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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.
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PMID:The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst. 39 80

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.
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PMID:Elevated plasma renin activity in patients with acute pyelonephritis. 69 21

The examination was conducted in 142 patients with coronary atherosclerosis, aged 33 to 74 years, and in 40 normal persons, aged 25 to 48 years. The pain form of the disease was observed in 96 patients, the arrhythmic one--in 38, the painless one--in 8 patients. The arterial pressure was within the normal limits in the examined patients. In 67.6% of the patients hypercholesterolemia was diagnosed, in 47.3%--hypertriglyceridemia. Type II hyperlipoproteinemia was found in 67.6% of the cases, types III and IV--in 5.3 and 9.1%, respectively, type V--in 0.5% of the patients; the type of hyperlipoproteinemia could not be identified in 10.6%, and in 6.9% of the cases the blood level of lipoproteins did not differ from the normal. The plasma renin activity examined by the radioimmunoassay in normals comprised 1.26 +/- 0.21 ng/ml/hour; in patients with the pain form of coronary atherosclerosis--6.67 +/- 0.72 ng/ml/hour; in those with arrhythmias--6.89 +/- 1.20 ng/ml/hour; in those with the painless form--2.39 +/- 1.02 ng/ml/hour. The highest renin activity was revealed in types IIa, IIb and III hyperlipoproteinemia, as well as in paroxysmal arrhythmia and cardiac fibrillation.
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PMID:[Plasma renin activity in patients with coronary arteriosclerosis with different types of hyperlipoproteinemia]. 96 46

Considerable evidence now indicates that a separate and distinct renin-angiotensin system (RAS) is present within the brain. The necessary precursors and enzymes required for the formation and degradation of the biologically active forms of angiotensins have been identified in brain tissues as have angiotensin binding sites. Although this brain RAS appears to be regulated independently from the peripheral RAS, circulating angiotensins do exert a portion of their actions via stimulation of brain angiotensin receptors located in circumventricular organs. These circumventricular organs are located in the proximity of brain ventricles, are richly vascularized and possess a reduced blood-brain barrier thus permitting accessibility by peptides. In this way the brain RAS interacts with other neurotransmitter and neuromodulator systems and contributes to the regulation of blood pressure, body fluid homeostasis, cyclicity of reproductive hormones and sexual behavior, and perhaps plays a role in other functions such as memory acquisition and recall, sensory acuity including pain perception and exploratory behavior. An overactive brain RAS has been identified as one of the factors contributing to the pathogenesis and maintenance of hypertension in the spontaneously hypertensive rat (SHR) model of human essential hypertension. Oral treatment with angiotensin-converting enzyme inhibitors, which interfere with the formation of angiotensin II, prevents the development of hypertension in young SHR by acting, at least in part, upon the brain RAS. Delivery of converting enzyme inhibitors or specific angiotensin receptor antagonists into the brain significantly reduces blood pressure in adult SHR. Thus, if the SHR is an appropriate model of human essential hypertension (there is controversy concerning its usefulness), the potential contribution of the brain RAS to this dysfunction must be considered during the development of future antihypertensive compounds.
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PMID:Regulatory role of brain angiotensins in the control of physiological and behavioral responses. 136 94

Endogenous opioids are known to be involved in the pathophysiology of idiopathic headache. In fact, decreased levels of enkephalin (E) or endorphin (BE) during headache attacks might be a marker of an altered pain-inhibiting system of central neurotransmission or could be secondary to alterations of brain circulation that often occur during the headache crisis. Recently, captopril (C) has been shown to be apt to restore the availability of endogenous opioids, to improve cerebral blood flow via the inhibition of both the cerebral and systemic renin-angiotensin system or of catecholamine release. It has also been reported to be able to restore the nociceptive-antinociceptive balance through an increase of serum kinin (K) or prostaglandin (Pr) levels. In the present study, the efficacy of C in reducing the frequency (F), duration (D), or severity (S) of headache paroxysm were investigated in a double blind trial vs. placebo (P). Twenty-six subjects (5 males and 21 females; mean age 37 +/- 11 years) suffering from idiopathic headache at least for one year have been allocated to treatment with C (25 mg three times/day) or P according to a double-blind randomized protocol for 4 months. The effects of C or P have been evaluated with Migraine Index Correct, related to changes in F, D or S of headache attacks. Our results indicate that C is effective in reducing F, D or S in subjects with idiopathic headache.
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PMID:[Captopril versus placebo in the prevention of hemicrania without aura. A randomized double-blind study]. 149 69

Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. GH caused a significant increase in ECV (L): 20.45 +/- 0.45 (GH), 19.53 +/- 0.48 (placebo) (P less than 0.01), whereas plasma volume (L) remained unchanged 3.92 +/- 0.16 (GH), 4.02 +/- 0.13 (placebo). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 +/- 0.54 (GH), 3.16 +/- 0.53 (placebo) P less than 0.01. Plasma aldosterone (pmol/L): 129 +/- 14 (GH), 89 +/- 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 +/- 12 (GH), 14 +/- 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 +/- 0.05 pmol/L vs. 1.90 +/- 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2-3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP.
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PMID:Expansion of extracellular volume and suppression of atrial natriuretic peptide after growth hormone administration in normal man. 182 8

The purpose of the present study was to measure plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction without heart failure, and also to assess the temporal sequence of changes of plasma ANP during the first hours of recovery from myocardial infarction. The study was performed in 22 patients who were admitted to the Intensive Care Unit with the diagnosis of acute myocardial ischaemia that had an evolution of less than 6 h. Blood samples were drawn on admission and at 1, 8, and 24 h, and plasma concentrations of ANP, renin, aldosterone, epinephrine, norepinephrine and vasopressin were measured. Compared with control subjects, on admission patients showed increased plasma levels of ANP, as well as increased plasma renin activity (PRA), aldosterone, norepinephrine, epinephrine, dopamine, and antidiuretic hormone (ADH). ANP, but not renin or aldosterone plasma values, decreased with time, and there was a significant correlation between ANP and time after onset of pain. No increase in plasma creatinine was observed during the hospital stay, and the patients showed a negative fluid balance. No relationship was found between the location or extension of the infarction, or morphine treatment and ANP plasma levels. The high levels of ANP seem to counteract the haemodynamic and fluid-retention effects of the vasoconstrictive factors released after myocardial infarction.
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PMID:Atrial natriuretic peptide in patients with acute myocardial infarction without functional heart failure. 182 81

A total of 119 patients with myocardial infarction hospitalized within 24 hrs from the disease onset were examined. He-Ne laser irradiation of the blood (daily 40 min sessions for 3-5 days) was carried out in 45 patients (Group 1). The rest 74 patients (Group 2) were administered common therapy. A number of biologically active substances were radioimmunoassayed in the blood of 12 Group 1 and 11 Group 2 patients on days 1, 3, and 7 of the disease. The pain syndrome was alleviated in Group 1 patients, in contrast to Group 2 patients, and the frequencies of ventricular arrhythmias, of heart failures, and of the condition recurrences were reduced, as was the mortality rate. Laser therapy resulted in reduction of the activities of the hypophyseoadrenocortical and aldosteron-renin-angiotensin systems. Besides blood levels of dilatants and proaggregants (PGF2 alpha, vasopressin, angiotensin II) reduced in these patients, whereas vasodilating and antiaggregation hormones (PGE, PGI2) levels increased and the PGI2/TxB2 ratio improved.
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PMID:[The use of low-intensity laser irradiation of the blood in myocardial infarction]. 236 94

From November 1979 to May 1982, I had the "honor" of serving time at Evin political prison, Teheran Iran. Evin is the historical prison which has set the pace of revolution in the country. At Evin it was discovered that increased regular intake of water improved the clinical picture of peptic ulcer disease. One of the main components of this picture was pain of varying severity, sometimes very severe indeed. Theoretical research to find the physiological reasons for the observed effect of water, in a condition currently classified as disease, has revealed a neurotransmitter, an osmoregulator, a water intake promoter status and a role for histamine. The action of histamine seems to be coupled to the efficient function of the cation pumps. Histamine and serotonin are involved in the regulation of the body's water balance. Cellular "free water" insufficiency produces a disturbance of tryptophan metabolism; it is this disturbance and induced functional deficiency altering the homeostatic balance that produces pain and eventually tissue transformation and/or damage. This pain is being introduced as a signal system denoting free water deficiency of the cell and, therefore, it should be classified as thirst pain. Histamine and the reninangiotensin system also coordinate the water intake and sodium balance of the body. With the induction of renin-angiotensin system for increase in water intake, threshold rates for water intake and the threshold rates for raising blood pressure seem close.
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PMID:Pain: a need for paradigm change. 282 4

It has been suggested that stimulation of adrenoreceptors could be responsible for some of the haemodynamic effects of isoflurane. But there are no solid data demonstrating the role of sympatho-adrenal stimulation induced by pain during isoflurane administration. The impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension has been investigated in 28 patients (47-76 years), scheduled for total hip arthroplasty. After premedication with morphine hydrochloride (0.1 mg/kg), patients were randomly assigned to receive either no fentanyl (control group) or fentanyl (5 micrograms/kg before tracheal intubation, 5 micrograms/kg before skin incision, and 2 micrograms/kg each 15 min during the 1st hour). Isoflurane was given to maintain mean arterial blood pressure in the range 6.7-8 kPa in both groups. Haemodynamic data and blood samples for determination of plasma renin activity (PRA) and epinephrine (E) and norepinephrine (NE) levels were collected before and during hypotension. The fentanyl group and the control group differed significantly during hypotension: heart rate, cardiac index, oxygen consumption and E, NE and PRA were lower (P less than 0.01) in the fentanyl group than in control group. Fentanyl lowered the required concentration of isoflurane to achieve the same degree of hypotension (end-tidal concentration: 0.8 +/- 0.2% in the fentanyl group and 1.4 +/- 0.15% in the control group; P less than 0.001). Our results demonstrate that the cardiovascular effects of higher isoflurane concentrations in the absence of narcotic analgesia are counterbalanced by adrenergic stress stimulation of released epinephrine and norepinephrine. Among the likely reasons for catecholamine release during isoflurane administration, inadequate analgesia may be considered.
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PMID:Impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension. 328 71


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