Nitroprusside abolishes the deleterious effects of surface cooling–induced hypothermia on immature pigs with ventricular septal defects

Gott, John Parker; Cox, S. Douglas; Mavroudis, Constantine

doi:10.1016/s0022-5223(19)36343-3

Cited by 3 publications

(2 citation statements)

References 42 publications

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“…In agreement with our previous studies [ 5 , 6 ] and findings from other laboratories [ 4 , 11 , 16 , 33 , 39 ], HT was found to be accompanied by a decline in RBF to about half of that under normal conditions. Since MAP remained largely unchanged, the depression of the blood flow resulted from a twofold increase in renal vascular resistance.…”

Section: Discussionsupporting

confidence: 93%

Effect of nitric oxide on renal autoregulation during hypothermia in the rat

Broman

Carlström

Källskog

et al. 2017

Pflugers Arch - Eur J Physiol

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Hypothermia-induced reduction of metabolic rate is accompanied by depression of both glomerular perfusion and filtration. The present study investigated whether these changes are linked to changes in renal autoregulation and nitric oxide (NO) signalling. During hypothermia, renal blood flow (RBF) and glomerular filtration rate (GFR) were reduced and urine production was increased, and this was linked with reduced plasma cGMP levels and increased renal vascular resistance. Although stimulation of NO production decreased vascular resistance, blood pressure and urine flow, intravenous infusion of the NO precursor L-arginine or the NO donor sodium nitroprusside did not alter RBF or GFR. In contrast, inhibition of NO synthesis by Nw-nitro-L-arginine led to a further decline in both parameters. Functional renal autoregulation was apparent at both temperatures. Below the autoregulatory range, RBF in both cases increased in proportion to the perfusion ±pressure, although, the slope of the first ascending limb of the pressure-flow relationship was lower during hypothermia. The main difference was rather that the curves obtained during hypothermia levelled off already at a RBF of 3.9 ± 0.3 mL/min then remained stable throughout the autoregulatory pressure range, compared to 7.6 ± 0.3 mL/min during normothermia. This was found to be due to a threefold increase in, primarily, the afferent arteriolar resistance from 2.6 to 7.5 mmHg min mL−1. Infusion of sodium nitroprusside did not significantly affect RBF during hypothermia, although a small increase at pressures below the autoregulatory range was observed. In conclusion, cold-induced rise in renal vascular resistance results from afferent arteriolar vasoconstriction by the autoregulatory mechanism, setting RBF and GFR in proportion to the metabolic rate, which cannot be explained by reduced NO production alone.

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Section: Discussionsupporting

confidence: 93%

Effect of nitric oxide on renal autoregulation during hypothermia in the rat

Broman

Carlström

Källskog

et al. 2017

Pflugers Arch - Eur J Physiol

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“…It is unclear why the patient in this case needed early banding, atypically, in the 1 st week of life; it may possibly be the result of the concomitant therapeutic hypothermia. Surface-induced hypothermia exacerbates pulmonary overcirculation in the patient with a left-to-right shunt, by increasing the systemic vascular resistance almost without changing the pulmonary vascular resistance,[ 5 ] which potentially gives a clue of the atypically progressing pulmonary overcirculation in this case. Although there remained a possibility of postponing the pulmonary trunk banding by vasodilator usage after the rewarming, the situation was difficult due to the additional complications regarding the hypotension and congestive heart failure with almost a maximum treatment.…”

Section: Discussionmentioning

confidence: 99%

Tricuspid atresia 1c accompanying neonatal encephalopathy treated with pulmonary trunk banding and therapeutic hypothermia

Cao,

Shibasaki,

Tachibana

2023

Annals of Pediatric Cardiology

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The influence of therapeutic hypothermia, known to improve neurodevelopmental outcomes in neonatal encephalopathy, remains unknown in newborns with severe congenital heart diseases. We report a neonate with tricuspid atresia type 1c suffering from moderate neonatal encephalopathy. A burst suppression pattern on amplitude-integrated electroencephalography recovered after inducing moderate therapeutic hypothermia, but exacerbated pulmonary overcirculation still persisted even after the rewarming. Since the medical treatment for pulmonary overcirculation had reached the limit, semi-urgent pulmonary trunk banding was performed on the 4th day of life. Postoperative brain magnetic resonance imaging showed no apparent brain injuries; the patient was discharged uneventfully. We share our perioperative management experience of a patient with tricuspid atresia type Ic who required therapeutic hypothermia for neonatal encephalopathy.

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