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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate whether prolonged water immersion (WI) results in reduction of central blood volume and attenuation of renal fluid and electrolyte excretion, these variables were measured in connection with 12 h of immersion. On separate days, nine healthy males were investigated before, during, and after 12 h of WI to the neck or during appropriate control conditions. Central venous pressure, stroke volume, renal sodium (UNaV) and fluid excretion increased on initiation of WI and thereafter gradually declined but were still elevated compared with control values at the 12th h of WI. Atrial natriuretic peptide (ANP) concentration in plasma initially increased threefold during WI and thereafter declined to preimmersion levels, whereas plasma renin activity, plasma aldosterone, and norepinephrine remained constantly suppressed. It is concluded that, compared with the initial increases, central blood volume (central venous pressure and stroke volume) is reduced during prolonged WI and renal fluid and electrolyte excretion is attenuated. UNaV is still increased at the 12th h of WI, whereas renal water excretion returns to control values within 7 h. The WI-induced changes in ANP, plasma renin activity, plasma aldosterone, and norepinephrine may all contribute to the initial increase in UNaV. The results suggest, however, that the attenuation of UNaV during the later stages of WI is due to the decrease in ANP release.
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PMID:Circulation, kidney function, and volume-regulating hormones during prolonged water immersion in humans. 139 77

This study was designed to determine whether or not atrial natriuretic factor (ANF) is present in the vascular walls and to observe the differences in ANF between control (WKY) and stroke-prone spontaneously hypertensive rats (SHRsp). It was found that ANF is indeed present in the vascular wall of the distal aorta. HPLC analysis of the extracts from cultured aortic smooth muscle cells (ASMC) and medium revealed that intracellular ANF was mainly in the form of ANF(1-126), at levels of 0.82 +/- 0.03 (SHRsp) and 1.04 +/- 0.10 ng/10(6) cells (WKY), while the major form in the medium was ANF(99-126), at levels of 0.40 +/- 0.06 and 0.60 +/- 0.06 ng/10(6) cells, respectively. Both forms were present in smaller amounts in SHRsp than in WKY rats. On the contrary, both renin activity and angiotensin I concentrations in SHRsp cells were significantly higher than those in the WKY controls. In addition, immunocytochemistry showed positive ANF staining in cultured ASMC of both strains. The results suggest that ANF can be synthesized and secreted by cultured ASMC from rats.
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PMID:Atrial natriuretic factor and renin synthesized in cultured aortic smooth muscle cells of rats. 145 Mar 93

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure. 153 81

Our review of the current literature and experience in caring for pacemaker patients suggests that a consideration of hemodynamics is a logical way to approach pacemaker selection and programming. Multiple clinical factors enter into the selection of a pacemaker or pacemaker programming settings in each case. It appears that in patients with sinus node disease, atrial-inhibited or dual-chamber pacing provides the best chance for preventing the development of chronic atrial fibrillation with its attendant risks of embolism and stroke. It is clear that AV synchrony has beneficial hemodynamic effects at rest in most patients. The results of Labovitz would suggest that in patients with marked left atrial enlargement, this may be less so. The results of Stewart et al would further suggest that in patients with retrograde VA conduction, dual-chamber pacing is preferable. Retrograde VA conduction can be intermittent and this makes it difficult to use its absence on a single test to decide on the type of pacemaker to use. It appears that baseline left ventricular function does not determine the relative improvement in cardiac output observed with AV synchrony or rate-adaptive pacing. However, in patients with severe congestive heart failure even a small improvement in cardiac output may result in significant clinical improvement. Studies have shown that in any given patient, there may be an optimal AV interval at rest. In general, this ranges from 100 to 150 milliseconds. In normal individuals the optimal AV interval shortens with increased heart rate during exercise in a predictable and linear fashion. The hemodynamic benefits of a shortened AV interval with faster heart rates in pacemaker patients have not yet been shown. Intuitively, however, this would appear to be a desirable approach and will probably be added to the design of future generations of dual-chamber pacemakers. Studies of the effect of different pacing modes on secretion of atrial natriuretic factor are intriguing and may contribute more to our understanding of pacing hemodynamics in the future. During exercise, heart rate increase is more important than AV synchrony and this has been shown by several studies. Thus, in active patients with chronotropic incompetence due to sick sinus syndrome, the addition of rate-adaptive pacing is important. Because single-chamber rate-adaptive atrial pacing leaves the patient exposed to the risk of future development of AV block and DDD pacing does not provide chronotropic support, it is likely that the new rate-adaptive dual-chamber (DDDR) devices will be used in a significant number of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pacemaker hemodynamics: clinical implications. 154 30

Plasma volume expansion usually occurs with acute endurance exercise and endurance training both in humans and in animals. In most cases, the increase in plasma volume is associated with lower haematocrit without red cell mass change or an actual reduction in red cell mass, causing relative or true anaemia, respectively. The combination of exercise and heat acclimation (which produces also hypervolaemia, but at a lesser degree than exercise) enhances hypervolaemia induced by exercise training alone. The onset of the phenomenon is extremely rapid: hypervolaemia is observed within minutes or hours of the cessation of exercise. However, 2 days are necessary to reach peak plasma volume expansion after a marathon run or longer race. The magnitude of this natural expansion ranges from 9 to 25%, corresponding to an additional 300 to 700 ml of plasma. The magnitude of this alteration depends on preceding exercise: ambient conditions, intensity and duration of exercise, body posture and frequency of the exercise bouts. The larger the reduction in plasma volume during exercise, the greater the subsequent hypervolaemia. The hydration status of the subjects before and during exercise might modify also plasma volume changes: sufficient fluid ingestion can lead to plasma volume expansion even during prolonged exercise. Fluid-regulating hormones (aldosterone, arginine vasopressin and atrial natriuretic factor) in conjunction with an elevation in plasma protein content promote hypervolaemia. However, the role and the mechanism of the increase in protein mass remain unclear and the hormonal role in the induction of chronic hypervolaemia is still an open question. Hypervolaemia can improve performance by inducing better muscle perfusion, and by increasing stroke volume and maximal cardiac output. By increasing skin blood flow, plasma volume expansion also enhances thermoregulatory responses to exercise. This leads to the important concept of optimal plasma volume and haematocrit, and performance.
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PMID:Hormonal and plasma volume alterations following endurance exercise. A brief review. 155 54

To assess further the effects of atrial natriuretic factor on autonomic nervous system reflexes in normal humans, the hemodynamic and neurohormonal responses to lower body negative pressure were measured at control and during infusions of atrial natriuretic factor and nitroglycerin in nine normal male subjects. The control -20 mm Hg lower body negative pressure was characterized by significant reductions in right atrial and pulmonary wedge pressures, as well as stroke volume and cardiac output. This was associated with a reflex increase in forearm vascular resistance and plasma norepinephrine. During the infusion of atrial natriuretic factor, the same -20 mm Hg lower body negative pressure produced a larger decrease in mean arterial pressure of 7.9 +/- 3.9 mm Hg (p less than 0.05), as well as a larger decrease in stroke volume (41.3 +/- 4.2 ml/beat) and cardiac output (2.0 +/- 0.3 L/min). Atrial natriuretic factor infusion did not affect the increase in forearm vascular resistance during lower body negative pressure, but did attenuate the increase in plasma norepinephrine. To control for nonspecific vasodilator actions, lower body negative pressure was also repeated during nitroglycerin infusion. Nitroglycerin infusion did not significantly change the responses of blood pressure, cardiac output, stroke volume, forearm vascular resistance, or plasma norepinephrine during lower body negative pressure. Thus, these data demonstrate that atrial natriuretic factor infusion can attenuate sympathetic nervous system reflexes evoked during lower body negative pressure. These inhibitory effects on the sympathetic nervous system may contribute to many of the observed hemodynamic actions of atrial natriuretic factor.
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PMID:Atrial natriuretic factor attenuates sympathetic reflexes during lower body negative pressure in normal men. 170 79

We examined the effect of atrial natriuretic peptide on cerebral edema in 96 rats. Forty-four rats were given 30 (n = 11), 120 (n = 26), or 150 (n = 7) micrograms/kg of the peptide intravenously over 24 hours after occlusion of the left middle cerebral artery to induce cerebral ischemia. We then measured the brain water content, the brain sodium and potassium contents, the in vitro proton nuclear magnetic resonance longitudinal (T1) and transverse (T2) relaxation times, and the area of the edematous regions. Compared with saline treatment (n = 39), peptide treatment decreased the brain water content in a dose-dependent manner and decreased the brain sodium content significantly (p less than 0.05). Peptide treatment also suppressed the lengthening of both T1 and T2 in edematous tissue (p less than 0.05 and p less than 0.01, respectively) and reduced the area of the edematous regions observed by magnetic resonance imaging (p less than 0.01). Atrial natriuretic peptide appears to have a pharmacological effect on ischemic brain edema, possibly by suppressing the elevation of water content through regulation of electrolyte transport in the brain.
Stroke 1991 Jan
PMID:Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method. 182 2

Following subarachnoid hemorrhage, the plasma concentration of atrial natriuretic factor is elevated and appears to be independent of atrial stretch. While the hypothalamus and circumventricular organs contribute to sodium and intravascular volume regulation, their influence on atrial natriuretic factor is not known. We tested the hypothesis that, following subarachnoid hemorrhage, suprasellar cisternal blood, intraventricular blood, or ventricular enlargement would be associated with elevated plasma levels of atrial natriuretic factor. Computed tomograms of 26 patients performed less than or equal to 3 days after hemorrhage were analyzed to determine the presence of suprasellar or intraventricular blood and enlargement of the third or lateral ventricle. These results were correlated with the plasma atrial natriuretic factor and serum sodium concentrations. The initial atrial natriuretic factor concentration was elevated and was higher in patients with suprasellar or intraventricular blood than in those without (suprasellar: 131 +/- 20 and 54 +/- 10 pg/ml, respectively; intraventricular: 137 +/- 25 and 84 +/- 31 pg/ml, respectively). The atrial natriuretic factor concentration remained higher over the week following hemorrhage in patients with suprasellar blood than in those without (127 +/- 16 and 68 +/- 12 pg/ml, respectively). The atrial natriuretic factor concentration was not correlated with hyponatremia (125-134 meq/l) or age-corrected ventricular size. Hyponatremia did not correlate with the presence of intraventricular or suprasellar blood. Our data suggest that suprasellar and intraventricular blood disturb hypothalamic function, resulting in an elevated plasma atrial natriuretic factor concentration. The presence of a direct relation between atrial natriuretic factor and hyponatremia remains unclear.
Stroke 1991 May
PMID:Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage. 182 48

The physiologic and potential pharmacologic roles of atrial natriuretic factor in congestive heart failure have remained confusing. We have evaluated the hemodynamic responses to human atrial natriuretic factor [ANF (102-126)] given as bolus intravenous doses of 2.0 or 4.5 micrograms/kg to 12 patients with congestive heart failure. Responses were monitored with pulmonary and systemic arterial catheters in place. By 30 minutes after 4.5 micrograms/kg ANF (n = 6), heart rate decreased from 97 +/- 16 to 91 +/- 15 beats/min, right atrial pressure from 14 +/- 4 to 12 +/- 3 mm Hg, and pulmonary capillary wedge pressure from 33 +/- 3 to 23 +/- 2 mm Hg (all p less than 0.05); responses persisted for 120 minutes. Mean arterial pressure, cardiac index, stroke volume index, and pulmonic and systemic vascular resistances did not change significantly. The 2.0 micrograms/kg ANF dose produced similar responses, but only heart rate and right atrial pressure decreased significantly. No clinically important side effects were noted. High-dose ANF bolus doses can be administered simply and safely and improve hemodynamic parameters in chronic heart failure. Therefore ANF does have pharmacologic activity in heart failure and may have therapeutic potential.
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PMID:Prolonged hemodynamic benefits from a high-dose bolus injection of human atrial natriuretic factor in congestive heart failure. 183 91

Sixteen patients presenting for abdominal aortic surgery were divided into two groups according to whether or not there was a history and clinical evidence of chronic heart failure (CHF). Atrial natriuretic peptide (ANP) and catecholamines were measured during a preoperative exercise test and then with induction of anaesthesia and surgery. Patients in the CHF group (n = 8) had a much-reduced cardiac output (CO) rise in response to exercise compared to the control group (13% vs. 75%, P less than 0.05). This difference was due to the absence of a stroke volume increase in the CHF group. Induction of anaesthesia resulted in a greater fall in mean arterial pressure in the CHF group prior to the start of surgery, due to a greater fall in CO. Plasma ANP levels were higher in the CHF group at rest and at each exercise stage (P less than 0.05). ANP levels were not altered by induction of anaesthesia or intubation, but increased with the start of surgery in the CHF group (P less than 0.05). Increases in plasma catecholamine levels in response to exercise and to surgery were similar in the two groups. Changes in endogenous ANP may be important in counteracting the undesirable effects of vasoconstrictor hormones during physical exercise or surgical stress.
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PMID:Influence of cardiac failure on atrial natriuretic peptide responses in patients undergoing vascular surgery. 183 63


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