Vital Organ Blood Flow During Deliberate Hypotension in Dogs

Abstract

Increasing the inspiratory concentration of isoflurane is a commonly used technique for producing deliberate hypotension (DH) when isoflurane is used as the principal anesthetic. When an intravenous anesthetic technique is used, DH can be produced by the administration of a peripheral vasodilator, eventually in association with low concentrations of isoflurane. The aim of this investigation was to compare the effects of these two different approaches on vital organ blood flow. DH was induced in 12 mongrel dogs with two different anesthetic techniques: inhaled anesthesia with isoflurane (ISO) or an intravenous anesthetic technique combining propofol and alfentanil in combination with the alpha-adrenoreceptor antagonist, urapidil, and isoflurane at low end-expiratory concentrations. Mean arterial pressure (MAP) was initially decreased by 20% of its baseline and then to 50 mm Hg. Vital organ blood flows and the cerebral metabolic rate for oxygen were determined at each decrement in MAP, and after discontinuation of DH. A decrease in cardiac output was observed in the ISO group when MAP was decreased to 50 mm Hg. Cerebral blood flow was constantly and significantly higher in the ISO group. The cerebral metabolic rate for oxygen did not change compared to baseline values in both groups. At a MAP of 50 mm Hg, a decrease in renal blood flow was observed in both groups. Splanchnic blood flow remained stable in the intravenous anesthetic group in contrast to the ISO group where splanchnic blood flow decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of anesthetic drugs on canine splenic volume determined via computed tomography

“…9 The authors of that study did not propose a mechanism for such a finding, but redistribution of blood from peripheral to central compartments may be implicated. Propofol causes systemic hypotension, which may result in blood redistribution to the spleen.…”

Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling

“…It is known that the degree of the decrease of cerebral perfusion is correlated to the severity of brain damage [3]. Taken together, less pronounced redistribution may explain the higher frequency of hypoxic-ischemic brain damage in the cortex as compared to the subcortex of patients with hemorrhagic shock [7,9,10,11,12]. …”

“…This is based on (i) the proven ability of urapidil to lower arterial blood pressure [39]; (ii) the selective inhibition of α1A-ARs by urapidil [35,37]; and (iii) the proven role (by gene knock-out) of α1A-AR in maintenance of arterial blood pressure [40]. Furthermore it has been shown previously that urapidil decreases vascular resistance in all tissues without affecting cardiac output [10] and does not affect baseline CBF [11,12]. From that, we hypothesized that cortical CBF might be preserved with urapidil treatment.…”

“…The origin of this vulnerability remains unclear. It is generally attributed to (1) high susceptibility of cortical neurons to ischemia or (2) to insufficient maintenance of cortical perfusion compared to subcortical structures [10,11,12]. Resolving this issue will be of crucial importance for clinical medicine since it may lead to development of new strategies for attenuating cortical damage during shock.…”

Redistribution of Tissue Blood Flow After Stellate Ganglion Block in the Rabbit

“…Renal blood flow was decreased by 40% during deliberate hypotension, although this decrease never reached the critical level. 21 In addition, there are no reports of impaired liver function during deliberate hypotension in patients with normal liver function. 22 In this study, changes in visceral blood flow after SGB might be of no clinical significance because the decreases in LBF and RBF were slight and blood pressure showed no major change.…”