Effect of carbon dioxide on renal blood flow

Norman, J N; Macintyre, James G.; Shearer,; Craigen, IM; Smith, George Van S.

doi:10.1152/ajplegacy.1970.219.3.672

Cited by 27 publications

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“…There have been no previous studies to our knowledge in newborn animals concerning the effects of hypocarbia and hypercarbia without hypoxia on organ blood flow other than to the brain. Even in adult animals, the effects of hypo-and hypercarbia with normoxemia on organ blood flow vary widely from study to study (8,17,19).…”

Section: Discussionmentioning

confidence: 99%

“…Paralysis was induced with 0.5 mg/kg of pancuronium and the ventilator was adjusted to obtain a predetermined Paco2 range of 35-45 mm Hg for the baseline blood flow measurement. Following the baseline determination, progressive hypocarbia was induced by increasing the ventilatory rate to achieve the predetermined P~c o~ ranges of [25][26][27][28][29][30][31][32][33][34][35][15][16][17][18][19][20][21][22][23][24][25], and less than 15 mm Hg. Following these three hypocarbic measurements, the ventilatory rate was returned to baseline and 15 min later, hypercarbia was induced by adding 15% COz to the inspired gases.…”

Section: Methodsmentioning

confidence: 99%

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The Effects of Variations in Paco2 on Brain Blood Flow and Cardiac Output in the Newborn Piglet

et al. 1984

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ABSTRAm. The acute effects of normoxemic hypocarbia and hypercarbia were examined in six newborn piglets. Brain blood flow was maintained during hypocarbia until extremely low Paco2 ( 4 5 mm Hg) levels were achieved at which time total brain and cerebral blood flow decreased significantly from baseline values. Blood flow to the thalamus, cerebellum and brain stem was unchanged from baseline conditions during hypocarbia. This suggests that the newborn brain is relatively insensitive to moderate degrees of hypocarbia. Extreme hypocarbia (Paco, e l 5 mm Hg) was associated with a significant increase in heart rate, accompanied by a significant decrease in mean arterial blood pressure; however, cardiac output was not significantly different from baseline determinations. Hypercarbia with normoxemia was associated with significant increases in total brain blood flow, with greater blood flow to the brain stem, cerebellum, and thalamus than to the cerebrum. The percentage of cardiac output received by the brain was also significantly increased, although total cardiac output was unchanged. This demonstrates that the newborn cerebral vasculature is sensitive to hypercarbia and that regional differences in sensitivity may account for the greater increments in blood flow to the caudal portions of the brain than that to the cerebrum. (Pediatr Res 18:1132-1136, 1984) Hyperventilation to extremely low Paco2 levels has been advocated as a form of therapy for pulmonary vasospasm in the human neonate (7,22). Hyperventilation has also been used in adults as a method of restoring autoregulation of the brain blood flow following brain injury (21). In the adult, there is no further reduction in cerebral blood flow below carbon dioxide tensions of approximately 20 mm Hg, presumably because ischemia induces metabolic changes in the brain that ovemde the C02 control of the cerebral vasculature (3,10,26 species whose brain maturation differs significantly from that of the term human neonate. The maturation of the newborn piglet brain is comparable to a human infant of 36-38 wk gestation (6, 23). Therefore, we utilized the newborn piglet to assess the acute effects of variations in Paco2 on brain blood flow and cardiac output, with a comparison of regional blood flow within the brain and the percentage of cardiac output received by the brain during hypo-and hypercarbia. MATERIALS AND METHODSSix, 1-to 4-day-old farm-bred piglets were subjects of this study. All piglets remained with the sows until the morning of the study. The weight of the piglets was 1.52 & 0.42 kg (mean +. SD).surgical procedures. All surgical procedures were performed under nitrous oxide inhalation anesthesia with local anesthesia using 1% xylocaine. A tracheotomy was performed and the piglets were ventilated with a pressure-limited Amsterdam infant ventilator using a gas mixture of 70% nitrous oxide and 30% oxygen. Polyvinyl catheters (OD127 ID86) were placed in the left axillary artery, abdominal aorta via the femoral artery and inferior vena cava via the femoral ...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The Effects of Variations in Paco2 on Brain Blood Flow and Cardiac Output in the Newborn Piglet

et al. 1984

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“…The effects of hypercapnic acidosis on renal function have been the subject of extensive investigation (Stone et al, 1958;Bersantes and Simmons, 1967;Norman et al, 1970;Farber et al, 1975Farber et al, , 1976Farber et al, , 1977Kurz and Zehr, 1978;Berns et al, 1979;Anderson et al, 1980). There are suggestions from clinical studies that chronic hypercapnic states are associated with renal sodium retention (Campbell and Short, 1960;Farber et al, 1975;Farber et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Henrich

Groß

Dillingham

1982

Circulation Research

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Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased Pco 2 from 23 to 74 nun Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 juEq/min, P < 0.001) and fractional excretion of sodium (4.0 to 1.2%, P < 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, Po 2 , glomerular filtration rate, renal blood flow, extraction of p-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of l-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal a-adrenergic nerves and the renin angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

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“…RBF and RVR in the distal occlusion group were essentially the same as in the untreated group, indicating that the effect of the baroreflex on RBF during cerebral ischemia was minimal in our BCO model and that the reduction in RBF was primarily caused by cerebral ischemia. Although the effect of hypocapnia on RBF was not examined in this study, the previous examination by Norman et al 16 indicated that variations in PcOj of < 20 mm Hg have little effect on RBF. We assume, therefore, that the PcOj levels in this study may not affect the renal vascular responses during cerebral ischemia.…”

Section: Figure 3 Percent Changes In Renal Blood Flow (Rbf) After Bimentioning

confidence: 74%

Renal blood flow in acute cerebral ischemia in spontaneously hypertensive rats: effects of alpha- and beta-adrenergic blockade.

Yao¹,

Sadoshima²,

Shiokawa³

et al. 1987

Stroke

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The influences of acute cerebral ischemia on renal hemodynamics were examined in spontaneously hypertensive rats in which cerebral ischemia was induced by bilateral carotid artery occlusion. Renal and cerebral blood flow were measured with a hydrogen clearance technique. Either phenoxybenzamine (0.5 mg/kg body wt) or propranolol (2 mg/kg) was given i.v. immediately after ischemia was induced to examine the drugs' effects on cerebral and renal hemodynamics. One hour after ischemia, cerebral blood flow was markedly reduced to 5, 3, and almost 0% of the preischemic value in the untreated, phenoxybenzamine-treated, and propranolol-treated rats, respectively. In contrast, renal blood flow at that time was decreased to 65, 88, and 67%, respectively. The calculated renal vascular resistance was similarly increased to 151 % In the untreated and 136% in the propranolol-treated rats, but decreased to 82% in the phenoxybenzamine-treated rats. The present results indicate that in acute cerebral ischemia renal blood flow was considerably decreased with concomitant increased renal vascular resistance, and that such reduction in renal blood flow was minimized by a-adrenergic blockade but not by /3-blockade. It is concluded that activation of the a-adrenergic system in acute cerebral ischemia causes renal vasoconstriction. (Stroke 1987;18:629-633) I t is known that cerebrovascular disease not only leads to severe derangements of the cerebral circulation and metabolism, but also to undesirable dysfunctions of various extracranial organs. Cardiac arrhythmias, electrocardiographic changes, and myocardial necrosis are not uncommon, 1 " 3 acute gastric erosion or ulcer sometimes causes massive hemorrhage, 4 -3 and pulmonary congestion and edema lead to respiratory distress. 67 Increased activity of the sympathetic nervous system is explained to be, in part, responsible for these extracranial changes.Renal blood flow (RBF) is mainly regulated by intrinsic (autoregulation) and extrinsic factors (autonomic nervous system and humoral elements), 8 " 10 although the renal hemodynamics in acute cerebral ischemia are not fully understood. In this study, we measured renal cortical blood flow in spontaneously hypertensive rats (SHR) in which acute cerebral ischemia was produced by bilateral carotid occlusion (BCO). The purposes of this study were to observe whether cerebral ischemia affects the regulation of RBF and, if so, to examine whether sympathetic nerve activity influences its regulation. Materials and MethodsTwenty-six male SHR aged 5-6 months, weighing 240-360 g, were used in this study. The rats were fed stock chow diet (Oriental Co., Japan) and tap water ad libitum. Under amobarbital anesthesia (100 mg/kg Received August 14, 1986; accepted January 13, 1987. body wt i.p.), both femoral arteries were cannulated, one for continuous recording of systemic arterial blood pressure and heart rate, and the other for anaerobic sampling of blood for pH, Poj, and Pco? determinations. A femoral vein was also cannulated for infusion of dr...

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Effect of carbon dioxide on renal blood flow

Cited by 27 publications

References 0 publications

The Effects of Variations in Paco2 on Brain Blood Flow and Cardiac Output in the Newborn Piglet

The Effects of Variations in Paco2 on Brain Blood Flow and Cardiac Output in the Newborn Piglet

Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Renal blood flow in acute cerebral ischemia in spontaneously hypertensive rats: effects of alpha- and beta-adrenergic blockade.

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