Defining the role of capillaries in “normal perfusion pressure breakthrough” and “occlusive hyperemia”

✓ The authors report two cases of treatment by intraarterial papaverine of cerebral vasospasm complicating the resection of an arteriovenous malformation (AVM). Both cases had successful reversal of vasospasm documented on angiography. In the first case sustained neurological improvement occurred, resulting in a normal outcome by the time of discharge. In the second case, neurological deterioration occurred with the development of cerebral edema. This complication was thought to be due to normal perfusion pressure breakthrough, on the basis of angiographic arterial vasodilation and increased cerebral blood flow. These two cases illustrate an unusual complication of surgery for AVMs and demonstrate that vasospasm (along with intracranial hemorrhage, venous occlusion, and normal perfusion pressure breakthrough) should be considered in the differential diagnosis of delayed neurological deterioration following resection of these lesions. Although intraarterial papaverine may be successful in dilating spastic arteries, it may also result in pathologically high flows following AVM resection. However, this complication has not been seen in our experience of treating aneurysmal subarachnoid hemorrhage by this technique.

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Normal Perfusion Pressure Breakthrough Theory

Neurosurgery ◽

10.1093/neurosurgery/25.cn_suppl_1.651 ◽

1978 ◽

Vol 25 (CN_suppl_1) ◽

pp. 651-672 ◽

Cited By ~ 561

Author(s):

Robert F. Spetzler ◽

Charles B. Wilson ◽

Phillip Weinstein ◽

Max Mehdorn ◽

Jeannette Townsend ◽

...

Keyword(s):

Perfusion Pressure ◽

Normal Perfusion Pressure Breakthrough

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Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00327.2001 ◽

2002 ◽

Vol 282 (4) ◽

pp. H1334-H1340 ◽

Cited By ~ 16

Author(s):

R. R. Lamberts ◽

M. H. P. van Rijen ◽

P. Sipkema ◽

P. Fransen ◽

S. U. Sys ◽

...

Keyword(s):

Ion Channels ◽

Perfusion Pressure ◽

Cardiac Contractility ◽

No Synthase ◽

Coronary Perfusion ◽

Channel Blockade ◽

No Release ◽

Sustained Increase ◽

Stretch Activated Ion Channels

The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3–4 s, perfusion pulse, n = 7), 10 repetitive perfusion pulses ( n = 4), or a sustained increase in perfusion pressure (150–200 s, perfusion step, n = 7) increase developed force by 2.7 ± 1.1, 7.7 ± 2.2, and 8.3 ± 2.5 mN/mm2 (means ± SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a perfusion step remains increased by 5.1 ± 2.5 mN/mm2 ( P < 0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 μmol/l) or streptomycin (40 and 100 μmol/l) blunts the perfusion-induced increase in developed force. Incubation with 100 μmol/l N ω-nitro-l-arginine [nitric oxide (NO) synthase inhibition], 10 μmol/l sodium nitroprusside (NO donation) and 0.1 μmol/l verapamil (L-type Ca2+ channel blockade) are without effect on the perfusion-induced increase of developed force. We conclude that brief, repetitive, or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca2+channels are not involved.

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Effects of meclofenamate on the renin response to aortic constriction in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1984.247.3.r546 ◽

1984 ◽

Vol 247 (3) ◽

pp. R546-R551 ◽

Cited By ~ 2

Author(s):

D. Villarreal ◽

J. O. Davis ◽

R. H. Freeman ◽

W. D. Sweet ◽

J. R. Dietz

Keyword(s):

Perfusion Pressure ◽

Plasma Renin ◽

Renal Perfusion ◽

Renin Release ◽

Aortic Constriction ◽

Renal Perfusion Pressure ◽

Inhibition Of Prostaglandin Synthesis ◽

Intact Kidney ◽

Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

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Role of Perfusion Pressure in Major Organ Blood Flow during Cardiopulmonary Bypass in Canines

Korean Journal of Anesthesiology ◽

10.4097/kjae.2000.39.5.748 ◽

2000 ◽

Vol 39 (5) ◽

pp. 748

Author(s):

Young Lan Kwak ◽

Young Hwan Park ◽

Sang Beom Nam ◽

Young Jun Oh ◽

Seung Ho Kim ◽

...

Keyword(s):

Blood Flow ◽

Cardiopulmonary Bypass ◽

Perfusion Pressure ◽

Organ Blood Flow ◽

Major Organ

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Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

Journal of the American Society of Nephrology ◽

10.1681/asn.v291371 ◽

1992 ◽

Vol 2 (9) ◽

pp. 1371-1387 ◽

Cited By ~ 1

Author(s):

J C Romero ◽

V Lahera ◽

M G Salom ◽

M L Biondi

Keyword(s):

Nitric Oxide ◽

Renal Function ◽

Perfusion Pressure ◽

Sodium Intake ◽

Systemic Circulation ◽

Renal Perfusion ◽

Renin Release ◽

High Sodium ◽

Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

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Effects of calcitonin gene-related peptide on vascular resistance in rats: role of sex steroids

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.6.h2063 ◽

1999 ◽

Vol 276 (6) ◽

pp. H2063-H2068 ◽

Cited By ~ 1

Author(s):

Michelle Grewal ◽

Janis Cuevas ◽

Gautam Chaudhuri ◽

Lauren Nathan

Keyword(s):

Sex Steroids ◽

Perfusion Pressure ◽

Pressor Response ◽

Calcitonin Gene Related Peptide ◽

Ovariectomized Rats ◽

Synthesis Inhibitor ◽

Pregnant Rats ◽

Related Peptide ◽

Calcitonin Gene

It has been demonstrated in reflex-intact animals that the sensitivity to calcitonin gene-related peptide (CGRP) is increased during pregnancy and that this action is mediated by sex steroids but not by nitric oxide (NO). We assessed the effects of CGRP in the following groups of anesthetized ganglion-blocked rats: 1) pregnant, 2) ovariectomized, and 3) ovariectomized and treated with estradiol and progesterone. Changes in mean arterial pressure (MAP) were assessed after the administration of varying doses of CGRP. Decreases in MAP after CGRP administration were significantly greater in pregnant rats and ovariectomized rats administered sex steroids than in ovariectomized controls. The CGRP antagonist CGRP8–37 produced a pressor response of similar magnitude in both pregnant and ovariectomized rats. We also assessed the effects of CGRP and the modulating role of NO in the isolated uterine vascular bed preparation. CGRP reduced perfusion pressure to a greater degree in ovariectomized animals treated with sex steroids than in ovariectomized animals. This response was attenuated by pretreatment with an NO synthesis inhibitor. CGRP8–37 produced a similar increase in perfusion pressure in both groups. We conclude that 1) the increased vascular sensitivity observed during pregnancy or after treatment with sex steroids is in part mediated by NO, and 2) CGRP8–37 has a vasoconstrictor action of its own.

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Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.6.h2541 ◽

1997 ◽

Vol 272 (6) ◽

pp. H2541-H2546 ◽

Cited By ~ 4

Author(s):

G. Dornyei ◽

G. Kaley ◽

A. Koller

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Perfusion Pressure ◽

Thromboxane A2 ◽

No Synthase ◽

Gracilis Muscle ◽

Vasoactive Agents ◽

Before And After ◽

Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

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Downregulation of ventricular contractile function during early ischemia is flow but not pressure dependent

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.275.5.h1520 ◽

1998 ◽

Vol 275 (5) ◽

pp. H1520-H1523 ◽

Cited By ~ 1

Author(s):

Miao-Xiang He ◽

H. Fred Downey

Keyword(s):

Coronary Artery ◽

Perfusion Pressure ◽

Contractile Function ◽

Coronary Perfusion Pressure ◽

Coronary Perfusion ◽

Rat Hearts ◽

Myocardial Contractile Force ◽

Myocardial Contractile ◽

Artery Obstruction

The mechanism responsible for the abrupt fall in myocardial contractile function following coronary artery obstruction is unknown. The “vascular collapse theory” hypothesizes that the fall in coronary perfusion pressure after coronary artery obstruction is responsible for contractile failure during early ischemia. To test the role of vascular collapse in downregulating myocardial contractile force at the onset of ischemia, coronary flow of isolated rat hearts was abruptly decreased by 50, 70, 85, and 100% of baseline, and subsequent changes in coronary perfusion pressure and ventricular function were recorded at 0.5-s intervals. At 1.5 s after flow reductions ranging from 50 to 100%, decreases in contractile function did not differ, although perfusion pressure varied significantly from 45 ± 1 to 20 ± 2 mmHg. When function fell to 50% of baseline, perfusion pressures ranged from 35 ± 0.5 to 2.5 ± 1 mmHg for flow reductions ranging from 50 to 100%. Identical contractile function at widely differing coronary perfusion pressures is incompatible with the vascular collapse theory.

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