Cardiovascular responses to diving and involuntary submergence in the rhinoceros auklet (Cerorhinca monocerata Pallas)

1992 ◽  
Vol 70 (12) ◽  
pp. 2303-2310 ◽  
Author(s):  
Richard Stephenson ◽  
Michael S. Hedrick ◽  
David R. Jones
Keyword(s):  
Steady State ◽  
Lung Ventilation ◽  
Cardiovascular Responses ◽  
Arterial Blood ◽  
Cerorhinca Monocerata ◽  
Arterial Blood Oxygen ◽  
Lactate Levels ◽  
Progressive Accumulation ◽  
Physiological Research ◽  
Rhinoceros Auklet

Cardiovascular responses during diving behaviour were recorded via a cannulated carotid artery in five rhinoceros auklets. Heart rate and mean arterial blood pressure were unchanged from predive values during both escape and feeding dives. The responses to feeding dives and escape dives did not differ. Acidosis, accompanying elevated steady-state plasma lactate levels during escape diving activity, was partially compensated by lung ventilation between dives. The absence of progressive accumulation of lactate in the blood implies that an aerobic steady state was attained, despite the short intervals between dives (2.4 ± 0.4 s). Arterial blood oxygen tension was maintained at reduced levels (50–60 mmHg; 1 mmHg = 133.322 Pa) for up to 32 min of continuous escape diving activity. Immersion of restrained auklets or capture of diving auklets in a net provoked a rapid and intense bradycardia. Growth of hand-reared auklet nestlings peaked at a time corresponding to the natural fledging age for this species but the urge to leave the nest box was not triggered by reduced food availability, as has been suggested for wild semi-precocial alcids. Potential pitfalls in the maintenance and use of alcids in physiological research are discussed.

Gas exchange and its control in non-steady-state systems: the consequences of evolution from water to air breathing in the vertebrates

1988 ◽  
Vol 66 (1) ◽  
pp. 109-123 ◽  
Author(s):  
G. Shelton ◽  
P. C. Croghan
Keyword(s):  
Steady State ◽  
Gas Exchange ◽  
Dynamic Models ◽  
Continuous Process ◽  
Circulatory System ◽  
Lung Ventilation ◽  
Burst Duration ◽  
Air Breathing ◽  
Arterial Blood ◽  
Dissociation Curves

Control of breathing and gas exchange has been extensively investigated in unimodal animals, particularly mammals, in which ventilation is characteristically a regular and continuous process and gas exchange approximates to a steady-state system. Both static and dynamic models have been developed in control-theory analyses. Similar analyses are possible in unimodal fish, though few have been carried out. Control in bimodal animals, such as air-breathing fish and amphibians, is more difficult to understand and model. The evolutionary change from water to air breathing in vertebrates involves not only the adjustment of many control processes but also the development, in the early stages, of non steady states in gas exchangers, blood, and tissues. A simple control-system model, differing from mammalian counterparts in its greater emphasis on storage functions and its intermittently activated controller, is described for two suggested stages in the evolution of air breathing. The first of these stages is air gulping, in which a fixed and rather brief pattern of air breathing is activated by internal signals generated as a result of the inadequacy of the gills to provide sufficient oxygen for tissue metabolism. The second stage is that of burst breathing, in which lung ventilation is both begun and ended by internal signals so that burst duration is variable. The effects of adjusting parameters on variables of evolutionary importance, such as dive duration, burst duration, store renewal, and metabolic rate, can be examined in these two versions of the model. Refinements to incorporate arterial and venous compartments in the circulatory system, the shunting of venous and arterial blood streams in the heart, realistic oxygen dissociation curves, controller inputs from a wider range of sources, and the capacity to respond to some conditions with changes in ventilation rate as well as in burst and dive durations, are being developed. They should make the complex, non-steady-state interactions between gas exchangers, circulating blood, and tissues easier to understand and indicate the likely steps toward the evolution of steady-state systems seen in birds and mammals.

Developmental changes in respiratory, febrile, and cardiovascular responses to PGE2 in newborn lambs

2000 ◽  
Vol 278 (6) ◽  
pp. R1460-R1473 ◽  
Author(s):  
T. C. Tai ◽  
S. L. Adamson
Keyword(s):  
Adult Life ◽  
Lung Ventilation ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Periodic Breathing ◽  
Developmental Changes ◽  
Postnatal Life ◽  
Newborn Period ◽  
Arterial Blood ◽  
Thyroarytenoid Muscle

PGE2 has centrally mediated respiratory, febrile, and cardiovascular effects that markedly differ between fetal and adult life. We hypothesized that the transition from fetal to adult responses to PGE2 occurs in the newborn period. Thus effects of an intracarotid infusion of PGE2 (3 μg/min for 60 min) were determined in unanesthetized newborn lambs at 5, 10, and 15 days after birth. At 5 days, PGE2 reduced central CO2 sensitivity, reduced lung ventilation due to a decrease in breathing frequency, and induced hypercapnia. By 15 days, these effects of PGE2 had waned significantly. In contrast, phasic (expiratory) thyroarytenoid muscle electromyogram activity, number of short apneas, and incidence of Biot periodic breathing were similarly increased at all three ages. PGE2 induced a sustained fever at 10 and 15 days. Heart rate and mean arterial blood pressure were unchanged in contrast to marked increases observed by others in adults. Results showed that the transition from fetal to adult respiratory and febrile responses to PGE2 occurs in early postnatal life, whereas adult cardiovascular responses develop later in life in sheep.

Effects of feeding on metabolism, gas transport, and acid-base balance in the bullfrog Rana catesbeiana

2000 ◽  
Vol 278 (1) ◽  
pp. R185-R195 ◽  
Author(s):  
Morten Busk ◽  
Frank B. Jensen ◽  
Tobias Wang
Keyword(s):  
Rana Catesbeiana ◽  
Sartorius Muscle ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Integrative Study ◽  
Base Balance ◽  
Arterial Blood Oxygen ◽  
Lactate Levels

Massive feeding in ectothermic vertebrates causes changes in metabolism and acid-base and respiratory parameters. Most investigations have focused on only one aspect of these complex changes, and different species have been used, making comparison among studies difficult. The purpose of the present study was, therefore, to provide an integrative study of the multiple physiological changes taking place after feeding. Bullfrogs ( Rana catesbeiana) partly submerged in water were fed meals (mice or rats) amounting to ∼[Formula: see text] of their body weight. Oxygen consumption increased and peaked at a value three times the predigestive level 72–96 h after feeding. Arterial[Formula: see text] decreased slightly during digestion, whereas hemoglobin-bound oxygen saturation was unaffected. Yet, arterial blood oxygen content was pronouncedly elevated because of a 60% increase in hematocrit, which appeared mediated via release of red blood cells from the spleen. Gastric acid secretion was associated with a 60% increase in plasma [Formula: see text]concentration[Formula: see text]]) 48 h after feeding. Arterial pH only increased from 7.86 to 7.94, because the metabolic alkalosis was countered by an increase in[Formula: see text] from 10.8 to 13.7 mmHg. Feeding also induced a small intracellular alkalosis in the sartorius muscle. Arterial pH and [Formula: see text] returned to control values 96–120 h after feeding. There was no sign of anaerobic energy production during digestion as plasma and tissue lactate levels remained low and intracellular ATP concentration stayed high. However, phosphocreatine was reduced in the sartorius muscle and ventricle 48 h after feeding.

Blood Sampling From Scalp Arteries in Infants

PEDIATRICS ◽  
1973 ◽  
Vol 51 (1) ◽  
pp. 120-122
Author(s):  
Mureen A. Schlueter ◽  
Barbara B. Johnson ◽  
Dorothy A. Sudman ◽  
Leslie Y. Wang ◽  
Paulette Namkung ◽  
...  
Keyword(s):  
Steady State ◽  
Superficial Temporal Artery ◽  
Temporal Artery ◽  
Blood Oxygen ◽  
The Past ◽  
Arterial Blood ◽  
Arterial Blood Oxygen ◽  
Intermittent Sampling ◽  
Inspired Oxygen ◽  
Scalp Arteries

Frequent measurements of arterial blood oxygen tension are necessary in order to regulate the amount of environmental oxygen needed by infants with cardiopulmonary disease.1 In 1964, Thomsen2 described a technique for intermittent sampling of arterial blood from the temporal artery of small infants. Since we have successfully used a modification of her method during the past 6½ years, we thought it useful to describe our procedure and our experience with it. Technique For sampling, we insert a needle into the lumen of the frontal or parietal branch of the superficial temporal artery which we located by palpation. We try to perform the puncture when the infant is in a "steady state," by which we mean that breathing is regular, the infant is not agitated, and the concentration of inspired oxygen has been constant for at least 15 minutes.

scholarly journals Accumulation of Prostacyclin in Rat Brain during Haemorrhagic Hypotension—Possible Role of PGI2 in Autoregulation

1984 ◽  
Vol 4 (1) ◽  
pp. 107-109 ◽  
Author(s):  
E. Shohami ◽  
A. Sidi
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Control Group ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Arterial Blood ◽  
Haemorrhagic Hypotension ◽  
Potent Vasodilator ◽  
Prostaglandin F

The effect of haemorrhagic hypotension on the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto prostaglandin F1α (6-keto-PGF1α) in cortical tissue of rats was studied. Lightly anesthetized rats were subjected to steady-state hypotension for 15 min, with a mean arterial blood pressure of 80, 60, and 40 mm Hg, and compared to a control group of normotensive rats. No significant change was found in the levels of PGE2 and TXB2. The level of 6-keto-PGF1α increased from 7.8 ± 0.9 to 14.1 ± 1.9 pg/mg protein (p < 0.02) at 80 mm Hg. Our findings suggest that prostacyclin, which is a potent vasodilator, might play a role in setting the lower limit of the autoregulation range.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

A model of anemic tissue perfusion after blood transfusion shows critical role of endothelial response to shear stress stimuli

2021 ◽  
Author(s):  
Weiyu Li ◽  
Amy G. Tsai ◽  
Marcos Intaglietta ◽  
Daniel M. Tartakovsky
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Blood Transfusion ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Arterial Blood Flow ◽  
Microvascular Blood Flow ◽  
No Production ◽  
Arterial Blood ◽  
Transfusion Requirements

­­ ­Although some of the cardiovascular responses to changes in hematocrit (Hct) are not fully quantified experimentally, available information is sufficient to build a mathematical model of the consequences of treating anemia by introducing RBCs into the circulation via blood transfusion. We present such a model, which describes how the treatment of normovolemic anemia with blood transfusion impacts oxygen (O2) delivery (DO2, the product of blood O2 content and arterial blood flow) by the microcirculation. Our analysis accounts for the differential response of the endothelium to the wall shear stress (WSS) stimulus, changes in nitric oxide (NO) production due to modification of blood viscosity caused by alterations of both hematocrit (Hct) and cell free layer thickness, as well as for their combined effects on microvascular blood flow and DO2. Our model shows that transfusions of 1- and 2-unit of blood have a minimal effect on DO2 if the microcirculation is unresponsive to the WSS stimulus for NO production that causes vasodilatation increasing blood flow and DO2. Conversely, in a fully WSS responsive organism, blood transfusion significantly enhances blood flow and DO2, because increased viscosity stimulates endothelial NO production causing vasodilatation. This finding suggests that evaluation of a patients' pre-transfusion endothelial WSS responsiveness should be beneficial in determining the optimal transfusion requirements for treating anemic patients.

scholarly journals Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses

2002 ◽  
Vol 93 (6) ◽  
pp. 1918-1924 ◽  
Author(s):  
Robert Carter ◽  
Thad E. Wilson ◽  
Donald E. Watenpaugh ◽  
Michael L. Smith ◽  
Craig G. Crandall
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Heat Dissipation ◽  
Sweat Rate ◽  
Local Heating ◽  
Cardiovascular Responses ◽  
Maximal Heart Rate ◽  
Exercise Recovery ◽  
Active Recovery ◽  
Arterial Blood

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 ± 3, forearm: 48 ± 3%max) compared with during inactive recovery (chest: 21 ± 2, forearm: 25 ± 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 ± 0.10, forearm: 0.46 ± 0.10 mg · cm−2 · min−1) compared with during inactive recovery (chest: 0.28 ± 0.10, forearm: 0.14 ± 0.20 mg · cm−2 · min−1); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.

scholarly journals Arterial blood sampling in male CD-1 and C57BL/6J mice with 1% isoflurane is similar to awake mice

2018 ◽  
Vol 125 (6) ◽  
pp. 1749-1759 ◽  
Author(s):  
Ashley M. Loeven ◽  
Candace N. Receno ◽  
Caitlin M. Cunningham ◽  
Lara R. DeRuisseau
Keyword(s):  
Cardiovascular Responses ◽  
Blood Chemistry ◽  
Blood Sampling ◽  
Optimal Time ◽  
Mouse Strains ◽  
Breathing Frequency ◽  
Breathing Patterns ◽  
Suitable Alternative ◽  
Arterial Blood Sampling ◽  
Arterial Blood

Isoflurane (ISO) is a commonly used anesthetic that offers rapid recovery for laboratory animal research. Initial studies indicated no difference in arterial Pco2 ([Formula: see text]) or pH between conscious (NO ISO) and 1% ISO-exposed CD-1 mice. Our laboratory investigated whether arterial blood sampling with 1% ISO is a suitable alternative to NO ISO sampling for monitoring ventilation in a commonly studied mouse strain. We hypothesized similar blood chemistry, breathing patterns, and cardiovascular responses with NO ISO and 1% ISO. C57BL/6J mice underwent unrestrained barometric plethysmography to quantify the pattern of breathing. Mice exposed to hypoxic and hypercapnic gas under 1% ISO displayed blunted responses; with air, there were no breathing differences. Blood pressure and heart rate were not different between NO ISO and 1% ISO-exposed mice breathing air. Oxygen saturation was not different between groups receiving 2% ISO, 1% ISO, or air. Breathing frequency stabilized at ~11 min of 1% ISO following 2% ISO exposure, suggesting that 11 min is the optimal time for a sample in C57BL/6J mice. Blood samples at 1% ISO and NO ISO revealed no differences in blood pH and [Formula: see text] in C57BL/6J mice. Overall, this method reveals similar arterial blood sampling values in awake and 1% ISO CD-1 and C57BL/6J mice exposed to air. Although this protocol may be appropriate in other mouse strains when a conscious sample is not feasible, caution is warranted first to identify breathing frequency responses at 1% ISO to tailor the protocol. NEW & NOTEWORTHY Conscious arterial blood sampling is influenced by extraneous factors and is a challenging method due to the small size of mice. Through a series of experiments, we show that arterial blood sampling with 1% isoflurane (ISO) is an alternative to awake sampling in C57BL/6J and CD-1 male mice breathing air. Monitoring breathing frequency during 1% ISO is important to the protocol and should be closely followed to confirm adequate recovery after the catheter implantation.

Intravenous morphine-induced activation of vagal afferents: peripheral, spinal, and CNS substrates mediating inhibition of spinal nociception and cardiovascular responses

1992 ◽  
Vol 68 (4) ◽  
pp. 1027-1045 ◽  
Author(s):  
A. Randich ◽  
C. L. Thurston ◽  
P. S. Ludwig ◽  
J. D. Robertson ◽  
C. Rasmussen
Keyword(s):  
Intravenous Administration ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Vagal Afferents ◽  
Spinothalamic Tract ◽  
Depressor Response ◽  
Arterial Blood ◽  
Intravenous Morphine ◽  
Cervical Vagotomy

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)

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