Cardiac Output in the Large Cephalopod Octopus Dofleini

1965 ◽  
Vol 42 (3) ◽  
pp. 475-480
Author(s):  
KJELL JOHANSEN

The cardiac output in Octopus dofleini has been measured, making use of the Fick principle. The measurements were made on intact animals, resting or free-swimming, after previous chronic implantation of intravascular catheters for collection of blood samples. The respiratory exchange was measured with a specially designed respirometer. In addition to cardiac output the following parameters were measured or computed: oxygen consumption; oxygen tension, oxygen content and percentage saturation of venous and arterial blood; arterial pressure; heart rate; stroke volume and stroke work. A detailed discussion of the results obtained is limited by the lack of comparable information for other invertebrates.

Perfusion ◽  
1987 ◽  
Vol 2 (1) ◽  
pp. 39-50 ◽  
Author(s):  
Esther P Hill ◽  
David C Willford ◽  
William Y Moores ◽  
Ronald Bellamy ◽  
William H Heydorn

Oxygen consumption was measured in 10 anaesthetized, surgically instrumented domestic pigs on cardiopulmonary bypass while cardiac output (pump flow rate) was decreased. Oxygen consumption data (calculated by the Fick principle from blood flow rate and arterial and mixed venous content measurements) were plotted against total oxygen transport (TOT=QCaO2, where Q is pump flow rate and CaO2 is arterial blood oxygen content). Oxygen consumption (VO2) measurements were made in each animal at two haematocrits (approximately 30%, which is normal for pigs, and approximately 15%). In five of the animals (Group I) the measurements were made with normal haematocrit first, the blood was then haemodiluted with plasma or Dextran, and the measurements were repeated. In the remaining five animals (Group II), the haematocrit orderwas reversed. The plots showed two regions: above a certain value of TOT which we call critical TOT, VO2 was relatively independent of TOT, while at lower values of TOT, VO2 decreased approximately linearly with TOT. At the low haematocrit, the critical TOT (±S.E.M) was significantly lower ( P <0.05) than at normal haematocrit (6.9 ± 0.9 vs. 10.7 ± 1.2 ml/min/kg). Below the critical TOT, the curves for the two haematocrit levels were not significantly different. Above the critical TOT, the average VO2 was lower at the low haematocrit than at the normal haematocrit (6.0 ± 0.6 vs. 8.8 ± 1.1 ml/min/kg).


1965 ◽  
Vol 43 (3) ◽  
pp. 411-420 ◽  
Author(s):  
M. A. Chiong ◽  
P. F. Binnion ◽  
J. D. Hatcher

The cardiovascular effects of an intravenous injection of pronethalol (2.5 mg/kg) and the effect of this agent on the cardiovascular changes induced by an infusion of adrenaline (0.2 μg/kg per minute) were investigated in intact anaesthetized dogs. Fifteen minutes after the administration of pronethalol, significant increases were observed in oxygen consumption, right ventricular systolic pressure, and haematocrit, and decreases in arterial blood pressure and total peripheral resistance. Arterial hypotension and a fall in stroke work were the only changes noted at 30 minutes. There was considerable variability in cardiac output, stroke volume, and heart rate but, on the average, no significant change was observed. Pretreatment with pronethalol abolished or significantly reduced the adrenaline-induced rises in cardiac output, heart rate, stroke volume, stroke work, oxygen consumption, right ventricular systolic pressure, and arterial haematocrit, and reversed the changes in diastolic arterial pressure and peripheral resistance. It is concluded that pronethalol is not devoid of sympathomimetic activity and that it effectively blocks the adrenaline responses mediated by β-receptors.


1966 ◽  
Vol 44 (1) ◽  
pp. 77-92
Author(s):  
VANCE A. TUCKER

1. Oxygen consumption, stroke volume, heart rate and the difference in oxygen contents of arterial and venous blood (AV difference) were measured in the resting iguana at body temperatures of 20, 30 and 38° C. Oxygen consumption increased by a factor of 4.4 as temperature changed from 20 to 38° C. This increase was accomplished by a decrease in stroke volume by a factor of 0.5, and increases in heart rate and AV difference by factors of 4.1 and 2.2, respectively. 2. During activity increases in oxygen consumption at a given temperature were accompanied by increases in heart rate and AV difference, but stroke volume did not change consistently. 3. The percentage saturation of arterial blood with oxygen in the iguana may differ in the right and left systemic arches. In some lizards, both arches carried equally saturated blood, but in others the left arch carried blood containing less oxygen than the right arch. 4. An hypothesis is presented concerning the function of the double systemic arches and incompletely divided ventricles of lizards. These structures may be a device for permitting increased cardiac output associated with thermoregulation to bypass the lungs while maintaining a supply of well-oxygenated blood to the head. 5. Data on oxygen capacity, percentage saturation of blood with oxygen, haematocrit and pH of iguana blood are included in this study.


1964 ◽  
Vol 207 (6) ◽  
pp. 1345-1348 ◽  
Author(s):  
Vojin Popovic

After chronic cannulation of the aorta and right ventricle with polyethylene tubes, ground squirrels re-entered hibernation and were used for cardiac output determinations (Fick principle). The cardiac output of a 210- to 220-g hibernating ground squirrel at a body temperature of 7 C was about 1.0 ml/min, about 65 times smaller than in the active state. A similar decrease occurred in the oxygen consumption of the hibernating animals. The arteriovenous difference of oxygen contents of the blood was unchanged in hibernation despite somewhat decreased oxygen content of arterial blood. The hematocrit ratio was 57 vol % in euthermic ground squirrels and only 40 in hibernating animals.


1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.


2020 ◽  
Vol 1 (1) ◽  
pp. 72-9
Author(s):  
Alfan Mahdi Nugroho ◽  
Yusmein Uyun ◽  
Annemarie Chrysantia Melati

Analgesia epidural telah diperkenalkan secara rutin sebagai salah satu modalitas analgesia pada proses persalinan sejak lama. Hubungan antara analgesia epidural persalinan dengan demam intrapartum pada maternal sudah disebutkan pada beberapa literatur. Demam didefinisikan sebagai peningkatan suhu tubuh lebih dari 38 oC yang didapat dari dua kali pemeriksaan. Beberapa teori yang disebutkan antara lain perubahan termoregulasi, infeksi pada ibu-janin dan inflamasi non-infeksi yang dimediasi oleh sitokin proinflamasi. Namun demikian berbagai mekanisme analgesia epidural dapat menyebabkan demam masih terus diteliti. Identifikasi demam pada ibu saat persalinan merupakan hal yang penting untuk dilakukan karena memiliki konsekuensi klinis pada ibu dan neonatus. Pada ibu ditemukan suhu yang meningkat dikaitkan dengan peningkatan denyut jantung ibu, curah jantung, konsumsi oksigen, dan produksi katekolamin. Sedangkan pada janin demam intrapartum dapat menyebabkan sepsis, perubahan skor APGAR, peningkatan kebutuhan bantuan napas dan kejadian kejang. Efek demam pada ibu dan janin masih terus dipelajari, sehingga suatu saat didapatkan cara pencegahan yang paling baik yang pada akhirnya menghindarkan keraguan untuk melakukan analgesia persalinan.   Fever during labour epidural analgesia Abstract Epidural analgesia has been routinely introduced as one of the analgesia modalities during labour. Literature has mentioned the relationship between epidural analgesia and intrapartum fever among mothers. Fever is defined as increased temperature above 38 oC in more than two measurements. Several theories have been proposed, inculing thermoregulation changes, mother-fetal infection, and non-infectious inflammation mediated by proinflammatory cytokines. However, these mechanisms have been continued to evolve. Fever identification in pregnant women is essential to recognize clinical consequences to both mothers and neonates. Increased temperature in mothers is associated with increased heart rate, cardiac output, oxygen consumption, and catecholamines production. Meanwhile, in neonates intrapartum fever is related to sepsis, APGAR score changes, the need of respiratory support and incidence of neonatal seizure. Therefore, these consequences are extensively studied in order to determine the appropriate prevention.


2001 ◽  
Vol 204 (10) ◽  
pp. 1719-1727 ◽  
Author(s):  
S. Imbrogno ◽  
L. De Iuri ◽  
R. Mazza ◽  
B. Tota

Nothing is known about the effects of nitric oxide (NO) on cardiac performance in fish. Using an in vitro working heart preparation that generates physiological values of output pressure, cardiac output and ventricular work and power, we assessed the effects of NO on the cardiac performance of the eel Anguilla anguilla. We examined basal cardiac performance (at constant preload, afterload and heart rate), the effects of cholinergic stimulation and the Frank-Starling response (preload-induced increases in cardiac output at constant afterload and heart rate). The NO synthase (NOS) inhibitors N(G)-monomethyl-l-arginine (l-NMMA) and l-N(5)(1-iminoethyl)ornithine (l-NIO), the guanylate cyclase inhibitor 1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ) and Triton X-100, a detergent that damages the endocardial endothelium, all increased stroke volume (V(S)) and stroke work (W(S)). In contrast, the endogenous NOS substrate l-arginine, tested before and after treatment with haemoglobin, the NO donor 3-morpholinosydnonimine, tested with and without the superoxide scavenger superoxide dismutase, and the stable cGMP analogue 8-bromoguanosine 3′,5′-cyclic monophosphate (8-Br-cGMP) decreased V(S) and W(S). Acetylcholine chloride produced a biphasic effect. At nanomolar concentrations, in 34 % of the preparations, it induced a NO-cGMP-dependent positive inotropism that required the integrity of the endocardial endothelium. Pretreatment with Triton X-100 or with NO-cGMP pathway inhibitors (l-NMMA, l-NIO, N(G)-nitro-l-arginine methyl ester, Methylene Blue and ODQ) abolished the positive effect of acetylcholine. In contrast, at micromolar concentrations, acetylcholine produced a negative effect that involved neither the endocardial endothelium nor the NO-cGMP pathway. Pre-treatment with l-arginine (10(−)(6)mol l(−)(1)) was without effect, whereas l-NIO (10(−)(5)mol l(−)(1)) significantly reduced the Frank-Starling response. Taken together, these three experimental approaches provide evidence that NO modulates cardiac performance in the eel heart.


1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.


1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.


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