Disease relevance of Vascular Resistance

• There was a strong correlation between the intensity of endothelin-1-like immunoreactivity and pulmonary vascular resistance in the patients with plexogenic pulmonary arteriopathy, but not in those with secondary pulmonary hypertension [1].
• In 20 patients with severe congestive heart failure, intravenous milrinone resulted in significant decreases in left ventricular end-diastolic pressure (from 27 +/- 2 to 18 +/- 2 mm Hg), pulmonary wedge pressure, right atrial pressure, and systemic vascular resistance, as well as a slight reduction in mean arterial pressure [2].
• Our findings indicate that preeclampsia is characterized by the absence of the normal pregnancy-related decrease in vascular resistance, which is preceded in most instances by an exaggerated response of platelet intracellular calcium to arginine vasopressin early in pregnancy [3].
• Thus, thiazide therapy effectively and safely lowers the BP in most patients with systolic hypertension by reducing systemic vascular resistance [4].
• Subsequent administration of NAA (20 mg/kg) rapidly and completely reversed the hypotension and increased systemic vascular resistance; these effects of NAA were reversed by L-arginine [5].

Psychiatry related information on Vascular Resistance

• Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man [6].

High impact information on Vascular Resistance

• However, the unexpected finding of zero flow during a prolonged diastole with a coronary artery pressure of 40 mmHg (PZF) is a reminder that the physical forces, including vascular smooth muscle contraction, that determine coronary vascular resistance are incompletely understood [7].
• Reduction in pulmonary vascular resistance with long-term epoprostenol (prostacyclin) therapy in primary pulmonary hypertension [8].
• Intravenous adenosine had a variable effect on pulmonary vascular resistance (mean reduction, 27 percent; range, 0 to 56; P<0.001) [8].
• CONCLUSIONS: In primary pulmonary hypertension, long-term therapy with epoprostenol lowers pulmonary vascular resistance beyond the level achieved in the short term with intravenous adenosine [8].
• Our data indicate that the increases in peripheral vascular resistance and blood pressure that characterize this disorder are mediated, at least in part, by a substantial increase in sympathetic vasoconstrictor activity [9].

Chemical compound and disease context of Vascular Resistance

• Similar erratic increases in coronary vascular resistance were observed with i.v. digoxin (1 mg) during ischemia in three dogs [10].
• In the remaining 27 patients, mobilization of ascites also induced a significant but smaller reduction in systemic vascular resistance (-5.0% +/- 1.6%; P < 0.05) without significant changes in renin, norepinephrine, and hepatic venous pressure gradient [11].
• METHODS: Mean arterial pressure (MAP), cardiac index, and systemic vascular resistance (SVR) were determined in cirrhotic rats with ascites undergoing long-term treatment with different doses of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (3 mg or 0.5 mg.kg-1.day-1) [12].
• When they become available, two investigational drugs, minoxidil and an oral converting enzyme inhibitor, both of which lower total peripheral resistance, will offer a new approach to controlling truly resistant hypertension [13].
• The present investigation was undertaken to study cardiac release of adenosine and prostacyclin (prostaglandin [PG] I2) in patients with ischemic heart disease (IHD), and to assess coronary vascular resistance before and after inhibition of synthesis in such patients [14].

Biological context of Vascular Resistance

• Raising serum triiodothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy [15].
• Despite marked decreases in systemic vascular resistance (40 per cent; P less than 0.001), hydralazine produced only moderate decreases in pulmonary arteriolar resistance (21 per cent), without improving stroke volume or pulmonary-artery pressure [16].
• Seven of the eight patients who had minimal pulmonary vasodilation in response to adenosine (mean reduction in resistance units, <20 percent) still had a significant reduction in pulmonary vascular resistance when treated with epoprostenol (mean, 39+/-14 percent; P=0.002) [8].
• These observations help explain why the newborn with a large ventricular septal defect and a high hemoglobin concentration does not have clinical signs of a large left-to-right shunt, and also suggest that the postnatal decline in hematocrit has a substantial role in the normal fall in pulmonary vascular resistance after birth [17].
• Neither dose of practolol altered base-line heart rate, forearm vascular resistance, and arterial pressure, Both low and high doses significantly attenuated heart rate responses to exercise [18].

Anatomical context of Vascular Resistance

• In contrast, BQ 123 did not change vascular resistance in a regional systemic circulation (the fetal hindlimb) [19].
• L-NMMA also significantly increased systemic and splanchnic vascular resistance; whereas blood flow to the stomach, small intestine, colon, pancreas, mesentery, spleen, and kidney was decreased significantly [20].
• INTERPRETATION: In pregnancies with umbilical-artery AEDF, betamethasone treatment is associated with decreased placental vascular resistance, possibly induced via increased placental CRH secretion [21].
• Cellular mechanisms that link sodium pump inhibition to increased vascular resistance involve increased norepinephrine release and reduced re-uptake and directly increased smooth muscle contractility and reactivity, as a result of increased cell sodium [22].
• These include acquired and inherited abnormalities of serum thyroid-hormone-binding proteins, peripheral resistance to thyroid hormones, acute nonthyroidal illness, acute psychiatric illness, and some drug-induced conditions associated with nonthyrotoxic elevations of serum thyroxine [23].

Associations of Vascular Resistance with chemical compounds

• The responses of blood flow and vascular resistance to acetylcholine were significantly reduced in the hypertensive patients (P less than 0.0001); maximal forearm flow was 9.1 +/- 5 ml per minute per 100 ml in the patients and 20.0 +/- 8 ml per minute per 100 ml in the controls (P less than 0.0002) [24].
• Left ventricular filling pressure and systemic vascular resistance decreased from 23.9 to 15.3 mm Hg and from 1642 to 921 dyn.sec.cm-5, respectively, with nitroprusside, but increased to 30.4 mm Hg and 2109 dyn.sec.cm-5 (both P less than 0.001) upon its discontinuation [25].
• However, there were no significant differences between groups in the responses of blood flow and vascular resistance to sodium nitroprusside [24].
• The vasodilator effect of phentolamine was also significantly greater in the morning (mean decrease in vascular resistance, 38 +/- 6 percent) than in the afternoon (26 +/- 6 percent) and evening (21 +/- 7 percent) (P less than 0.05) [26].
• RESULTS--Dopamine increased the MAP largely by increasing the cardiac index whereas norepinephrine increased the MAP by increasing the systemic vascular resistance index while maintaining the cardiac index [27].

Gene context of Vascular Resistance

• The acute administration of an inhibitor of HO to cirrhotic rats, at a dose that normalized aortic HO activity, was associated with significantly greater effects on arterial pressure, total peripheral vascular resistance, and cardiac index, compared with effects in sham rats [28].
• Endothelin-1 contributes to increased systemic and pulmonary vascular resistance, vascular dysfunction, myocardial ischemia and renal impairment in CHF [29].
• 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 [30].
• Increased counteracting effect of eNOS and nNOS on an alpha1-adrenergic rise in total peripheral vascular resistance in spontaneous hypertensive rats [31].
• MEASUREMENTS AND MAIN RESULTS: Administration of r-hTNF binding protein-1 resulted in improvement of mean arterial pressure, cardiac output, and systemic vascular resistance, as compared with the vehicle-treated group (p < .05) [32].

Analytical, diagnostic and therapeutic context of Vascular Resistance

• Intravenous infusion of endothelin (50 ng/kg per min) increases arterial pressure by increasing peripheral vascular resistance but in association with an increase in coronary vascular resistance and decreases in cardiac output [33].
• Administration of a heme oxygenase inhibitor zinc protoporphyrin IX (1 microM) eliminated the baseline CO generation, and the vascular resistance exhibited a 30% elevation concurrent with discrete patterns of constriction in sinusoids and reduction of the sinusoidal perfusion velocity [34].
• Adoptive immunotherapy with IL 2 is associated with severe cardiovascular toxicities including peripheral and pulmonary edema, hypotension decreased systemic vascular resistance, increased heart rate, and an increased cardiac index [35].
• There was a mean decrease of 21.2% in coronary vascular resistance after a bolus of 1 mg of nitroglycerin was injected in the study group (p less than .001, n = 15); there was no significant change in resistance in the control group [36].
• Responses of mean arterial pressure, forearm vascular resistance, and plasma norepinephrine were assessed during lower-body negative pressure and the cold pressor test [37].

References