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

Although hemodynamic benefit has been shown with sodium nitroprusside (NP) in acute coronary pump failure, complete understanding of the mechanisms of action of the agent on the cardiocirculation and its value in chronic ventricular dysfunction are lacking. This investigation evaluates the effects of NP on the systemic and regional arterial and venous beds and on cardiac dynamics, ventricular volumes, contractile state and myocardial energetics in long-standing congestive heart failure. Twelve patients with chronic coronary pump dysfunction received NP infusion to lower systolic pressure to 95-105 mm Hg. Left ventricular (LV) function was assessed directly by angiographic volumes and high fidelity pressure, and peripheral circulatory dynamics were determined simultaneously by forearm arterial and venous plethysmography. NP reduced mean arterial pressure (MAP) from 88.2 to 73.4 mm Hg (P less than 0.05) and significantly (P less than 0.05) enhanced the variables of LV performance: LV end-diastolic pressure (EDP) diminished from 18.5 to 9.9 mm Hg; ejection fraction rose from 0.47 to 0.55; percent of LV segmental shortening increased; and isovolumic and ejection indices of contractility improved. Concomitantly, NP reduced the indices of myocardial oxygen demands of ventricular tension time index and LVED volume index. These salutary effects on LV performance and energetics occurred secondary to peripheral arterial and venous dilation (P less than 0.05) produced by NP: total systemic vascular resistance was lowered from 1590 to 1310 dynes sec cm--5; forearm vascular resistance diminished from 46 to 37 mm Hg/ml/100 gm/min; and forearm venous tone fell from 14.2 to 10.1 mm Hg/cc. Depressed stroke index (SI) and cardiac index (CI) increased (P less than 0.05) with NP: despite the fall in LVEDP, when ventricular filling pressures with the agent were at levels slightly above normal. Dextran infusion given with NP to restore LVEDP to moderately elevated values increased SI and CI (P less than 0.05) when NP alone produced no change in stroke output. Thus, the peripheral vasodilator properties of nitroprusside improve LV function by reducing impedance to ventricular ejection, while MVO2 is diminished by decreasing LV preload and afterload through relaxing actions
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PMID:Clinical use of sodium nitroprusside in chronic ischemic heart disease. Effects on peripheral vascular resistance and venous tone and on ventricular volume, pump and mechanical performance. 111 13

The cardiac response to intravenous administration of the ultrashort-acting oxybarbiturate anesthetic, methohexital sodium, was studied in trained dogs. Heart rate increased immediately and gradually declined to the control value 60 minutes later. Stroke volume decreased immediately, reversed transiently, and decreased again, to return gradually to the control value at one hour. Peak aortic flow velocity and peak aortic flow acceleration paralleled the triphasic response of stroke volume. Cardiac output decreased initially, then increased to above the control value to a maximum at the time of maximum heart rate, then decreased again to below the control value by 30 minutes. From 30 minutes to 60 minutes cardiac output gradually returned to the control value.
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PMID:Left ventricular dynamics of trained dogs anesthetized with methohexital. 111 61

We examined the hemodynamic response to afterload reduction by sodium nitroprusside in 7 patients with severe mitral regurgitation of purely valvular origin. Lowering of systemic vascular resistance was associated with major reductions in pulmonary capillary mean (29 +/- 2 to 13 +/- 1 mm Hg) and left ventricular end diastolic (20 +/- 3 to 9 +/- 1 mm Hg) pressures, while substantial increases were noted in cardiac index (2.2 +/- 0.5 to 3.1 +/- 0.4 litres/min per m2 body surface area) and forward stroke volume (23 +/- 4 to 34 +/- 4 ml/beat/m2 body surface area). Angiographic calculations showed significant decreases in regurgitant volume (73 +/- 19 to 55 +/- 12 ml/beat/m2 body surface area) and regurgitant fraction (0.70 +/- 0.07 to 0.57 +/- 0.06). No significant change occurred in left ventricular ejection fraction or heart rate, suggesting that the improved cardiac function was not due to a reflex increase in adrenergic stimulation. These observations support the concept that afterload reduction may be therapeutic in severe mitral regurgitation by reducing impedance to forward left ventricular output, thereby promoting greater forward and small regurgitant fractions of the total stroke volume.
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PMID:Reduced systemic vascular resistance as therapy for severe mitral regurgitation of valvular origin. 118 Apr 26

Changes in oxygen uptake, cardiac output, heart rate, stroke volume, central blood volume, arteriovenous oxygen difference, aortic, pulmonary arterial, and right atrial blood pressure, systemic vascular resistance, hematocrit, circulating plasma volume, urine flow, fractional sodium excretion, and free water clearance were studied in eight healthy volunteers in stable water diuresis, exposed to cold by means of air at +15 degrees C and at a speed of 0.5 m/sec. A decrease in circulating plasma volume and systemic vascular resistance was found during cold stress. Mean aortic blood pressure, sodium excretion, cardiac output, oxygen uptake, arteriovenous oxygen difference, and hematocrit increased. No changes in urine flow or in clearance of free water could be demonstrated. Heart rate, stroke volume, and central blood volume showed significant increases in cold. The results are interpreted to suggest that exposure to cold raises the arterial blood pressure by an increase in cardiac output, thereby increasing capillary hydrostatic pressure in certain vascular areas, including the renal vascular bed. This negatively affects capillary reabsorption processes in the kidney, causing a reduction in tubular sodium reabsorption, thus giving rise to a natriuresis. In other areas it seems to cause a shift of fluid towards the intersitial space.
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PMID:Cardiovascular and renal responses to acute cold exposure in water-loaded man. 118 88

The influence of controlled hypotension (mean arterial pressure 60 mmHg) induced by sodium nitroprusside and trimethaphan on systemic circulation and myocardial oxygen consumption was studied in 7 anaesthetized closed chest dogs. The hypotensive effect of both drugs was primarily mediated by a reduction in total peripheral resistance. No change in cardiac output was observed. Stroke volume decreased in the presence of tachycardia. Left ventricular max dp/dt remained unaffected during sodium nitroprusside hypotension and was reduced by trimethaphan. Max dp/dt, load data and heart rate indicated that trimetaphan possesses negative inotropic properties. Sodium nitroprusside induced a hyperperfusion of the heart with a marked decrease in myocardial arteriovenous difference in oxygen. Myocardial oxygen consumption remained unchanged. Trimethaphan, on the other hand, induced only small increments in coronary blood flow and a rise in the arteriovenous difference in oxygen of the heart. This resulted in a higher myocardial oxygen consumption (+16%). Cardiac efficiency was lessened by trimethaphan and remained unaffected in the presence of sodium nitroprusside. As sodium nitroprusside neither affects myocardial oxygen consumption nor alters myocardial contractility, we conclude that sodium nitroprusside has advantages over trimethaphan in the management of controlled hypotension and in the therapy of hypertensive crisis and cardiogenic shock.
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PMID:[The effects of sodiumnitroprusside and trimethaphan induced hypotension on haemodynamics and myocardial oxygen consumption (author's transl)]. 125 27

Twenty-nine patients received no anticoagulant therapy after aortic valve replacement with a Starr-Edwards Model 2400 prosthesis. Hemodynamic studies were performed at 3 to 26 months (average 12 months) in 18 of 29 patients. Mean aortic valve gradients ranged from 14 to 62 mm. Hg and averaged 34 mm. Hg. Calculated aortic valve area varied from 0.20 to 1.75 sq. cm. and averaged 0.98 sq. cm. Thirteen of 18 patients had critically stenotic valve orifices. At reoperation or autopsy, examination of the prostheses consistently revealed pannus and thrombus which narrowed the inflow orifice and usually extended to the struts. Of the remaining 11 patients, 3 have died (2 suddenly and one after a cerebrovascular accident), 2 have had embolic episodes, and 6 have refused a repeat study but are being given anticoagulant therapy. Clinical examination, serum lactic dehydrogenase (LDH) levels, phonocardiography, echocardiography, and fluoroscopy of the prosthesis were often unrevealing. Cardiac catheterization was the only reliable method for critically evaluating prosthetic function. In conclusion, close follow-up, preferably with cardiac catheterization, is recommended in any patient who received a Starr-Edwards Model 2400 aortic valve prosthesis without anticoagulation. Long-term anticoagulation with sodium warfarin is indicated in all patients with a Model 2400 aortic valve prosthesis unless there is a contraindication to such therapy.
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PMID:Thrombotic phenomena with nonanticoagulated, composite-strut aortic prostheses. 126 50

To test the efficacy of exogenous prostaglandins for vasodilator therapy in heart failure, we studied the hemodynamic, hormonal, and renal effects of prostaglandin E2 (1.5-150 ng/kg/min) in six conscious dogs before and after induction of heart failure by right ventricular pacing (250 beats/min, 10 days). In healthy dogs, PGE2 decreased the mean arterial pressure (MAP) by a reduction in total peripheral resistance (TPR), increased cardiac output (CO), stroke volume (SV), and heart rate with no effect on right atrial pressure (RAP). Plasma levels of renin (PRC) and norepinephrine (NE) were increased at the highest dosage. Renal plasma flow (RPF) and sodium excretion (UNaV) were augmented without a change in the glomerular filtration rate (GFR) and urine flow (UF). In dogs with heart failure, PGE2 lowered the MAP and TPR and elevated the CO and SV without an effect on the RAP, PRC, and NE. The RPF and GFR were not changed, but the increase in UNaV was preserved and UF significantly augmented. In experimental heart failure, PGE2 increases the CO due to arteriolar dilation and afterload reduction without inducing further neurohumoral activation and exerts potent natriuretic and diuretic action. Therefore, PGE2 may have beneficial effects in heart failure therapy.
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PMID:Prostaglandin E2 in dogs with heart failure: hemodynamic, hormonal, and renal effects. 128 Jul 9

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

The main points covered in this review are as follows: 1. Hypertension is a major determinant of cardiovascular disease (CVD). As such it is a major cause of mortality, potential years of life lost, morbidity and long-term disability. 2. The incidence of CVD is directly related to BP. It is likely that this extends over the full range of BP although some writers believe that a J-curve of risk exists for CHD. 3. The relationship between long-term disability from CVD and BP requires further study. 4. Because of regression dilution bias, the gradient in risk of stroke and CHD with BP has been underestimated in the past. Recent research suggests that the risk of stroke increases at least tenfold and CHD sixfold over a range of usual DBP of 30 mmHg (equivalent to approximately 50 mmHg baseline DBP). 5. The population attributable risk (PAR) of CVD related to general elevation of BP in the population from a mean daily excess of sodium intake of 100 mmol/day is at least 30%. In typical industrialised countries the PAR for stroke and CHD from clinical hypertension is 36% and 22%, respectively. These estimates of PAR provide a guide to the maximum benefit that could result from either restriction of sodium intake in the whole population or ideal management of all persons with hypertension. In practice such targets are unlikely to be realised. 6. Recent analyses of clinical trials of treatment of hypertension suggest that the risk of stroke is reduced at all levels of initial BP to the extent predicted from observational studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Review of the benefits of treating hypertension. 129 6

Fifty-three patients with traumatic shock were injected 200-400 ml of a 10% solution of sodium chloride in combination with 100 ml of the 40% solution of glucose. The continuous, for 1-2 h, elevation of arterial pressure, increased minute blood circulation volume, cardiac index, stroke volume were noted. At the same time base deficiency in blood was growing. So, in the last 5 patients the infusion therapy at the prehospital stage was completed by injecting 200 ml of 3% sodium solution and the acid-base state in them was thus leveled. When using the "internal autotransfusion" lethality was reliably less than in patients who were treated by routine (polyglucon, gelatinole) infusion therapy.
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PMID:[The use of the "internal autotransfusion" method in complex shock-control measures at the prehospital stage]. 130 53


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