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

The effects of central venous bolus injections of potassium chloride (KCl) on arterial potassium concentration were studied in patients undergoing cardiopulmonary bypass. Ten subjects were studied, and each received a rapid bolus injection of KCl, 33 microEq/kg, both before and after cardiopulmonary bypass. Injections were delivered through the proximal infusion port of a 7.5F pulmonary artery catheter, which was situated in either the superior vena cava or the right atrium. Monitored variables included the electrocardiogram, mean arterial, central venous, and pulmonary artery pressures, end-tidal carbon dioxide and inspired oxygen concentrations, and temperature. Blood was sampled continuously at either the radial artery alone or both the radial artery and aortic root at 2 mL/4.3 s. The difference in magnitude between the maximal potassium concentration achieved and the prebolus baseline potassium concentration (delta K) was correlated with cardiac output, stroke volume, and prebolus baseline potassium concentration (baseline [K+]), using simple linear regression analysis. Although significant hyperkalemia (eg, 7 to 9 mEq/L) developed in both the aortic root and radial artery, this was of no electrocardiographic or hemodynamic consequence, presumably because of the transient nature of the hyperkalemic response, following bolus injection of KCl. There was no significant correlation between delta K and cardiac output or stroke volume; however, delta K did correlate significantly with the Baseline [K+] in a direct linear relationship. It is concluded that central bolus injections of KCl through the proximal infusion port of the pulmonary artery catheter at 33 microEq/kg are safe. This technique should be used cautiously in patients with extremely low cardiac outputs or where intracardiac shunting of blood may exist, as these situations could potentially result in greater hyperkalemic responses than those observed in the current study.
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PMID:Effects of central bolus injections of potassium chloride on arterial potassium concentration in patients undergoing cardiopulmonary bypass. 213 35

The effect of varying amounts of dietary magnesium (Mg) in conjunction with potassium (K) on hypertension and stroke mortality in hypertensive stroke-prone (SHRsp) rats was studied. These results show that high K (2.1%) diets strongly protect against stroke mortality and rises of blood pressure, while high Mg (0.26%) diets appeared to increase stroke mortality and accelerate the rise of blood pressure in SHRsp rats. Similarly, medium high (1.3%) levels of K in the diet significantly reduced blood pressure and stroke mortality but not nearly as much as the 2.1% K in the high K diet.
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PMID:Deleterious effects of high magnesium diets and beneficial effects of high potassium diets in hypertensive stroke-prone rats. 213 72

Antihypertensive management reduces the incidence of congestive heart failure, malignant hypertension and stroke; however, the overall incidence of events due to ischemic heart disease was not influenced by antihypertensive treatment. One of the possible explanations might be some negative metabolic effects of antihypertensive drugs. Hypokalemia develops in 20 to 50% patients who receive a thiazide diuretic. An association between hypokalemia and malignant arrhythmias (including ventricular fibrillation), in acute myocardial infarction, has been observed. 24-hour ambulatory electrocardiographic monitoring demonstrated a higher frequency of ventricular ectopic beats in hypertensive patients taking thiazides. There is, however, no convincing evidence of a simple causative relation between ventricular extrasystoles and low concentrations of serum potassium. Hypertensives with left ventricular hypertrophy (ECG criteria) had significantly more premature ventricular contractions than patients with established hypertension without left ventricular hypertrophy or normotensive subjects. These data could provide an electrophysiologic substrate for the epidemiologic findings of increased morbidity and mortality in patients with left ventricular hypertrophy.
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PMID:The heart in hypertension and arrhythmias. 213 16

Endothelin-3 (ET-3), a recently described vasoconstricting peptide was infused in Inactin anesthetized rats at 0, 40, 170 or 340 ng/kg/min for 45 minutes (n = 8 in each group). ET-3 infusion increased mean arterial pressure at all infusion rates by increasing total peripheral resistance. Cardiac output (delta CO) was significantly decreased at the two highest ET-3 infusion doses. The decrease in cardiac output was associated with a decrease in central venous pressure and stroke volume and an increase in hematocrit. ET-3 infusion at 40 ng/kg/min increased sodium excretion (delta UNaV) by 0.14 +/- 0.08 microEq/min (p less than 0.05 compared to vehicle infusion) without affecting the glomerular filtration rate (GFR). At higher infusion rates ET-3 markedly decreased the GFR, urine flow and urinary potassium excretion. ET-3 infusion significantly increased circulating levels of ANF. The present study demonstrates that ET-3 increases blood pressure by increasing total peripheral resistance but decreases cardiac output. Further, ET-3 has natriuretic effects at low doses but markedly attenuates renal function at high doses.
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PMID:Cardio-renal effects of endothelin-3 in the rat. 214 3

We have recently demonstrated that K(+)-induced dilation of cerebral resistance-sized vessels has two independent components, only one of which seemed sodium pump dependent. In our current investigation, potassium-induced dilation of spontaneous tone was compared in cerebral arteries from normotensive Wistar-Kyoto rats and age-matched stroke-prone spontaneously hypertensive rats. Branches of the posterior cerebral artery were cannulated and pressurized, and these vessels developed spontaneous tone. After a 5-minute period in K(+)-free physiological saline solution, K+ was increased in 1-mM increments to a final concentration of 15 mM. In the normotensive arteries, K+ concentrations between 0 and 5 mM K+ resulted in dilations that had a transient (sodium pump-dependent) component, and K+ concentrations in excess of 7 mM produced dilations that lacked a transient (sodium pump-independent) component. Similar branches from the hypertensive rat also responded with transient dilations to K+ (less than 5 mM), and these were significantly greater at 3 mM K+. However, the maintained dilations to K+ (greater than 7 mM), noted in preparations from Wistar-Kyoto rats, were absent in seven of eight preparations. Thus, the impaired dilations, in the hypertensive vessels, to K+ described here is a consequence of altered function of some sodium pump-independent component rather than altered Na+,K(+)-ATPase activity.
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PMID:Impaired potassium-induced dilation in hypertensive rat cerebral arteries does not reflect altered Na+,K(+)-ATPase dilation. 217 51

We studied the effects of dietary Ca2+ on blood pressure, survival, and calcium channel function to investigate cardiovascular disease mechanisms in stroke-prone spontaneously hypertensive rats. Beginning at 3 weeks of age, rats were fed high sodium chloride diets (8.0%) in combination with either high (2.0%) or low (0.2%) Ca2+ diets for 8 weeks. At 12 weeks of age, survival was 90% in the high Ca2+ group and 30% in the low Ca2+ group. The higher blood pressure and lower survival in the low Ca2+ group suggest an intensification of altered vascular muscle cell mechanisms by a dietary Ca2+ deficit. Nimodipine (1-10 nM) effectively blocked L-type Ca2+ currents in isolated vascular muscle cells from both groups. Contraction of isolated cells that were not patch clamped to high potassium solutions were also blocked by 1 nM nimodipine. Disappearance of the L-type Ca2+ channel current was accelerated by holding at depolarizing potentials (positive to -50 mV) and by depolarizing steps to 0 mV. Nimodipine block of the L-type Ca2+ currents in vascular muscle is believed to contribute substantially to antihypertensive properties and stroke prevention, actions that may develop fully only in stroke-prone spontaneously hypertensive rats on a diet of at least normal Ca2+.
Stroke 1990 Dec
PMID:Effects of dietary calcium on nimodipine-sensitive calcium channel function in stroke-prone spontaneously hypertensive rats. 217 63

Prehistoric animals and humans consumed a diet low in sodium but high in potassium, and thus, evolutionary forces fostered the development of physiologic systems that conserved sodium and excreted potassium. With the advent of civilized societies, food cooking and processing have greatly increased the sodium but decreased the potassium content of the diet. However, there has been little time for physiologic systems to adapt. The resulting excess of sodium has been implicated as an important factor in the development of hypertension and congestive heart failure. This traditional focus on sodium has ignored the potential role that an inadequate dietary intake of potassium might play in the degenerative diseases of the heart, brain and kidney. Yet dietary potassium may be as powerful a determinant of cardiovascular morbidity and mortality as dietary sodium. In experimental and clinical hypertension, an increased intake of potassium (without a change in dietary sodium) can reduce blood pressure, may suppress the activity of the sympathetic nervous and renin-angiotensin systems, and can prevent the development of vascular injury; conversely, potassium depletion has been associated with an increase in stroke and sudden death. In patients with chronic heart failure, potassium can modify both the mechanical and electrical properties of the heart, it can exert diuretic effects, and it can reduce the frequency and complexity of potentially lethal ventricular tachyarrhythmias. Given this central role, the effects of many pharmacologic interventions on the morbidity and mortality of patients with hypertension or chronic heart failure can be enhanced or diminished by the effect that these treatments might have on potassium homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potential role of potassium as a determinant of morbidity and mortality in patients with systemic hypertension and congestive heart failure. 217 78

Endothelin, a potent vasoconstrictor peptide synthesized by the vascular smooth muscle endothelium, was chronically infused into male Sprague-Dawley rats to determine whether a long-term increase in circulating endothelin levels would cause a sustained elevation in mean arterial pressure. Rats were catheterized, housed in metabolic cages, and maintained on a fixed 6 meq/day sodium intake throughout the experiment with daily measurements including mean arterial pressure, heart rate, water intake, urine output, urinary sodium excretion, urinary potassium excretion, cardiac output, total peripheral resistance, and stroke volume. Infusion of endothelin-1 (ET-1) at rates of 3, 5, or 7.5 pmol/kg/min for 7 days was associated with significant, sustained, and dose-dependent increases in mean arterial pressure and smaller less consistent elevations in total peripheral resistance. Other parameters were unaffected. Similar results were observed in rats receiving endothelin-3 (ET-3), except that a higher dose of ET-3 was required. These results indicate that elevated blood levels of endothelin could produce a maintained hypertension without sodium or water retention and that the hemodynamic basis for the increased mean arterial pressure is similar to that seen in most other forms of experimental and clinical hypertension.
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PMID:Chronic hypertension produced by infusion of endothelin in rats. 219 Sep 24

Experimental prevention of hypertension and related cardiovascular diseases has been studied in rat models for hypertension and stroke and not only salt reduction but also increased intakes of potassium, calcium, magnesium, protein, some amino acids and fatty acids and dietary fibers have been proven to be effective and indicated the importance of nonpharmacological dietary prevention of cardiovascular diseases. These experimental findings contribute to dietary risk factor analyses and the prevention of hypertension and its complications in man, as demonstrated by a cross-sectional epidemiological study on cardiovascular diseases and alimentary comparison (WHO-CARDIAC Study).
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PMID:Experimental intervention of hypertension and cardiovascular diseases. 220 60

Among the many classes of diuretics available, thiazides have emerged as the most appropriate category for the treatment of uncomplicated hypertension. Potassium-sparing agents may be added according to need or in fixed-combination therapy. Thiazides act on the cortical diluting segment of the renal tubule. The potassium-sparing agents interfere with the Na(+)-K+ exchange process in the terminal part of the distal tubule. Thiazides have been the cornerstone of therapy in nearly all prospective therapeutic, mild and moderate hypertension trials conducted to date. They have, therefore, proved their value in the prevention of hypertensive cardiovascular complications such as stroke and congestive heart failure. The physiologic changes occurring during antihypertensive treatment with thiazides have been extensively studied. The initial response to a thiazide is characterized by a mildly negative change in sodium and fluid balance. The resulting slight contraction in plasma volume is followed by reductions in cardiac output and blood pressure. Because these reductions are disproportionate, vascular resistance rises initially. In the longer term, plasma volume is partly restored, and cardiac output re-attains the baseline level. Thus, the reduction in blood pressure ultimately appears to be based on vasodilation. The mechanisms of this biphasic vascular response are not completely understood. This lack of insight, however, does not detract from the proven value of thiazides in treating hypertensive subjects.
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PMID:Diuretics and blood pressure reduction: physiologic aspects. 221 85


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