Rapid effects of parathyroid hormone(1–34) and prostaglandin E2 on bone blood flow and strontium clearance in the rat in vivo

1991 ◽  
Vol 131 (3) ◽  
pp. 359-365 ◽  
Author(s):  
E. Cochrane ◽  
I. D. McCarthy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Parathyroid Hormone ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Prostaglandin E ◽  
Bone Blood Flow ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Mineral Ions

ABSTRACT The vascular effects of noradrenaline, ATP, parathyroid hormone (PTH) and prostaglandin E2 (PGE2) were investigated in the rat. Additionally, the exchange of mineral ions between bone and blood was assessed by measuring strontium clearance, with the aim of investigating whether the vascular effects of these agents altered uptake of mineral ions or if this exchange could be changed independently of blood flow. Radioactive microspheres and 85Sr were used to establish bone blood flow and mineral clearance. Measurements of bone blood flow and arterial pressure were made in each animal and used to calculate vascular resistance. A measurement of 85Sr clearance was also obtained. Arterial blood pressure was significantly affected by noradrenaline (P ≤ 0·003) and ATP (P ≤ 0·015). Additionally, noradrenaline significantly (P ≤ 0·03) reduced bone blood flow. This decrease was related to a significant increase in vascular resistance. Arterial blood pressure and bone blood flow were significantly reduced by both bovine PTH(1–34) (P ≤ 0·001, P ≤ 0·02) and PGE2 (P ≤ 0·005, P ≤ 0·001). Vascular resistance to bone was increased by both agents but this was only statistically significant in the case of PGE2 (P ≤ 0·01). A significant (P ≤ 0·001) reduction in strontium was also produced by PGE2. In each group the relationship between bone blood flow and strontium clearance was then analysed. Only the PGE2-treated group had a slope of the regression which was statistically different from both the control animals and the other drug-treated groups. Treatment with PGE2 therefore resulted in a dose-related decrease in 85Sr clearance which was not related to the reduction in bone blood flow. Journal of Endocrinology (1991) 131, 359–365

Renal Vascular Responses to Dopamine: Haemodynamic and Angiographic Observations in Normal Man

1973 ◽  
Vol 45 (6) ◽  
pp. 733-742 ◽  
Author(s):  
N. K. Hollenberg ◽  
D. F. Adams ◽  
P. Mendell ◽  
H. L. Abrams ◽  
J. P. Merrill
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Cardiovascular Effects ◽  
Normal Subjects ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Normal Man ◽  
Renal Vascular

1. The renal vascular response to intravenously administered dopamine was assessed in normal man by selective renal arteriography and xenon washout. Infusion of 3 μg min−1 kg−1 induced renal vasodilatation with an increase in the cortical component of blood flow. Arterial blood pressure was not influenced and a systemic effect was not demonstrable. Lower doses did not induce a renal response. Increasing dosage raised arterial blood pressure and induced subjective symptoms, but did not result in a further increase in renal blood flow. 2. Renal vascular resistance increased with increasing age in the normal subjects. A significant inverse relationship was found between the initial vascular resistance and the renal vasodilator response to dopamine. It thus appears that the vascular effects of increasing age (nephrosclerosis) may limit the dilator response to dopamine. 3. It is concluded that dopamine is an effective renal cortical vasodilator when administered intravenously at doses which are free from other systemic cardiovascular effects. The dose-response relationship must be considered in attempts at reversal of conditions characterized by renal vasoconstriction.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Patterned cardiovascular responses to sleep and nonrespiratory arousals in a porcine model

1998 ◽  
Vol 85 (4) ◽  
pp. 1285-1291 ◽  
Author(s):  
Sandrine H. Launois ◽  
Joseph H. Abraham ◽  
J. Woodrow Weiss ◽  
Debra A. Kirby
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Arterial Blood

Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by −29.6 ± 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 ± 4.0%), tachycardia (heart rate increase: +23.8 ± 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

Validity of fluorescent microspheres method for bone blood flow measurement during intentional arterial hypotension

2003 ◽  
Vol 95 (3) ◽  
pp. 1153-1158 ◽  
Author(s):  
H. Anetzberger ◽  
E. Thein ◽  
M. Becker ◽  
A. K. Walli ◽  
K. Messmer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Bone Blood Flow ◽  
Control Mechanisms ◽  
Arterial Blood ◽  
Severe Hypotension ◽  
New Zealand White Rabbits ◽  
Blood Pressures

In this study, we compared bone blood flow values obtained by simultaneously injected fluorescent (FM) and radiolabeled microspheres (RM) at stepwise reduced arterial blood pressure. Ten anesthetized female New Zealand White rabbits received simultaneous left ventricular injections of FM and RM at 90, 70, and 50 mmHg mean arterial blood pressure (MAP). After the experiments, both kidneys and long bones of all four limbs were removed and dissected in a standardized manner. Radioactivity (corrected for decay, background, and spillover) and fluorescence were determined, and blood flow values were calculated. Relative blood flow values estimated for each bone sample by RM and FM were significantly correlated ( r = 0.98, slope = 0.99, and intercept = 0.04 for 90 mmHg; r = 0.98, slope = 0.94, and intercept = 0.09 for 70 mmHg; r = 0.98, slope = 0.96, and intercept = 0.07 for 50 mmHg). Blood flow values (ml · min-1 · 100 g-1) of right and left bone samples determined at the different arterial blood pressures were identical. During moderate hypotension (70 mmHg MAP), blood flow in all bone samples remained unchanged compared with 90 mmHg MAP, whereas a significant decrease of bone blood flow was observed at severe hypotension (50 mmHg MAP). Our results demonstrate that the FM technique is valid for measuring bone blood flow. Differences in bone blood flow during altered hemodynamic conditions can be detected reliably. In addition, changes in bone blood flow during hypotension indicate that vasomotor control mechanisms, as well as cardiac output, play a role in setting bone blood flow.

Effect of Chronic Smoking on Endothelium-Dependent Vascular Relaxation in Humans

1993 ◽  
Vol 85 (1) ◽  
pp. 51-55 ◽  
Author(s):  
Marie-Cécile Jacobs ◽  
Jacques W. M. Lenders ◽  
Jan A. Kapma ◽  
Paul Smits ◽  
Theo Thien
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cigarette Smoking ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Vascular Relaxation ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

1. Cigarette smoking is one of the major risk factors for the development of atherosclerosis. It is not clear, however, whether chronic cigarette smoking impairs the normal physiological function of the endothelium before the development of morphological vascular lesions. To test this, we investigated endothelium-dependent vascular relaxation in young habitual smoking subjects. 2. In 11 non-smokers and 10 habitual smokers we measured the changes in bilateral forearm blood flow, arterial blood pressure and forearm vascular resistance (ratio between mean arterial blood pressure and forearm blood flow) during three interventions: postocclusive forearm hyperaemia, intrabrachial infusion of methacholine which causes vasodilatation by stimulating the release of endothelium-dependent relaxing factor, and intrabrachial infusion of sodium nitroprusside which causes vasodilatation independently from the endothelium by a direct effect on the vascular smooth muscle wall. 3. During infusion of the highest dose of methacholine, forearm vascular resistance decreased by 91.7 ± 1.4% in the smokers and by 89.9 ± 1.8% in the non-smokers. During infusion of sodium nitroprusside, forearm vascular resistance decreased by 80.0 ± 3.8% in the smokers as compared with 80.7 ± 6.1% in the non-smokers. There was no difference in basal forearm vascular resistance or in post-ischaemic reactive hyperaemia between smokers and non-smokers. Thus, vasodilatation induced by both methacholine and sodium nitroprusside was not significantly different between smokers and non-smokers. 4. We conclude that in young habitual cigarette smokers the endothelium-dependent vasodilatation in the forearm seems to be preserved, suggesting that habitual smoking does not result in permanent endothelial dysfunction in the human forearm.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Renal and iliac vascular responses to left ventricular receptor stimulation in conscious dogs

1984 ◽  
Vol 246 (5) ◽  
pp. R788-R798
Author(s):  
A. J. Gorman ◽  
K. G. Cornish ◽  
I. H. Zucker
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cholinergic Receptor ◽  
Left Ventricular ◽  
Conscious Dog ◽  
Arterial Blood

The purpose of the present study was to investigate the relative responses of the renal and iliac vascular beds to the selective chemical stimulation of left ventricular receptors in the conscious dog. Twenty dogs were chronically instrumented to obtain measurements of arterial blood pressure, renal blood flow, and iliac blood flow before and after a bolus intracoronary injection of veratridine (0.4-1.0 micrograms/kg in 0.5-ml vol) with the heart paced. The responses to intracoronary veratridine were a significant reduction in arterial blood pressure averaging 25 mmHg accompanied by a simultaneous reduction in renal blood flow of 25%. Renal resistance did not change throughout the course of the response analyzed (50 s). Iliac blood flow, however, increased, reaching a peak of 35% above control due to a 51% decrease in iliac resistance. After sinoaortic denervation, renal resistance still failed to show a decrease, although the recovery of arterial blood pressure and iliac resistance was prolonged. After a mild hypotensive hemorrhage (20 ml/kg), a greater decrease in iliac resistance occurred with intracoronary veratridine injections, but renal resistance still did not change. The reduction in iliac resistance with intracoronary veratridine was significantly attenuated after phentolamine administration (2 mg/kg iv) but not after atropine alone (0.2 mg/kg iv). A significant cholinergic receptor component of iliac vasodilation was observed only after prior alpha-adrenergic-receptor blockade. The results of this study are consistent with the conclusion that in the conscious dog, left ventricular receptors exert a preferential neural control over skeletal muscle vascular resistance and do not influence renal vascular resistance.

Effect of hypovolemia on forearm vascular resistance control during exercise in the heat

1991 ◽  
Vol 71 (4) ◽  
pp. 1382-1386 ◽  
Author(s):  
T. S. Nishiyasu ◽  
X. G. Shi ◽  
G. W. Mack ◽  
E. R. Nadel
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Cycle Ergometer ◽  
Dynamic Exercise ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Forearm Vascular Resistance

To determine the influence of hypovolemia on the control of forearm vascular resistance (FVR) during dynamic exercise, we studied five physically active men during 60 min of supine cycle ergometer exercise bouts at 35 degrees C in control (normovolemic) and hypovolemic conditions. Hypovolemia was achieved by 3 days of diuretic administration and resulted in an average decrease in plasma volume of 15.9%. Relative to normovolemia, hypovolemia caused an attenuation of the progressive rise in forearm blood flow (P less than 0.05) and an increase in heart rate (P less than 0.05) during exercise. Because mean arterial blood pressure during hypovolemic exercise was well maintained, the attenuation of forearm blood flow was due entirely to a relative increase in FVR. At the onset of dynamic exercise, FVR was increased significantly in control and hypovolemic conditions by 13.2 and 27.1 units, respectively. The increase in FVR was significantly different between control and hypovolemic conditions as well. We attributed the increased vasoconstrictor bias during hypovolemia to cardiopulmonary baroreceptor unloading and/or an increased sensitivity to cardiopulmonary baroreceptor unloading. We concluded that reduced blood flow to the periphery during exercise in the hypovolemic condition was caused entirely by an increase in vascular resistance, thereby preserving arterial blood pressure and adequate perfusion to the organs requiring increased flow.

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