Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Long-lasting haemorrhagic hypotension (4.5 hr at 35 mmHg) leading to irreversible haemorrhagic shock, has been studied in normal dogs, in dogs treated with a bradykinin potentiating nonapeptide (BPP(9a)), which blocks the conversion of angiotensin I to angiotensin II, and in dogs with experimental chronic diabetes insipidus (DI dogs). BPP(9a) was given by I.V. injection before the start of bleeding (BPP pre-treated group), 45 min after blood pressure had reached 35 mmHg (BPP early treated group) or 2 hr after blood pressure had reached 35 mmHg (BPP late-treated group). After retransfusion of blood all dogs were allowed to recover and observed for a further period of 3 days.2. Untreated control dogs developed haemorrhagic shock with tachycardia, low cardiac output, low total peripheral conductance and low stroke volume. All died within 24 hr of retransfusion, with pathological lesions typical of irreversible haemorrhagic shock.3. BPP pre-treated dogs developed haemorrhagic shock with bradycardia (during early shock), high cardiac output, high peripheral vascular conductance and high stroke volume when compared with the untreated controls. All pre-treated animals survived the 3 day observation period. They were then killed and on post-mortem showed no signs of irreversible haemorrhagic shock.4. BPP early-treated animals behaved like controls before BPP, but like pre-treated animals after the drug. Only one out of eight died within the 3 day observation period.5. BPP late-treated dogs behaved like controls before BPP. They responded to the drug with a rise in cardiac output, peripheral vascular conductance and stroke volume, and with a fall in heart rate. These responses were, however, short-lived. Four out of these eight animals died within the 3 day observation period, with lesions of irreversible haemorrhagic shock.6. DI dogs developed haemorrhagic shock with tachycardia (like controls), but with high cardiac output and peripheral vascular conductance (like BPP pre-treated dogs). The stroke volume of DI dogs was intermediate between those of controls and pre-treated groups. All six dogs survived the 3 day observation period.7. BPP(9a) had no measurable effect on the course of endotoxic shock.8. It is suggested that the normally severe vasoconstriction of the mesenteric vascular bed, which is thought to be responsible for irreversible haemorrhagic shock, is absent or attenuated in the absence of vasopressin or angiotensin. The consequences of this on the development of irreversibility are discussed.
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PMID:On the role of vasopressin and angiotensin in the development of irreversible haemorrhagic shock. 437 70

The spontaneously hypertensive rat (SHR) and the stroke-prone substrain (sp-SHR) have been reported to have several abnormalities in levels of peptides both in tissue and in plasma (beta-endorphin, prolactin, thyroid stimulating hormone and vasopressin) when compared to the Wistar Kyoto (WKY) normotensive control rat. As the secretion of these peptides is under dopaminergic control and the abnormalities consistently suggest under-activity of the dopaminergic control system in the brain, injections of dopamine (0.4 mg/kg) were given i.c.v. to 10 SHR, 10 renal artery stenosis hypertensive rats (LRAS) and 10 genetically hypertensive rats of the New Zealand strain (GHR). Mean blood pressure fell from 205 +/- 6 (SEM) mmHg to 128 +/- 8 mmHg in the SHR (p less than 0.001), from 184 +/- 7 mmHg to 176 +/- 7 mmHg in the LRAS (p greater 0.05) and from 157 +/- 5 mmHg to 138 +/- 6 mmHg in he GHR (p less than 0.02). These effects were unlikely to be due to leakage of dopamine out into the periphery as i.v. dopamine (0.4 mg/kg) increased blood pressure in these animals.
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PMID:Neuropeptide abnormalities suggest a dopaminergic basis for high blood pressure in the spontaneously hypertensive rat. 609 77

Twelve male patients were given high dose fentanyl (75-100 microgram.kg-1) anaesthesia with oxygen during elective aorto-coronary bypass operations, and their haemodynamic and vasopressin responses were determined during induction, sternotomy, cardiopulmonary bypass, post-bypass and recovery periods. For comparison, a group of 12 male patients were anaesthetized with morphine, halothane 0.5 per cent, nitrous oxide and oxygen, and were similarly studied. Significant alterations in haemodynamics included increased mean arterial pressure after sternotomy in the fentanyl group, increased heart rate in both groups, increased systemic vascular resistance after sternotomy only in the halothane group, and decreased left ventricular stroke work index in both groups following induction, bypass, and during the recovery periods. Plasma vasopressin levels increased significantly in both groups during the bypass period, but returned to baseline levels following bypass. Serum sodium and osmolality did not change significantly, and urinary sodium and potassium excretion rose with the progress of the operation in both groups. A positive correlation was found between mean arterial pressure and vasopressin only in the halothane group. Systemic vascular resistance was correlated to vasopressin levels in both groups. Vasopressin response in both groups was similar, with significant but relatively low increases in levels during cardiopulmonary bypass. Fentanyl-oxygen anaesthesia did not provide haemodynamic stability in eight of 12 patients.
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PMID:Haemodynamic and plasma vasopressin responses with high-dose fentanyl anaesthesia during aorto-coronary bypass operations. 612 67

An increased activity of vasoconstrictor mechanisms may play an important role in circulatory adjustments to heart failure. Thus, hemodynamic data and the plasma hormones epinephrine (E), norepinephrine (NE) and arginin vasopressin (AVP) as well as the plasma renin activity (PRA) were assessed in 50 patients undergoing coronary angiography and right heart catheterization. Patients were classified into three groups according to severity of left ventricular (LV) dysfunction as assessed by ejection fraction (LVEF): those with normal left ventricular function (group 1 (n = 12): LVEF greater than or equal to 55%, mean 70 +/- 3%) and those with moderate (group 2 (n = 16): LVEF 54-35%, mean 43 +/- 2%) or severe LV dysfunction (group 3 (n = 22): LVEF less than 35%, mean 22 +/- 1%). At rest plasma NE concentrations in patients with heart failure (group 2: 187 +/- 17 pg/ml; group 3: 299 +/- 27 pg/ml) did not differ significantly from control values (199 +/- 26 pg/ml). During exercise, NE concentrations increased in all patients (p less than 0.001). This increase in plasma NE was more pronounced in group 3 (753 +/- 71 pg/ml) than in group 1 (262 +/- 37) and group 2 (388 +/- 64). A significant inverse correlation was found between plasma NE and stroke index at rest (r = -0.592, p less than 0.001) as well as during exercise (r = -0.659, p less than 0.001). PRA was elevated at rest and during exercise in patients of group 3 but not of group 2 as compared with control patients (p less than 0.05). Plasma E and AVP were similar in all groups. Patients of group 3 were subdivided according to exercise capacity into patients who tolerated a maximum work load of 50 watts or more (group 3A) and those who did not tolerate a work load exceeding 25 watts (group 3B). At rest and during exercise, patients of group 3A had a higher stroke index than patients of group 3B. In contrast, there was no significant difference in LVEF between group 3A and 3B (22 +/- 2 vs 20 +/- 1%). During exercise patients with low exercise capacity (group 3B) had higher NE levels than patients with less impaired exercise capacity (group 3A) (948 +/- 86 vs 590 +/- 65 pg/ml, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Left ventricular function and activity of vasoconstrictor systems in patients with chronic heart insufficiency]. 637 88

Vasopressin (0.01-0.3 IU/ml) contracted isolated segments of rat basilar arteries from stroke-prone SHR (SP-SHR) and normotensive Wistar-Kyoto rats (WKY) unequally. Basilar arteries from SP-SHR were more responsive to vasopressin than were those from WKY when adrenergic nerve endings were present in both preparations. After destruction of adrenergic nerve endings by in vitro 6-hydroxydopamine treatment, the ED50 for vasopressin in both WKY and SP-SHR arteries decreased by a factor of three, indicating that the contractions caused by vasopressin were similarly modulated by prejunctional neurotransmitter release. However, only arteries from WKY showed prominent rhythmic relaxation-contraction cycles superimposed upon the vasopressin-induced tone. The tension cycles were 20-100 dyn in amplitude and occurred at 1-3 cycles/min. These tension oscillations of WKY were pronounced and obvious, sometimes amounting to as much tension as the underlying tonic contraction. Tension cycles could reflect a physiological contraction-relaxation phasing mechanism that fails to occur in basilar arteries of SP-SHR. The rhythmic activity was enhanced by K+-free solution and abolished by 30 mM K+ solution, suggesting that pacemaker changes in K+ conductance may underlie the WKY tension oscillations. It is suggested that the absence of rhythmic contractions in SP-SHR basilar arteries may be explained by greater activity of the electrogenic Na+-pump, which would tend to prevent the rhythmic oscillations in tension. These observations suggest that vasopressin has a differential action on basilar arteries of SP-SHR and WKY.
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PMID:Difference in vasopressin-induced contraction of basilar arteries from stroke-prone spontaneously-hypertensive rats (SP-SHR) and control Wistar-Kyoto rats (WKY). 644 11

There is evidence for an increased secretion of vasopressin in most models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension, one- and two-kidney renal hypertension, partial nephrectomy-salt hypertension, the spontaneously hypertensive rat (SHR), the Dahl salt-sensitive rat on a high-salt diet, and human essential hypertension. In most forms of hypertension, there is also an increased pressor responsiveness to vasopressin as well as to other pressor agents. Blockade of vasopressin with either a competitive antagonist or a specific antiserum lowered blood pressure substantially in DOC-salt hypertension, two-kidney, one-clip hypertension, the stroke-prone SHR with well-established hypertension, and the Dahl S rat treated with captopril. In rats with diabetes insipidus, one- and two-kidney renal hypertension, but not DOC-salt hypertension, can be produced. There is evidence that vasopressin can contribute to some models of hypertension as either a pressor or an antidiuretic agent.
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PMID:The role of vasopressin in hypertension. 669 Mar 29

A 47-year-old patient with severe decompensated alcoholic liver disease developed a progressive deterioration of her renal function (serum creatinine 4.0 mg/dL) with a renal failure index (RFI: UNa/U/PCr) consistently less than 1.0. In the absence of other causes of renal failure, these values supported the diagnosis of hepatorenal syndrome (HRS). A five-hour head-out water immersion (HWI) in a sitting position was carried out to increase the patient's "effective" blood volume (EBV) in an attempt to reverse the HRS. Hemodynamic monitoring (Swan-Ganz) was performed during the entire HWI procedure. Cardiac index increased by 64% during HWI (2.57 to 4.22 L/min/m2). Stroke volume index doubled (32.9 to 65.0 mL/m2) and systemic vascular resistance decreased by 48% (1426 to 754 dyne sec/cm). Increases in right atrium (RA) pressure (7.5 to 17.5 mm Hg) and pulmonary wedge (PW) capillary pressure (7.5 to 16.3 mm Hg) also occurred. Hemoglobin, hematocrit, and plasma protein concentrations decreased by 18% during HWI. Only a modest improvement in creatinine, urea, inulin, and para-aminohippurate (PAH) clearances was observed during HWI, and the RFI remained below 1.0. Plasma levels of antidiuretic hormone (ADH), aldosterone, and renin activity decreased during HWI. The patient's renal function progressively deteriorated over the next 15 days, but tubular function, as assessed by an RFI less than 1.0, was still intact seven days after our study. Our results indicate that a considerable increase in effective blood volume does not restore renal function in HRS.
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PMID:Effect of head-out water immersion on hepatorenal syndrome. 669 41

The effect of arginine-vasopressin (AVP) on potassium ion-evoked release of [3H]noradrenaline (NA) from rat brainstem slices was investigated. In normotensive Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats, AVP inhibited release of [3H]NA in a dose-dependent fashion, the magnitude and time course of inhibition at 10(-12)M AVP being similar to that observed using the alpha 2-adrenoceptor agonist, clonidine at 10(-7) M. However, it is unlikely that AVP functions through alpha-receptors since its effect is not blocked by phentolamine (10(-6) M). When brainstems from spontaneously-hypertensive (SH) rats (stroke-prone strain) were used, AVP was found to be without effect on [3H]NA-release at concentrations up to 10(-8) M. The potassium ion-evoked release appeared to have two components. The early phase of release was tetrodoxotin (TTX)-sensitive and was probably due to action potential conduction within the slices. The later phase, which was unaffected by tetrodotoxin, was probably a result of potassium-induced depolarization of nerve endings. AVP appeared to affect principally the early, TTX-sensitive release. In the presence of TTX (0.3 microM) the inhibitory effects of AVP were no longer seen. Thus, AVP may affect generation or conduction of action potentials within this tissue. There is published evidence that central vasopressinergic neurons may play a role in controlling the baroreceptor reflex arc. The present study provides a possible biochemical basis for this effect and is consistent with a neuromodulatory role of AVP in the CNS.
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PMID:Normotensive and spontaneously-hypertensive rats show differences in sensitivity to arginine-vasopressin as a modulator of noradrenaline release from brainstem slices. 669 13

A number of experiments were performed in order to investigate the possible importance of vasopressin (AVP) in the pathogenesis of high blood pressure in spontaneously hypertensive rats of the stroke prone strain (SHRSP). Radioimmunological studies revealed reduced concentrations of AVP in the plasma and brain of SHRSP as compared to normotensive controls. Intravenous administration of an AVP pressor antagonist had no significant influence on mean arterial blood pressure, cardiac output and total peripheral resistance in SHRSP. Crossbreeding of SHRSP with rats homozygous for hypothalamic diabetes insipidus resulted in the development of a new strain of rats which show high blood pressure despite of a complete lack in AVP. These results argue strongly against a pressor role of AVP in the development or maintenance of hypertension in SHRSP.
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PMID:Pathogenesis of hypertension in spontaneously hypertensive rats: definite evidence against a pressor role of vasopressin. 669 49

During hemodiafiltration, solutes are removed simultaneously by diffusion and convection. Increase of the fraction removed by diffusion, by using large surface area hemodiafilters, allows a further reduction of treatment time by hemodiafiltration. To assess the efficiency and biochemical safety of ultrashort treatment (mean duration 3 X 105 +/- 14 min/week) six patients (age 22-64) have been observed for six months. There were no differences in the clinical state or in the biochemical parameters compared to those found during the preceding hemodialysis period (3 X 240 min/week). In a second study, hemodynamic measurements in six individual patients aged 34-72 have been compared during a 90 min ultrashort hemodiafiltration (90 min) and during a 240 min hemodialysis. Circulatory stability was maintained during hemodiafiltration despite a rate of fluid removal that was 2.5 times that which occurred during hemodialysis. During both techniques there was a reduction of stroke volume and an adequate norepinephrine-induced rise of peripheral resistance. Plasma levels of vasopressin did not change during treatment. There were no differences in the frequency and quality of premature ventricular beats between the two treatments. The data from the two studies suggests that ultrashort hemodiafiltration (3 X 1.5-2 hr/week) provides biochemical safety as well as hemodynamic stability.
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PMID:Ultrashort hemodiafiltration: efficiency and hemodynamic tolerance. 683 75


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