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Results for “VASOMOTOR SYSTEM”

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At least 487 records · Page 27Linked to original sources
PubMed1995

Effect of regional and systemic changes in vasomotor tone on finger pressure amplification.

Pulse wave amplification, which leads to increased peripheral systolic pressure, is observed during vasoconstriction after head-up tilt and during exercise. This may influence finger pressure measurements with the Finapres. To distinguish between changes in regional vascular tone and changes in systemic hemodynamics as a cause of pulse wave amplification, we measured finger pressure, intra-arterial brachial artery pressure, heart rate, and left ventricular ejection time during high-dose intravenous and low-dose intra-arterial infusions of phenylephrine and sodium nitroprusside in eight subjects. Forearm blood flow was measured by means of venous occlusion plethysmography. Intravenous phenylephrine at the highest dose caused an increase in mean brachial artery pressure of 24 +/- 3 mm Hg, a decrease in heart rate of 10 +/- 11 beats per minute, and an increase in ejection time of 23 +/- 9 milliseconds (all P < .01), whereas pulse wave amplification was reduced. Finapres underestimated the rise in systolic brachial artery pressure of 41 +/- 9 mm Hg by 11 +/- 12 mm Hg (P < .01). Forearm blood flow did not change. Intravenous nitroprusside caused a decrease in mean brachial artery pressure of 23 +/- 9 mm Hg, an increase in heart rate of 18 +/- 11 beats per minute, and a decrease in ejection time of 36 +/- 31 milliseconds (all P < .01), whereas pulse wave amplification increased. Finapres underestimated the fall in systolic brachial artery pressure of 30 +/- 13 mm Hg by 9 +/- 10 mm Hg (P < .05). Forearm blood flow did not change. During regional infusion of phenylephrine and nitroprusside forearm flow halved and doubled, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Nonrespiratory rhythmic fluctuations in systemic arterial pressure in anesthetized humans.

STUDY OBJECTIVE: To clarify the frequency of nonrespiratory rhythmic fluctuations in systemic arterial pressure (vasomotor waves) and to identify the clinical conditions in which the vasomotor waves develop in humans under anesthesia. DESIGN: Retrospective analysis of collected data. SETTING: Inpatient surgery clinic at a university hospital. PATIENTS: Five hundred thirteen consecutive ASA physical status II-V patients. INTERVENTIONS: Direct arterial pressure monitoring and general anesthesia, including high-dose fentanyl, enflurane, enflurane plus fentanyl, cervical or thoracic epidural, and lumbar epidural anesthesia. MEASUREMENTS AND MAIN RESULTS: Among the anesthesia techniques used, vasomotor waves occurred most frequently in patients anesthetized with high-dose fentanyl (31.1%) and least frequently in those with high-level epidural blockade (7.4%). As a result of multiple logistic analysis, the contributing factors to the appearance of vasomotor waves were the institution of cardiopulmonary bypass (CPB) and the patient's age. It is also a novel finding that nearly one-third of the vasomotor waves developed in patients under stable hemodynamic conditions. CONCLUSIONS: Vasomotor waves are a common phenomenon in relatively high-risk patients during general anesthesia. The appearance of vasomotor waves is significantly related to CPB and patient age.

Adolescent↗
PubMed1991

Systemic hypertension alters vasomotor function in experimental vein grafts.

Hypertension is an established risk factor for atherosclerosis, a disease that is important in the pathophysiology of vein graft failure. Hypertension can also alter arterial vasoreactivity. The vasomotor function and histologic characteristics of autogenous vein grafts in hypertensive rabbits were assessed in this study. Hypertension was induced in 13 male New Zealand white rabbits by use of the Goldblatt one clip two kidney method. The right carotid artery was divided and bypassed with the reversed right external jugular vein 7 days later in these animals and in 13 normotensive controls. Blood pressure and renal function were assessed serially, and all the grafts were harvested after 28 days. Three grafts in each group were examined by light microscopy. The responses of the remaining grafts to norepinephrine, histamine, serotonin, and angiotensin II were determined in vitro under isometric tension. Endothelium-dependent relaxation to acetylcholine and calcium ionophore (A23187) was assessed in precontracted grafts. The mean arterial pressure was significantly increased after the Goldblatt procedure was performed. Intimal hyperplasia was observed in both groups, but the grafts in the hypertensive groups showed increased adventitial and medial fibrosis and a reduced number of vasa vasora. The grafts in the hypertensive rabbits were hypersensitive to all agonists as indicated by a significant reduction in their median effective dose values, and their maximal responses to all agonists were also significantly reduced. No graft relaxed in response to acetylcholine, and whereas precontracted grafts in normotensive rabbits had a maximal relaxation of 24% +/- 6% of precontraction with A23187, this was absent in the grafts in the hypertensive rabbits. The results suggest that angiotensin-induced hypertension may adversely affect vein graft patency by inducing hypersensitivity to physiologically important agonists and reducing the effect of receptor-independent endothelium-derived relaxation on vasomotor tone.

Acetylcholine↗
PubMed2001

Role of K(ATP)(+) channels in regulation of systemic, pulmonary, and coronary vasomotor tone in exercising swine.

The role of ATP-sensitive K(+) (K(ATP)(+)) channels in vasomotor tone regulation during metabolic stimulation is incompletely understood. Consequently, we studied the contribution of K(ATP)(+) channels to vasomotor tone regulation in the systemic, pulmonary, and coronary vascular bed in nine treadmill-exercising swine. Exercise up to 85% of maximum heart rate increased body O(2) consumption fourfold, accommodated by a doubling of both cardiac output and body O(2) extraction. Mean aortic pressure was unchanged, implying that systemic vascular conductance (SVC) also doubled, whereas pulmonary artery pressure increased almost in parallel with cardiac output, so that pulmonary vascular conductance (PVC) increased only 25 +/- 9% (both P < 0.05). Myocardial O(2) consumption tripled during exercise, which was paralleled by an equivalent increase in O(2) supply so that coronary venous PO(2) was maintained. Selective K(ATP)(+) channel blockade with glibenclamide (3 mg/kg iv), decreased SVC by 29 +/- 4% at rest and by 10 +/- 2% at 5 km/h (both P < 0.05), whereas PVC was unchanged. Glibenclamide decreased coronary vascular conductance and hence myocardial O(2) delivery, necessitating an increase in O(2) extraction from 76 +/- 2% to 86 +/- 2% at rest and from 79 +/- 2% to 83 +/- 1% at 5 km/h. Consequently, coronary venous PO(2) decreased from 25 +/- 1 to 17 +/- 1 mmHg at rest and from 23 +/- 1 to 20 +/- 1 mmHg at 5 km/h (all values are P < 0.05). In conclusion, K(ATP)(+) channels dilate the systemic and coronary, but not the pulmonary, resistance vessels at rest and during exercise in swine. However, opening of K(ATP)(+) channels is not mandatory for the exercise-induced systemic and coronary vasodilation.

Adenosine Triphosphate↗