles of mice, rats and guinea pigs were investigated in vitro. Cooling of the bathing solution prolonged the time parameters of single twitches and tetanic contractions in a non-linear manner in both muscle types of all animals. In muscles containing predominately fast twitch fibres like the EDL of all animals cooling was followed by an increase of the single twitch tension (cold potentiation) with a maximum of 160-180% at about 20 degrees C. The influence of a decrease of the temperature on the twitch tension was different in the SOL of the three animals. In SOL of mice (containing about 50% slow twitch fibres) the twitch tension was virtually unchanged, in SOL of rats (about 70% slow twitch fibres) a moderate cold depression and in SOL of guinea pigs (composed by slow twitch fibres only) a strong cold depression was observed. The maximum tetanic tension decreased progressively on cooling in all muscles and independently of their fibre type composition. Cooling increased the twitch-tetanus-ratio in fast twitch and decreased it in pure slow twitch muscles. It is concluded that the temperature dependence of the single twitch and the twitch-tetanus-ratio can be used as a physiological measure of the fibre type composition of a given muscle.
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PMID:Temperature effects on isometric contractions of slow and fast twitch muscles of various rodents--dependence on fibre type composition: a comparative study. 275 27

Deep interscapular temperature measured just below the brown fat lobes was studied in rats during sleep at two ambient temperatures (24 degrees C and 4 degrees C) before and after adaptation (9 days) to cold (4 degrees C). The results show that in the cold ambient deep interscapular temperature decreases during desynchronized sleep independently of adaptation. Such change in temperature is probably the result of the depression in sympathetic vasoconstrictor influences on heat exchangers producing blood and brown fat cooling in sequence during this stage of sleep.
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PMID:[Deep interscapular temperature and thermogenesis of brown fat during sleep]. 275 18

Fifteen patients with chronic stable angina pectoris and a history of reduced exercise tolerance in cold weather (cold intolerance) underwent symptom limited treadmill exercise tests at 20 degrees C and 0 degrees C in a specially constructed cold chamber while taking no antianginal medication. Their mean time to onset of angina (5.8 v 4.2 min), to 1 mm ST depression (5.1 v 3.8 min), and to peak exercise (7.4 v 5.7 min) was significantly shorter on exercise at 0 degrees C than at 20 degrees C. The double product of heart rate and systolic blood pressure at each of these end points was the same in both exercise tests. Eight of these patients were treated with nifedipine 10 mg three times a day for two weeks and then with propranolol 40 mg three times a day for another two weeks. Repeat exercise testing was performed at the end of each two week treatment period. The mean time (SD) to peak exercise at the end of the nifedipine treatment period was 9.1 (2.0) min at 20 degrees C and 8.5 (2.3) min at 0 degrees C. The double product at peak exercise was the same for both exercise tests. At the end of the propranolol treatment period the mean time to peak exercise was significantly less at 0 degrees C (7.8 (2.6) min) than at 20 degrees C (8.9 (2.4) min). The double product at peak exercise was the same for both exercise tests but was significantly less than that on nifedipine. Cold intolerance was shown in patients with a positive history by symptom limited treadmill exercise testing at 0 degrees C. It persisted when they were treated with propranolol, albeit to a lesser extent, but not when they were treated with nifedipine.
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PMID:Cold intolerance in patients with angina pectoris: effect of nifedipine and propranolol. 275 65

Of 57 patients with panic disorder with agoraphobia, more had their first panic in late spring and summer than in fall and winter, and in warm weather than in cold weather. In the month before the first panic 52% of the patients had prodromal depression or anxiety. Agoraphobic avoidance preceded the first panic in 23%, began within days after the first panic in 32% (without prodromal anxiety or depression in only 20%), and after more than one panic (1 week to 11 years later) in 41%. The site of the first panic was from the agoraphobic cluster (public places) in 81%, at work or school in 11%, and inside the home in 8%. Thirty-eight percent of patients were with a familiar adult at the time. Many features of the syndrome can be explained by an integrated model with several interacting factors contributing in varying degrees to the different routes by which it develops. To the learning and biological factors already suggested we add an evolutionary factor to explain why most first panics occur outside the home and mainly in public places. Certain extraterritorial cues constituting an agoraphobic cluster seem to be prepotent and prepared triggers or modifiers of fear during stress.
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PMID:Onset of panic disorder with agoraphobia. Toward an integrated model. 206 99

Sustained left ventricular pressure development during each infusion of a cold calcium-containing hyperkalemic cardioplegic solution has been observed in rat hearts. The present study was undertaken to relate such contraction (i.e., increase in resting pressure) to myocardial preservation and to the calcium and magnesium contents of a crystalloid hyperkalemic cardioplegic solution. Isolated perfused rat hearts with a left ventricular isovolumic balloon were arrested at 8 degrees C by the fully oxygenated cardioplegic solution infused every 15 minutes for 2 hours. Cardioplegic solutions containing ionized calcium in concentrations of 0, 0.1, or 1.2 mmol/L were each studied with (groups 2, 4, and 6) and without (groups 1, 3, and 5) the addition of magnesium (16 mmol/L). Hearts arrested by the cardioplegic solution with no calcium or magnesium (group 1) developed a pressure (averaged over the second to eighth infusion and expressed as percent prearrest left ventricular pressure) of 6.0% +/- 0.4% during cardioplegic infusions. This solution maintained end-arrest myocardial adenosine triphosphate (13.1 +/- 1.0 nmol/mg dry weight) and phosphocreatine (21.7 +/- 2.8 nmol/mg dry weight) contents near the prearrest contents and preserved left ventricular function at 95% +/- 3% of prearrest developed left ventricular pressure at 15 minutes of reperfusion at 37 degrees C. Calcium (groups 3 and 5) increased pressure development during cardioplegic infusions (10.4% +/- 0.5% and 15.1% +/- 0.9%), depleted adenosine triphosphate (7.2 +/- 1.0 and 7.4 +/- 0.9) and phosphocreatine (13.3 +/- 1.8 and 10.7 +/- 1.5), and depressed left ventricular functional recovery (71% +/- 1% and 73% +/- 3%). Magnesium alone (group 2) decreased pressure development during cardioplegic infusions (3.0% +/- 0.3%), maintained adenosine triphosphate (15.6 +/- 0.9), augmented phosphocreatine (38.3 +/- 1.2), and preserved left ventricular function (99% +/- 4%). Magnesium added to calcium (groups 4 and 6) prevented the calcium-induced increased pressure development during cardioplegic infusions (4.0% +/- 0.5% and 6.7% +/- 0.6%), maintained adenosine triphosphate (13.6 +/- 1.4 and 14.9 +/- 0.7), augmented phosphocreatine (31.3 +/- 1.6 and 32.2 +/- 2.4), and ameliorated the depression of functional recovery (82% +/- 2% and 86% +/- 2%). These data suggest that left ventricular pressure development during arrest contributed to calcium-induced energy depletion and impairment of functional recovery and that these deleterious effects were inhibited by magnesium. The inhibitory effects of magnesium on left ventricular pressure development were rapidly reversed on reperfusion. The data support the addition
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PMID:The effects of calcium and magnesium in hyperkalemic cardioplegic solutions on myocardial preservation. 275 59

Three aspects of trigeminal pain are considered: the peripheral mechanisms of pain from teeth and from the cornea, and the role of the trigeminal brainstem nuclei in pain. Pain is probably the only sensation that can be evoked by stimulation of dentin or dental pulp in man. Five nerve-endings enter dentinal tubules from the pulp but do not extend into the outer dentine, which is nevertheless sensitive. In teeth of limited growth in experimental animals, the dental pulp is supplied by A beta, A delta and C fibres and these are associated with two categories of receptor: one responds to cooling and to other stimuli that cause displacement of the contents of the dentinal tubules such as probing and drying the dentine, and the other group responds most vigorously to heating. Some cold sensitive units have A beta fibres and the evidence suggests that stimulation of these is capable of evoking both muscle reflexes and pain and, near threshold, 'pre-pain' sensations. Thermal stimulation of the cornea produces sensations of pain and, with less intense stimuli, irritation, Mechanical stimulation also produces pain but it is not clear whether, below the pain threshold, such stimuli produce touch sensation or some other sensation related to pain. Histologically, the nerve-endings in the corneal epithelium consist of fine, bare processes closely associated with the surface of the epithelial cells. Recordings in experimental animals have shown that many of the receptors respond to several different forms of stimulus and their properties correlate well with those predicted from psychophysical experiments in man. The results of trigeminal tractotomy in man and recordings from the trigeminal brainstem nuclei in anaesthetized animals, have generally indicated that nucleus caudalis is the main relay in the pain pathway from the face and associated structures. Recent observations have, however, shown that tractotomy does not produce complete analgesia of this region and responses to thermal stimulation of teeth and noxious stimulation of other oro-facial tissues have been recorded from the more rostral parts of the brainstem nuclear complex. The surgical procedures employed to set up an animal for stereotaxic recording may induce long-lasting depression in the excitability of neurons in these nuclei, which masks some of their properties. The mechanism of this depression has not been established.
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PMID:Peripheral and central aspects of trigeminal nociceptive systems. 285 85

The side-effect profile of labetalol was assessed in 34 patients with mild to moderate essential hypertension who had previously experienced side effects during beta-blocker therapy. The most frequently reported beta-blocker side effects were fatigue, impotence, cold extremities, and depression. After discontinuing their previous beta-blocker for 4 weeks, labetalol was titrated (100-400 mg b.i.d.) to achieve blood pressure control. Twenty-seven of 34 patients did not have a recurrence of a beta-blocker related side effect while receiving labetalol. The most common new side effect with labetalol was dizziness (3 patients). As judged by the attending physician and the patient, labetalol was better tolerated than conventional beta-blocker therapy in 30 of 34 patients (88%). Twenty-four of 34 patients (71%) preferred labetalol over previous therapy. Labetalol controlled blood pressure in 30 of 34 patients (88%). At equal antihypertensive doses, some side effects common to beta-blockers are seen less frequently with labetalol.
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PMID:Comparative tolerability of labetalol versus propranolol, atenolol, pindolol, metoprolol, and nadolol. 287 65

The value of beta blockade after myocardial infarction is extremely well documented. Close to 50 randomized trials have been performed, involving about 40,000 patients with short- or long-term follow-up. Over 20,000 patients have been included in more than 20 placebo-controlled trials with a follow-up period of 3 months or more. In long-term follow-up studies, about 1 to 2 weeks to 1 year after myocardial infarction, mortality was reduced by 21% and reinfarction by 24% (about 20,000 patients in 24 trials). The trial medication was withdrawn in about 20% in both placebo and beta-blocker groups in the major trials. In addition to reduction of mortality and reinfarction rate, benefits have clearly been demonstrated on severity of chest pain, arrhythmias, and other thromboatherosclerotic complications, as well as on readmissions. Significantly more patients experienced congestive heart failure, hypotension, bradycardia, and cold hands with beta-blocker treatment, whereas no clear-cut difference was found for atrioventricular block, bronchial constriction, and intermittent claudication. Some studies have reported more tiredness, depression, and gastrointestinal disturbances. In the Stockholm metoprolol trial, analyses on quality of life have been performed. In this trial, 3 years of metoprolol treatment after myocardial infarction resulted in a prolongation of both survival and time spent completely asymptomatic, as well as in an optimal functional state. Furthermore, less time was spent disabled after serious atherosclerotic complications. Long-term beta blockade after myocardial infarction reduces mortality and morbidity but causes adverse reactions in some patients. With proper selection of patients and type and dosage of beta blocker, survival without atherosclerotic complications and side effects can be prolonged.
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PMID:Use of beta blockers in postinfarct prophylaxis: aspects on quality of life. 288 38


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