Effect of General Anaesthesia on Renal Haemodynamics in the Rat

Koeppen, Bruce M.; Katz, A I; Lindheimer, M. D.

doi:10.1042/cs0570469

Cited by 18 publications

(15 citation statements)

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“…A possible criticism of the study is that the anaesthetic might have affected the responses. There is evidence that both cardiac output and renal blood flow are reduced in the rat following anaesthesia with pentobarbitone (Koeppen, Katz & Lindheimer, 1979;Seyde, McGowan, Lund, Duling & Longnecker, 1985;Tuma, Irion, Vasthare *& Heinel, 1985), and it is claimed that during pentobarbitone anaesthesia the haemorrhage-induced reduction in renal blood blood flow is exaggerated (Seyde et al 1985). One study has also reported a modest reduction in renal blood flow following Inactin anaesthesia (Koeppen et al 1979), but no systematic investigation of the possible influence of Inactin on the cardiovascular and renal responses to haemorrhage has been performed.…”

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“…There is evidence that both cardiac output and renal blood flow are reduced in the rat following anaesthesia with pentobarbitone (Koeppen, Katz & Lindheimer, 1979;Seyde, McGowan, Lund, Duling & Longnecker, 1985;Tuma, Irion, Vasthare *& Heinel, 1985), and it is claimed that during pentobarbitone anaesthesia the haemorrhage-induced reduction in renal blood blood flow is exaggerated (Seyde et al 1985). One study has also reported a modest reduction in renal blood flow following Inactin anaesthesia (Koeppen et al 1979), but no systematic investigation of the possible influence of Inactin on the cardiovascular and renal responses to haemorrhage has been performed. Our control values for both cardiac output and renal blood flow in Inactin-anaesthetized rats were very similar to those reported in conscious animals (Koeppen et al 1979;Stanek et al 1983;Kobrin, Kardon, Oigman, Pegram & Frohlich, 1984;Tuma et al 1985), and, although fewer opportunities for comparison exist, the haemorrhage-induced renal vasoconstriction in our animals was much less marked than that reported in pentobarbitone-anaesthetized rats (Sapirstein, Sapirstein & Bredemeyer, 1960;Seyde et al 1985).…”

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“…One study has also reported a modest reduction in renal blood flow following Inactin anaesthesia (Koeppen et al 1979), but no systematic investigation of the possible influence of Inactin on the cardiovascular and renal responses to haemorrhage has been performed. Our control values for both cardiac output and renal blood flow in Inactin-anaesthetized rats were very similar to those reported in conscious animals (Koeppen et al 1979;Stanek et al 1983;Kobrin, Kardon, Oigman, Pegram & Frohlich, 1984;Tuma et al 1985), and, although fewer opportunities for comparison exist, the haemorrhage-induced renal vasoconstriction in our animals was much less marked than that reported in pentobarbitone-anaesthetized rats (Sapirstein, Sapirstein & Bredemeyer, 1960;Seyde et al 1985). These observations suggest that the thiobarbiturate Inactin might be a more suitable anaesthetic than pentobarbitone in studies of renovascular function in the rat (see Buelke-Sam, Holson, Bazare & Young, 1978).…”

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The renal vascular response to mild and severe haemorrhage in the anaesthetized rat.

Shirley

MacRae

Walker

1991

The Journal of Physiology

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SUMMARY1. In order to document the characteristics of the renal vascular response to blood losses of varying severity, Inactin-anaesthetized rats were subjected to a haemorrhage of 5, 10, 15 or 20 ml (kg body weight)-1, while a fifth group (control rats) remained unbled. Radioactive microspheres (diameter 10 ,um) were used to determine cardiac output, total renal blood flow and the distribution of blood flow within the kidneys; measurements were made before and 5-120 min after haemorrhage.2. In control animals none of the variables studied changed significantly during the experimental period.3. Immediately after haemorrhage there were reductions in arterial pressure and cardiac output which were roughly proportional to the severity of haemorrhage. Arterial pressure recovered to some extent during the next 30 min, then stabilized; cardiac output recovered only slightly.4. Total renal blood flow fell to an extent dependent on the degree of haemorrhage, with no evidence of subsequent recovery. The approximate reductions in renal blood flow were 2 % (n.s.), 15%, 30% and 50% after bleeds of 5, 10, 15 and 20 ml kg-1, respectively. Renal vascular resistance increased consistently only in the groups bled 15 and 20 ml kg-1. When renal blood flow was expressed as a fraction of cardiac output, it increased during the period immediately after haemorrhage, indicating some degree of 'protection' of the renal circulation in the face of hypotension.5. Measurements of intrarenal blood flow indicated a significantly reduced flow to the superficial cortex after every degree of haemorrhage. Inner cortical flow was less affected and fell significantly only in the groups bled 15 and 20 ml kg-1; blood flow to the mid-cortex was intermediate.

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The renal vascular response to mild and severe haemorrhage in the anaesthetized rat.

Shirley

MacRae

Walker

1991

The Journal of Physiology

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“…has been shown to decrease CI and HR in mice. 20 Koeppen et al 21 have also demonstrated that pentobarbitone significantly reduced renal blood flow. Mechanical ventilation can also affect hemodynamic parameters.…”

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confidence: 97%

“…There are reports documenting the effect of anesthetic agents on hemodynamic measurements. 20,21 Pentobarbitone (50 mg kg À1 , i.p.) has been shown to decrease CI and HR in mice.…”

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confidence: 99%

Hemodynamics of dexamethasone-induced hypertension in the rat

et al. 2009

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Although dexamethasone (DEX) is known to cause hypertension in humans and in animals, the hemodynamic characteristics of DEX-induced hypertension (DEX-HT) in the rat remain unclear. This study evaluated central and regional hemodynamics, and the role of total peripheral resistance (TPR) using a vasodilator minoxidil. Rats were divided into four groups, namely saline (n¼20), DEX (n¼21), minoxidil+saline (n¼10) and minoxidil+DEX (n¼10). Tail-cuff systolic blood pressure was recorded every second day. After 10-14 days of treatment, central (saline: n¼9, DEX: n¼10) and regional (saline: n¼11, DEX: n¼11) hemodynamic parameters were measured. Central hemodynamic data were also obtained from minoxidil-treated rats. DEX increased blood pressure (Po0.0005) in association with an increase in TPR (Po0.05). However, individual assessments of renal, mesenteric and hindquarter circulations did not detect any significant increase in resistance in these beds. Minoxidil increased cardiac output (P ¢o0.01) and cardiac index (P ¢o0.005) as well as decreased TPR (P¢o0.05) without affecting DEX-HT. DEX prevented weight gain and decreased thymus weight. The increase in TPR in DEX-HT in rats was not simply explained by isolated alterations to resistance in the renal, mesenteric or hindquarter circulations. Minoxidil effectively prevented the increase in TPR but not the increase in blood pressure, suggesting that an increase in TPR is not essential for DEX-induced blood pressure increase. Keywords: dexamethasone; hemodynamics; minoxidil; total peripheral resistance INTRODUCTION Synthetic glucocorticoid dexamethasone (DEX) is commonly used in clinical settings for the treatment of various medical conditions. It is used in adrenal insufficiency as a glucocorticoid hormone replacement treatment, in multiple myeloma together with other chemotherapeutic agents, to decrease cerebral edema due to intracranial pathology and as an anti-emetic in patients with cancer. When used chronically at a supra-physiological dose, DEX results in hypertension. The underlying mechanism for DEX-induced hypertension (DEX-HT) remains unclear. We have recently reviewed postulated mechanisms of DEX-HT. 1 There is evidence against plasma volume expansion 2 or sympathetic nerve activation 3 as key mechanisms of DEX-HT in humans. The roles of endogenous vasoconstrictors and vasodilators in DEX-HT are variable, with possible associations with nitric oxide, prostanoids, angiotensin II, arginine vasopressin, endothelins, catecholamines, neuropeptide Y and atrial natriuretic peptide. 1 Studies on DEX-HT in rodents have indicated that nitric oxide deficiency 4 and oxidative stress 5 are implicated in this form of hypertension. Nevertheless, the hemodynamic profile has not been fully evaluated in this model.The hemodynamics of DEX-HT has been evaluated in both humans 6 and dogs. 7 DEX-HT in humans (3 mg per day) was associated with increased total peripheral resistance (TPR) without any

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The effect of renal perfusion pressure on renal vascular resistance in the spontaneously hypertensive rat

Hsu

Slavicek

1982

Pflugers Arch.

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Renal hemodynamics and renal vascular resistance (RVR) were measured in the spontaneously hypertensive rat (SHR) and in the normotensive Wistar-Kyoto rat (WKY). In addition, the autoregulatory response and segmental RVR in the SHR were studied after aortic constriction. Mean arterial pressure (MAP) and RVR were higher in the SHR than in the WKY, but renal blood flow (RBF) and glomerular filtration rate were similar in both groups. Measurement of mean afferent arteriolar diameter (AAD) by a microsphere method showed a significantly smaller AAD in SHR (17.7 +/- 0.35 micrometers) than in the WKY (19.5 +/- 0.20 micrometers). This decrease in AAD could account for a 47% increase in preglomerular resistance. Aortic constriction in the SHR, sufficient to reduce renal perfusion pressure from 152 to 115 mmHg, did not alter the AAD. Since RBF and glomerular filtration were also well maintained following aortic constriction, these autoregulatory responses suggest that vessels proximal to the afferent arteriole rather than postglomerular vasculature are primarily involved in the changes on intrarenal vascular resistance in SHR.

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Effect of General Anaesthesia on Renal Haemodynamics in the Rat

Cited by 18 publications

References 3 publications

The renal vascular response to mild and severe haemorrhage in the anaesthetized rat.

The renal vascular response to mild and severe haemorrhage in the anaesthetized rat.

Hemodynamics of dexamethasone-induced hypertension in the rat

The effect of renal perfusion pressure on renal vascular resistance in the spontaneously hypertensive rat

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