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

The indices of central hemodynamics were determined in 112 patients with hypertensive disease during a crisis and in its arrest with hyperstat by means of integral rheography. The condition of the sympatheticoadrenal and kallikrein-kinin systems was studied. It was found that hyperstat normalizes arterial pressure in 5--6 minutes by reducing the initially increased general peripheral resistance and increasing the blood stroke and minute volumes as well as by reducing the content of adrenaline. The indices of the blood kallikrein-kinin system showed a tendency to return to normal values 24 hours after hyperstat administration. The drug caused no complications, only in two patients deterioration of myocardial blood supply was noted. The authors claim that hyperstat is a highly effective agent for arresting hypertensive crises.
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PMID:[Use of Hyperstat for arresting hypertensive crises]. 36 67

We investigated the effect of two oral (p.o.) doses of cicletanine (5 and 30 mg/kg/day) for 4 weeks on urinary excretion (UKE), renal concentration (RKC) of kallikrein, and prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha urinary excretion of stroke-prone (SP) spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) rats submitted to a high sodium intake (1%). Both doses of cicletanine induced a significant antihypertensive effect in treated SHR as compared with hypertensive untreated controls (HC). After 4-week treatment, a significant difference in mortality was observed between normotensive controls (NC) (0%) and HC (84%). Both doses of cicletanine reduced the mortality of hypertensive animals (8% SHR with 5 mg and 24% SHR with 30 mg vs. 84% in HC). Whereas UKE and RKC were decreased in HC during the progression of untreated hypertension from week 1 to week 4, both doses of cicletanine administration significantly prevented this decrease. Consistently with maintenance of UKE during the course of hypertension, the level of tissue kallikrein was higher in hypertensive cicletanine-treated than in untreated SHR. This increased RKC was associated with a significantly higher rate of kallikrein biosynthesis. The increased level of the urinary excretion and tissue concentration of PGE2 and 6-keto-PGF1 alpha in cicletanine-treated SHR as compared with untreated animals was also of interest. This protective effect on PG excretion correlated with that on kallikrein excretion. The results confirm the efficiency of cicletatine as an antihypertensive treatment. The antihypertensive action includes protective effects on potential vasodepressor kallikrein-kinin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of cicletanine on hypertension-induced decreases in the renal kallikrein-kinin and prostaglandin systems in stroke-prone spontaneously hypertensive rats. 128 Jul 17

Thirty-one healthy young pigs were studied to evaluate the effects of methylprednisolone sodium succinate (MP) on cellular, proteolytic, and hemodynamic parameters in normal and endotoxin-exposed animals. Fourteen animals served as controls, whereas 17 test animals received a continuous infusion of endotoxin, 0.01 mg/kg/3hr. Seven of the test animals and seven of the control group received a total of 200 mg/kg body weight over 5 hr of MP, 100 mg/kg as pretreatment before the endotoxin infusion was started. The administration of MP to control animals did not cause changes in the plasma kallikrein-kinin system, as determined with chromogenic peptide substrate assays. Only temporary effects, which normalized during the observation period, were seen in hemodynamic parameters. The pretreatment with MP significantly counteracted the increases in plasma kallikrein activity (KK) and the decreases in functional kallikrein inhibition capacity (KKI) seen after endotoxin infusion in untreated animals. Marked reductions in the number of circulating leukocytes and platelets were observed in untreated endotoxemia, together with increases in hematocrit. Furthermore, increases in pulmonary vascular resistance (PVR) and decreases in cardiac output (CO), left ventricular stroke work (LVSW), and mixed venous oxygen saturation (SvO2) ensued. The changes in circulating cells, PVR, and SvO2 were significantly counteracted by MP treatment, whereas changes in hematocrit, CO, and LVSW were only moderately improved.
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PMID:Plasma kallikrein generation in endotoxemia is abolished by ultra high doses of methyl-prednisolone: in vivo studies in a pig model. 177 78

Blood proteins could play a critical role in the pathogenesis of cerebral vasospasm in subarachnoid hemorrhage (SAH) as agonists and as antagonists of vasoconstriction. The present study was designed primarily to quantify the inhibition produced by antithrombin III of the phasic responses elicited by cumulative doses of KCl, serotonin (5-HT), uridine triphosphate (UTP), and thrombin in isolated canine basilar arteries, and to ascertain whether other proteins might act similarly. Antithrombin III (1 unit/ml and 3 units/ml) given 2 min beforehand inhibited all agonists. The inhibition was not dependent on a functional endothelium nor due to stimulation of the electrogenic sodium pump. Alpha2-macroglobulin (0.1 mg/ml and 0.4 mg/ml) inhibited the contractile responses to high K+, 5-HT and thrombin. Kallikrein (1 and 4 units/ml) did not inhibit UTP but inhibited high K+ and 5-HT through an effect on the endothelium. Kallikrein (1 unit/ml) irreversibly blocked the responses to thrombin. Globulins (3 mg/ml) and fibrinogen (0.3 mg/ml) were not inhibitory. The results demonstrate that anticoagulant proteins are very effective nonspecific inhibitors of the vasoconstriction, whereas the serine protease kallikrein selectively blocks thrombin. The remarkable potency of antithrombin III suggests that it may protect cerebral arteries from exhibiting vasospasm in SAH.
Stroke
PMID:Vasodilator proteins: role in delayed cerebral vasospasm. 242 60

The relationship between hypertension and cardiovascular damage was assessed in three groups of spontaneously hypertensive rats (SHR): 1. stroke prone SHR (SHR-SP) treated orally with an angiotensin I converting enzyme inhibitor (captopril) (100-400 mg/L in the drinking water) from 6 to 35 weeks of age, 2. SHR-SP maintained on tap water until 30 weeks of age, 3. stroke resistant SHR (SHR-SR) maintained on tap water. The controls were Wister Kyoto rats (WKY) maintained on tap water. Captopril-treated SHR-SP showed blood pressure lower than that of untreated SHR-SP, similar to SHR-SR. The ratio of heart weight to body weight was 0.55% in SHR-SP, 0.39% in captopril-treated SHR-SP, 0.46% in SHR-SR, and 0.39% in WKY. The kidneys of SHR-SP showed glomerular sclerosis, glomerular fibrosis, tubular casts, interstitial cell infiltration and vascular wall thickening or hyperplasia of the small arteries and arterioles. The severe glomerular sclerosis was mostly distributed in the inner and middle portions of cortex. Immunohistological study showed IgG, C3 and fibrinogen in the glomeruli and arterioles in SHR-SP. In captopril-treated SHR-SP, similar to SHR-SR, only minor histological changes were seen and there was no deposition of IgG, C3 or fibrinogen. No changes were seen in WKY. Thus, it was concluded that nephrosclerosis and cardiac hypertrophy in SHR-SP are prevented by captopril. The role of the renin-angiotensin and kallikrein-kinin systems in organ pathogenesis in SHR-SP is discussed.
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PMID:Prevention of nephrosclerosis and cardiac hypertrophy by captopril treatment of spontaneously hypertensive rats. 294

In investigating the role of urinary kallikrein in the pathophysiology of hypertension, we measured 12-hour kallikrein excretion in 1,100 persons in 68 Utah kindreds. The kallikrein excretion was statistically adjusted to account for variations in body size and urine output. Adjusted kallikrein excretion was greater in youths than in adults and correlated with potassium excretion and sodium excretion in persons with normal blood pressure. It was decreased in normotensive subjects with strong family histories of stroke and hypertension, but was not significantly different in adults with hypertension. Adjusted kallikrein excretion was correlated between pairs of siblings, parent-offspring pairs and spouses. Our results indicate that kallikrein excretion is a familial variable, with the familiality due more to shared environmental than genetic factors.
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PMID:Evidence for environmental familiality of kallikrein excretion in Utah kindreds. 363 40

We have previously shown that topical brain application of kallikrein, an enzyme which converts kininogen to bradykinin, induces rabbit pial arteriole dilation. The purpose of the present investigation was to utilize a newly developed competitive kinin receptor antagonist to test the hypothesis that kallikrein-induced dilation was due to the conversion of brain kininogen to vasoactive kinins. As in our previous study, we measured rabbit pial arteriole diameter with a microscope using the closed cranial window technique. The kinin antagonist (6 microM) reduced the dose-dependent dilation produced by bradykinin and blocked the dilation induced by kallikrein. In addition, the kinin antagonist was specific since it did not alter the cerebral arteriole dilation produced by adenosine, acetylcholine, or vasoactive intestinal polypeptide. These experiments provide further evidence for a possible role of the endogenous brain kallikrein-kinin system in the modulation of the cerebral circulation and provide the necessary pharmacologic foundation for future use of this antagonist in testing the role of kinins in the normal or altered cerebral circulation.
Stroke
PMID:Inhibition of bradykinin- and kallikrein-induced cerebral arteriolar dilation by a specific bradykinin antagonist. 364 92

Intraocular pressure (IOP) and arterial blood pressure (BP) were recorded manometrically in normotensive Wistar Kyoto rats (NR) and stroke-prone spontaneously hypertensive rats (SHR). IOP was significantly lower in SHR (7.8 +/- 0.2 mm Hg) compared to NR (15.9 +/- 0.4 mm Hg). In NR, administration of vasoactive substances (kallikrein, bradykinin, angiotensin I and II) or bloodletting resulted in significant IOP reactions, which ran nearly parallel to the acute BP changes. In SHR, however, IOP showed little reaction after comparable changes in BP. The cause of the low IOP in SHR is unknown. It is assumed that in SHR rarefaction of arterioles and capillaries and a decrease in the compliance of eye vessels, in combination with an increase in the distensibility of the bulbus at this low IOP level, contribute to the lack of IOP response after administration of vasoactive drugs.
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PMID:Intraocular pressure and systemic blood pressure after administration of vasoactive substances in hypertensive and normal rats. 384 58

The authors studied the correlation between the activity of renin, angiotensin-converting enzyme, the activity of prekallikrein and the blood prekallikrein level in men performing veloergometric exercise. At the same time they recorded the hemodynamic parameters (systolic and diastolic arterial pressure, the systolic rate, stroke volume and cardiac index, specific peripheral resistance). The blood samples collected before and immediately after the exercise showed a 41.4%-increase in the activity of renin and a 95%-increase in that of kallikrein, whereas the level of prekallikrein and the activity of the converting enzyme declined by 19 and 13% (P less than 0.05). These changes were accompanied by an increase in the systolic rate (by 107%) and in the systolic arterial pressure (by 36.7%), as well as by a reduction of the specific peripheral resistance (by 41.4%).
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PMID:[Renin, kallikrein and angiotensin converting enzyme in human physical loading]. 629 25

In male spontaneously hypertensive rats (SHRSP) of the stroke prone strain (Okamoto) and in normotensive Wistar-Kyoto rats (WKY) urinary kallikrein excretion was investigated at different age and at drug-induced diuresis. In rats of both strains from 7th till 19th week of age urinary kallikrein excretion increased with age. In SHRSP of 7th till 11th week of age kallikrein excretion was higher than in WKY rats, while it was lower in the 48-week-old SHRSP. No correlation was found between urinary kallikrein excretion and systolic blood pressure. In SHRSP and WKY rats a similar daily rhythm of kallikrein excretion in urine was found being high in the early morning and low in the afternoon. Kallikrein excretion correlated significantly with urine volume. The loop diuretic bumetanide (4 and 40 mg/kg) induced diuresis and natriuresis in both strains, however more marked in the WKY rats than in the SHRSP. Urinary kallikrein excretion, however, showed in both strains the same biphasic course with a short lasting increase and a secondary decrease. Thus, in the average urinary kallikrein excretion was not effected by the drug. Prolonged treatment with furosemide over 5 days (125 mg/kg) resulted in an increase in kallikrein excretion in urine, more pronounced in the WKY rats than in the SHRSP. The observed results suggest that renal kallikrein-kinin system is not involved in the development of spontaneous hypertension as a pathogenetic factor, but rather is influenced by other factors like hormone interactions, i.e. mineralocorticoids and catecholamines, as well as renal function and acute changes in urine flow.
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PMID:The renal kallikrein-kinin system in spontaneously hypertensive rats. 657 82


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