Blood Volume in the Hypothermic Dog

D'Amato, Henry E.; Hegnauer, A. H.

doi:10.1152/ajplegacy.1953.173.1.100

Cited by 60 publications

(6 citation statements)

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“…If the results we obtained with mild perfusion hypothermia can be applied to the more profound cooling produced by Chen and Chien, our experiments offer an explanation consistent with both the observations of Chen and Chien and others; i.e., pure plasma volume can leave the vascular compartment at the liver due to elevated sinusoid pressures, secondary to constriction of the hepatic outflow vessels. Our additional observation that water can also be lost during hypothermia as an ultrafiltrate is consistent with some (Svanes et al, 1970;Rodbard et al, 1951;Barbour, 1953;D'Amato and Hegnauer, 1953), but not all, of the observations of a decrease in plasma volume during hypothermia.…”

Section: Discussionsupporting

confidence: 88%

Mechanism of the increased vascular capacity produced by mild perfusion hypothermia in the dog.

Green¹,

Jackman²

1979

Circulation Research

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SUMMARY The mechanism of the increased vascular capacity produced by perfusion hypothermia was investigated in 20 anesthetized dogs. A right heart bypass preparation separated cardiac output (CO) into splanchnic (Q.) and nonsplanchnic (termed peripheral, Q p ) flows. Each channel drained by gravity into an external reservoir. Blood was then returned to the pulmonary artery at a constant flow of 80 ml/kg per min. Venous resistance and compliance of splanchnic (Ry, and C,) and peripheral (Rv p and Cp) channels were calculated from transient and steady state volume shifts which occurred following rapid drops in venous pressure. Arterial pressure (P.), hematocrit (H), plasma protein concentration, and changes in reservoir volume (AV^.) were also measured. PERFUSION hypothermia is the means by which body temperature can be lowered by selectively cooling the temperature of blood passing through an extracorporeal circuit. It has been long recognized that mild perfusion hypothermia (decreasing temperature to around 30°C) produces a decrease in extracorporeal reservoir blood volume at constant pump flow or a decrease in venous return at constant blood volume (i.e., an increase in vascular capacity) in both man and dog (Brown, 1962;Drew, 1966;Gollan et al., 1952;Yeh et al., 1961;Lindberg, 1959;Oz et al., 1960;Pierucci et al., 1960). Although there are several books (Cooper and Ross, 1960;Blair, 1964;Popovic and Popovic, 1974) and innumerable papers in the literature covering the subject of hypothermia, there are relatively few physiological reports of the effects of perfusion hypothermia. Furthermore, a review of the literature indicates that differences of opinion exist concern- ing the mechanism(s) of the increase in vascular capacity produced by perfusion hypothermia. This study was undertaken in an attempt to clarify the mechanism(s) responsible for this increase in vascular capacity. Methods Surgical ProceduresTwenty mongrel dogs with a mean weight of 23.0 ± 0.53 (SE) kg were anesthetized with sodium thiamylal, 18 mg/kg, iv. The anesthesia was maintained with 70% nitrous oxide in oxygen and halothane. A tracheotomy was performed and the dog was ventilated at an appropriate tidal volume and frequency for its size. A ventral laparotomy was then performed, followed by a splenectomy. The abdominal incision was not closed. The extracorporeal perfusion system used in this study (Fig. 1) has been described previously (Green, 1977;Green et al., 1978aGreen et al., , 1978b. In brief, the hepatic venous outflow of the splanchnic circulation and the circulation from the rest of the body, the peripheral channel, were isolated and cannulated. The venous return from these beds drained by gravity through separate Starling resistors and a Carolina Medical square wave electromagnetic flowmeter into an exby guest on

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Section: Discussionsupporting

confidence: 88%

Mechanism of the increased vascular capacity produced by mild perfusion hypothermia in the dog.

Green¹,

Jackman²

1979

Circulation Research

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“…Furthermore, intravascular distribution volume is reduced at low temperatures. From different studies using intact animal models, it has been reported that intravascular volume during hypothermia is reduced by 10 -35% (7,8,10,17,23). In our experiments, low and high Epi doses differed by a factor of 10, and we, therefore, think that concentration differences are comparable also at low temperatures, despite possible changes in distribution volume.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model

Kondratiev¹,

Myhre²,

Simonsen³

et al. 2006

Journal of Applied Physiology

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Rewarming from accidental hypothermia is often complicated by "rewarming shock," characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study, we tested whether epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1, 2, and 3 for dose-finding studies, and hypothermic groups 4, 5, and 6. At 20 and 24 degrees C during rewarming, group 4 (low-dose Epi) and group 5 (high-dose Epi) received bolus injections of 0.1 and 1.0 microg Epi, respectively. At 28 degrees C, Epi infusion was started in groups 4 and 5 with 0.125 and 1.25 microg/min, respectively. Group 6 served as saline control. After rewarming, both CO and stroke volume were restored in group 4, in contrast to groups 5 and 6, in which both CO and stroke volume remained significantly reduced (30%). Total peripheral resistance was significantly higher in group 5 during rewarming from 24 to 34 degrees C, compared with groups 4 and 6. This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature-dependent adrenoreceptor affinity.

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“…There was then a progressively steady decline in pressure as the hours of hypothermia progressed. By 8,16,and 24 hours the mean values for blood pressure were 33%, 44%, and 67%, respectively, less than before cooling. In general, we have found that the higher the blood pressures before cooling the higher the pressure remained during hypothermia.…”

Section: Resultsmentioning

confidence: 77%

Experimental Evaluation of Prolonged Hypothermia

Fisher¹

1955

Arch Surg

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Blood Volume in the Hypothermic Dog

Cited by 60 publications

References 0 publications

Mechanism of the increased vascular capacity produced by mild perfusion hypothermia in the dog.

Mechanism of the increased vascular capacity produced by mild perfusion hypothermia in the dog.

Cardiovascular effects of epinephrine during rewarming from hypothermia in an intact animal model

Experimental Evaluation of Prolonged Hypothermia

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