Vasodilation and Vasoconstriction: Real Story

Vasodilation of Blood Vessels

What is vasodilation? Definition of vasodilation

Vasodilation = (definition) is the increase in the internal diameter of blood vessels that is caused by relaxation of smooth muscle within the wall of the vessels thus causing an increase in blood flow. The opposite effect is vasoconstriction. When blood vessels dilate, the blood flow is increased due to a decrease in vascular resistance. However, for practical purposes, dilation of arteries and arterioles has the most significant therapeutic value since these blood vessels are the main contributors to systemic vascular resistance and, therefore, dilation of arteries and arterioles leads to an immediate decrease in arterial blood pressure and heart rate (hence, chemical arterial dilators are used to treat heart failure, systemic and pulmonary hypertension, and angina). Dilation of venous blood vessels decreases venous blood pressure. Such agents can be used to reduce cardiac output, venous and arterial pressure, tissue edema (due to better capillary fluid filtration), and myocardial oxygen demands. Let us consider, unlike useless official medical sources, practical or real-life aspects of vasodilation and vasoconstriction.

Content of this page:
Vasodilation and CO2: most potent vasodilator
Who is going to suffer from vasoconstriction?
Studies related to CO2-induced vasodilation and vasoconstriction
Vasodilation and vasoconstriction in simple terms
YouTube Video about CO2 - Vasodilation effect
References

Vasodilation, vasoconstriction and CO2: most potent vasodilator

Brain: normal breathing - vasodilation, hyperventilation - vasoconstriction Among arterial dilators, natural vasodilation agent CO2 is probably the most powerful chemical. The vasodilation effect is present in healthy people due to normal arterial CO2 concentration. According to Dr. M. Kashiba, MD and his medical colleagues from the Department of Biochemistry and Integrative Medical Biology, School of Medicine, Keio University in Tokyo, CO2 is a "potent vasodilator" (Kashiba et al, 2002), while Dr. H. G. Djurberg and his team from the Department of Anesthesia, Armed Forces Hospital, in Riyadh, Saudi Arabia suggested that "Carbon dioxide, a most potent cerebral vasodilator..." (Djurberg et al, 1998).

Nitric oxide is another very potent vasodilator that is generated within the human body from foods. More about Most Pot ent Natural Vasodilators: CO2 and NO.

Who is going to suffer from vasoconstriction?

Since CO2 is the most potent vasodilator, vasoconstriction should be a problem for those people who suffer from arterial hypocapnia. This relates to people with hyperventilation (or breathing more than the medical norms) and normal or nearly normal ventilation-perfusion ratio (e.g., no problems with lungs). Indeed, people with, for example, COPD, may hyperventilate, but their blood CO2 is generally higher than normal. Here are some studies that explain blood flow and vasodilation-vasoconstriction in the healthy and sick people.

Minute ventilation rates (chronic diseases)

Condition	Minute ventilation	Number of people	All references or click below for abstracts
Normal breathing	6 L/min	-	Medical textbooks
Healthy Subjects	6-7 L/min	>400	Results of 14 studies
Heart disease	15 (±4) L/min	22	Dimopoulou et al, 2001
Heart disease	16 (±2) L/min	11	Johnson et al, 2000
Heart disease	12 (±3) L/min	132	Fanfulla et al, 1998
Heart disease	15 (±4) L/min	55	Clark et al, 1997
Heart disease	13 (±4) L/min	15	Banning et al, 1995
Heart disease	15 (±4) L/min	88	Clark et al, 1995
Heart disease	14 (±2) L/min	30	Buller et al, 1990
Heart disease	16 (±6) L/min	20	Elborn et al, 1990
Pulm hypertension	12 (±2) L/min	11	D'Alonzo et al, 1987
Cancer	12 (±2) L/min	40	Travers et al, 2008
Diabetes	12-17 L/min	26	Bottini et al, 2003
Diabetes	15 (±2) L/min	45	Tantucci et al, 2001
Diabetes	12 (±2) L/min	8	Mancini et al, 1999
Diabetes	10-20 L/min	28	Tantucci et al, 1997
Diabetes	13 (±2) L/min	20	Tantucci et al, 1996
Sleep apnea	15 (±3) L/min	20	Radwan et al, 2001
Liver cirrhosis	11-18 L/min	24	Epstein et al, 1998
Hyperthyroidism	15 (±1) L/min	42	Kahaly, 1998
Epilepsy	13 L/min	12	Esquivel et al, 1991
CHV	13 (±2) L/min	134	Han et al, 1997
Panic disorder	12 (±5) L/min	12	Pain et al, 1991
Bipolar disorder	11 (±2) L/min	16	MacKinnon et al, 2007
Dystrophia myotonica	16 (±4) L/min	12	Clague et al, 1994

Studies related to CO2-induced vasodilation and vasoconstriction

Dr. K. P. Buteyko and his colleagues found vasoconstrictive effects of hypocapnia (CO2 deficiency) on arteries and peripheral blood vessels (Buteyko et al, 1964a; Buteyko et al, 1964b; Buteyko et al, 1964c; Buteyko et al, 1965; Buteyko et al, 1967), while additional CO2 causes vasodilation, which is a normal state of arteries and arterioles.

Patients and doctors As western physiological studies found, vasodilation requires normal arterial CO2 concentration, while hypocapnia (low CO2 concentration in the arterial blood) decreased perfusion of the following organs due to vasoconstriction:
- brain (Fortune et al, 1995; Karlsson et al, 1994; Liem et al, 1995; Macey et al, 2007; Santiago & Edelman, 1986; Starling & Evans, 1968; Tsuda et al, 1987),
- heart (Coetzee et al, 1984; Foëx et al, 1979; Karlsson et al, 1994; Okazaki et al, 1991; Okazaki et al, 1992; Wexels et al, 1985),
- liver (Dutton et al, 1976; Fujita et al, 1989; Hughes et al, 1979; Okazaki, 1989),
- kidneys (Karlsson et al, 1994; Okazaki, 1989),
- spleen (Karlsson et al, 1994),
- colon (Gilmour et al, 1980).
Some abstracts from these studies are provided at the bottom of this page.

Vasodilation and vasoconstriction in simple terms

Vasodilation effect due to CO2 What is the physiological mechanism of the reduced blood flow to vital organs? Arteries and arterioles have their own tiny smooth muscles that can constrict or dilate (vasodilation) depending on CO2 concentrations. When the breathe more, CO2 level becomes smaller, blood vessels constrict and vital organs (like the brain, heart, kidneys, liver, stomach, spleen, colon, etc.) get less blood supply. Similarly, hypocapnia causes spasm of all other smooth muscles of the human body: airways or bronchi and bronchioles, diaphragm, colon, bile ducts, etc.

This effect explains why sick people have less blood going to their brains, heart, liver, and other vital organs. Normal breathing pattern provides people with normal perfusion and oxygen supply for all vital organs due to CO2 vasodilation. However, since modern people breathe more than the medical norm (hyperventilate), they have to suffer from CO2 deficiency effects.

Are there any related systemic effects? The state of these blood vessels (arteries and arterioles) define total resistance to the systemic blood flow in the human body. Hence, hypocapnia increases strain on the heart. Normal CO2 parameters make resistance to blood flow in the cardiovascular system small. Hence, breathing directly participates in regulation of the heart rate. The father of cardiorespiratory physiology, Yale University Professor Yandell Henderson (1873-1944), investigated this effect about a century ago.

Among his numerous physiological studies, he performed experiments with anaesthetized dogs on mechanical ventilation. The results were described in his publication "Acapnia and shock. - I. Carbon dioxide as a factor in the regulation of the heart rate". In this article, published in 1908 in the American Journal of Physiology, he wrote, "... we were enabled to regulate the heart to any desired rate from 40 or fewer up to 200 or more beats per minute. The method was very simple. It depended on the manipulation of the hand bellows with which artificial respiration was administered... As the pulmonary ventilation increased or diminished the heart rate was correspondingly accelerated or retarded" (p.127, Henderson, 1908).

Be observant. When you get a small bleeding cut or a wound, deliberately hyperventilate and see if that can help stop the bleeding. It should due to vasoconsctriction. As an alternative, perform comfortable breath holding and breathe less and accumulate CO2. What would happen with your bleeding? (It should increase due to vasodilation.) Now you know what to do after dental surgeries, brain traumas, and other accidents involving bleeding. It is natural for humans and other animals to breathe heavily in such conditions. Hence, hyperventilation can be life-saving in cases of severe bleeding.

Group of doctors As many health professionals found, blood flow to vital organs is directly proportional to blood CO2 concentrations. Consider this example of vasodilation - vasoconstriction. According to the Handbook of Physiology (Santiago & Edelman, 1986), cerebral blood flow decreases 2% for every mm Hg decrease in CO2 pressure. When people have 20 mmHg CO2 in their blood (half of the official norm), they have about 40% less blood supply to the brain in comparison with normal conditions. Only skeletal muscles can get more blood in conditions of hyperventilation.

"…cerebral blood flow decreases 2% for every mm Hg decrease in CO2" Professor Newton, University of Southern California Medical Center, Hyperventilation Syndrome, 2004 June 17, Topic 270, p. 1-7 (www.emedicine.com).

Personal experiment. Take 100 deep and fast breaths through the mouth and you can pass out due to ... lack of oxygen and poor blood supply for the brain. Why? Because CO2 is a vasodilator (dilator of blood vessels).

Note that there is another powerful chemical NO (nitric oxide) that is also able to produce vasodilation, while its lack causes vasoconstriction. Humans generate nitric oxide in sinuses and, hence, mouth breathing prevents us from inhaling our own nitric oxide (see web page: Nasal Nitric Oxide Effects). Meanwhile, as some medical studies claim, CO2 is a most powerful known vasodilator.

YouTube Video about CO2 - Vasodilation-Vasoconstriction effect

A first part of this video clip explains how and why voluntary forceful hyperventilation leads to fainting: when we start to breathe heavily, CO2 content in the arterial blood sharply falls within seconds and blood vessels (arteries and arterioles) constrict since CO2 is the key factor in vasodilation.

Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and Body Oxygen in Healthy, Normal and Sick People
Breathing norms Parameters, graph, and description of the normal breathing pattern
6 breathing myths 6 myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the Sick. Table 1. Western scientific evidence about prevalence of CHV (chronic hyperventilation) in patients with various chronic conditions (34 medical studies)
Normal Minute Ventilation in Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of Normal People (24 medical publications)
HV and hypoxia How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
Body oxygen test How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy Table 4. CP (body oxygen level) in healthy people (27 medical studies)
Body oxygen in sick Table 5. CP (body oxygen level) in sick people (14 medical studies)
Buteyko Table of Health Zones with clinical description of most common zones
Morning HV Morning hyperventilation effect or how and why critically ill people are most likely to die during early morning hours

References: CO2 Effects Web Pages
Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
The Bohr effect How and why oxygen is released by red blood cells in tissues
Cell Oxygen Levels and oxygen transport are controlled by alveolar CO2 and breathing
Oxygen Transport depends on breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by breathing since hypoxia leads to or intensifies chronic inflammation through over-expression of the hypoxia-inducible factor 1, while normal breathing reduces these processes
Nerve stabilization takes place due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
Brochodilation - dilation of airways (bronchi and bronchioles) by carbon dioxide, and their constriction due to hypocapnia
CO2: Best Natural Cough Suppressant and "home remedy" since it calms urge-to-cough nerve receptors located in the tracheobronchial tree and larynx
Blood pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions
CO2 myth "CO2 is a toxic waste gas" myth
Breathing control How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic?

Some quotes from medical studies about CO2 - (most) potent vasodilator

Coetzee A, Holland D, Foëx P, Ryder A, Jones L, The effect of hypocapnia on coronary blood flow and myocardial function in the dog, Anesthesia and Analgesia 1984 Nov; 63(11): p. 991-997.

The effect of hypocapnia on global and regional myocardial function and coronary blood flow (CBF) was studied in dogs anesthetized with halothane before and after critical constriction of the left anterior descending (LAD) coronary artery. Coronary blood flow decreased 29% (P less than 0.05) when hypocapnia was induced in dogs with a normal LAD artery. Critical constriction reduced CBF by 42% (P less than 0.05)...

Dutton R, Levitzky M, Berkman R, Carbon dioxide and liver blood flow, Bull Eur Physiopathol Respir. 1976 Mar-Apr;12(2): p. 265-273.

... Thus, hypercapnia alone increases total liver blood flow, primarily by an increase in portal vein flow. Hypoxia results in a decrease in portal vein flow. The superimposition of hypercapnia on hypoxia restores blood flow to a level close to that found with hypercapnia alone. Hypercapnia in the range of 63 +/- 4 mmHg PCO2 overwhelms the tendency toward a reduction of portal vein blood flow induced by an arterial PO2 of 42 +/- 5 mmHg in the presence of mild hypocapnia (PCO2 : 30.2 +/- 1 mmHg).

Foëx P, Ryder WA, Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions, Bull Eur Physiopathol Respir 1979 Jul-Aug; 15(4): p.625-638.
...The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption.

Fortune JB, Feustel PJ, deLuna C, Graca L, Hasselbarth J, Kupinski AM, Cerebral blood flow and blood volume in response to O2 and CO2 changes in normal humans, J Trauma. 1995 Sep; 39(3): p. 463-471.

Changes in cerebral blood volume (CBV) after head injury may be an important determinant of intracranial pressure (ICP). To determine the normal response of CBV to hypoxemia, hypercapnia, and hypocapnia, eight normal subjects (5 males and 3 females; ages 25 to 43) were studied under these conditions... For conditions of hypocapnia, hypercapnia, and hypoxemia, the percentage of change in CBV was: -7.2 +/- 0.01, 12.8 +/- 0.01, and 5.2 +/- 0.03, respectively. The simultaneous percentage of change in CBF for the same conditions was -30.7 +/- 4.0, 29.5 +/- 9.2, and 18.4 +/- 6.9, respectively...

Fujita Y, Sakai T, Ohsumi A, Takaori M, Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle, Anesthesia and Analgesia 1989 Aug; 69(2): p. 152-157.

... Hypocapnia caused a decrease in HABF (hepatic artery blood flow) without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure...

Karlsson T, Stjernström EL, Stjernström H, Norlén K, Wiklund L, Central and regional blood flow during hyperventilation. An experimental study in the pig, Acta Anaesthesiol Scand. 1994 Feb; 38(2): p.180-186.

Blood flow to the cerebellum decreased soon after the induction of hyperventilation, whereas the cerebral blood flow did not decrease until the second hour of hyperventilation. Cardiac output, splanchnic perfusion and portal vein blood flow all decreased. Myocardial perfusion and arterial blood flow to spleen and kidney decreased while pancreatic and liver arterial blood flows were unaffected...

Liem KD, Kollée LA, Hopman JC, De Haan AF, Oeseburg B, The influence of arterial carbon dioxide on cerebral oxygenation and haemodynamics during ECMO in normoxaemic and hypoxaemic piglets, Acta Anaesthesiol Scand Suppl. 1995; 107: p.157-164.

OBJECTIVE. To investigate the cerebrovascular response to changes in arterial CO2 tension during extracorporeal membrane oxygenation (ECMO) in normoxaemic and hypoxaemic piglets. METHODS. Four groups of six anaesthetized, paralysed and mechanically ventilated piglets: group 1-normoxaemia without ECMO, group 2-ECMO after normoxaemia, group 3-hypoxaemia without ECMO, and group 4-ECMO after hypoxaemia, were exposed successively to hypercapnia and hypocapnia. Changes in cerebral concentrations of oxyhaemoglobin (cO2Hb), deoxyhaemoglobin (cHHb), (oxidized-reduced) cytochrome aa3 (cCyt.aa3) and blood volume (CBV) were continuously measured using near infrared spectrophotometry. Heart rate, arterial O2 saturation, arterial blood pressure, central venous pressure, intracranial pressure (ICP) and left common carotid artery blood flow (LCaBF) were measured simultaneously. RESULTS. Hypercapnia resulted in increased CBV, cO2Hb and ICP in all groups, while cHHb was decreased...

Macey PM, Woo MA, Harper RM, Hyperoxic brain effects are normalized by addition of CO2, PLoS Med. 2007 May; 4(5): e173.

... CONCLUSIONS: In this group of children, hyperoxic ventilation led to responses in brain areas that modify hypothalamus-mediated sympathetic and hormonal outflow; these responses were diminished by addition of CO2 to the gas mixture. This study in healthy children suggests that supplementing hyperoxic administration with CO2 may mitigate central and peripheral consequences of hyperoxia.

Okazaki K, Okutsu Y, Fukunaga A, Effects of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation of liver, kidney and skeletal muscle in the dog [Article in Japanese], Masui 1989 Apr, 38 (4); p. 457-464.

We investigated the effects of carbon dioxide on the splanchnic visceral organs (liver and kidney) as well as skeletal muscle in the anesthetized dog. Thirty two adult mongrel dogs were anesthetized with sodium pentobarbital, intubated and ventilated mechanically with 100% oxygen to maintain normocapnia. After laparotomy, miniature Clark-type polarographic oxygen electrodes were placed on the surfaces of liver, kidney and rectus femoris muscle. Electromagnetic blood flow (BF) probes were also applied to hepatic artery (HA), portal vein (PV), left renal artery (RA) and left femoral artery (FA). After a stable normocapnic ventilation, the hypocapnia was produced by increasing respiratory rate, and the hypercapnia was induced by adding the exogenous carbon dioxide. Results: Hyperventilation resulted in a significant decrease in HABF, PVBF, liver surface PO2 and kidney surface PO2 in parallel with the decreased PaCO2, but these parameters increased dose dependently when the carbon dioxide was added to the inspired gas (hypercapnic hyperventilation)...

Okazaki K, Hashimoto K, Okutsu Y, Okumura F, Effect of arterial carbon dioxide tension on regional myocardial tissue oxygen tension in the dog [Article in Japanese], Masui 1991 Nov; 40(11): p. 1620-1624.

... Hypocapnic hyperventilation (PaCO2: 22 mmHg) invariably resulted in a significant reduction of coronary blood flow (LADBF) and left ventricular myocardial tissue PO2 in both epicardial and endocardial layers, while addition of carbon dioxide to the inspired gas (hypercapnic hyperventilation) reversed the change by increased LADBF and arterial PaCO2 in a dose-dependent manner. These results indicate that injudicious and severe hypocapnic hyperventilation may induce impaired myocardial tissue perfusion and oxygenation although normal cardiac output and arterial blood oxygenation are maintained.

Okazaki K, Hashimoto K, Okutsu Y, Okumura F, Effect of carbon dioxide (hypocapnia and hypercapnia) on regional myocardial tissue oxygen tension in dogs with coronary stenosis [Article in Japanese], Masui 1992 Feb; 41(2): p. 221-224.

Carbon dioxide (CO2) has been well documented to act as a potent vasodilator of coronary vessels under normal conditions...

Wexels JC, Myhre ES, Mjøs OD, Effects of carbon dioxide and pH on myocardial blood-flow and metabolism in the dog, Clin Physiol. 1985 Dec; 5(6): p.575-588.

... During hypercapnia, however, MBF (myocardial blood-flow) increased more than 40%.

Ashkanian M, Gjedde A, Mouridsen K, Vafaee M, Hansen KV, Ostergaard L, Andersen G, Carbogen inhalation increases oxygen transport to hypoperfused brain tissue in patients with occlusive carotid artery disease: increased oxygen transport to hypoperfused brain, Brain Res. 2009 Dec 22; 1304: 90-5.

... Thus, carbogen improves oxygen transport to brain tissue more efficiently than oxygen alone.

Ashkanian M, Borghammer P, Gjedde A, Ostergaard L, Vafaee M, Improvement of brain body oxygen level by inhalation of carbogen, Neuroscience. 2008 Oct 28;156(4):932-8. Epub 2008 Aug 22.

Hyperoxic therapy for cerebral ischemia is suspected to reduce cerebral blood flow (CBF), due to the vasoconstrictive effect of oxygen on cerebral arterioles. We hypothesized that vasodilation predominates when 5% CO(2) is added to the inhaled oxygen (carbogen)... Oxygen and carbogen were equally potent in increasing oxygen saturation of arterial blood (Sa(O2)). The present data demonstrate that inhalation of carbogen increases both CBF and Sa(O2) in healthy adults. In conclusion we speculate that carbogen inhalation is sufficient for optimal oxygenation of healthy brain tissue, whereas carbogen induces concomitant increases of CBF and Sa(O2).

Kallinen J, Didier A, Miller JM, Nuttall A, Grénman R, The effect of CO2- and O2-gas mixtures on laser Doppler measured cochlear and skin blood flow in guinea pigs, Hear Res. 1991 Oct;55(2):255-62.

The effects of carbogen (5% CO2: 95% O2) 10% CO2-in-air and 100% O2 on cochlear blood flow (CBF), skin blood flow (SBP), blood pressure (BP) and arterial blood gases were investigated in the anesthetized, respired or self-respiring guinea pig. In respired animals, CBF and SBF were increased with carbogen and 10% CO2-in-air and decreased with O2...

Brown JJ, Meikle MB, Lee CA, Reduction of acoustically induced auditory impairment by inhalation of carbogen gas. II. Temporary pure-tone induced depression of cochlear action potentials, Acta Otolaryngol. 1985 Sep-Oct;100(3-4):218-28.

... Carbon dioxide is a potent stimulator of cerebral and cochlear vasodilatation...

Kisilevsky M, Hudson C, Mardimae A, Wong T, Fisher J, Concentration-dependent vasoconstrictive effect of hyperoxia on hypercarbia-dilated retinal arterioles, Microvasc Res. 2008 Mar;75(2):263-8. Epub 2007 Aug 28.

BACKGROUND/AIMS: The relative effects of simultaneously administered oxygen and carbon dioxide on vascular resistance are unknown. The purpose of the study was to investigate the independent effect of oxygen partial pressure on hypercarbia-induced vasodilation in the retinal arterioles. METHODS: Twelve young healthy volunteers participated in the study. End-tidal partial pressure of carbon dioxide was raised 23% from the baseline (i.e. air) at normoxia and then maintained constant while end-tidal partial pressure of oxygen (PETO(2)) was raised in a stepwise incremental fashion. Retinal vessel diameter and blood velocity were measured in the superior-temporal arteriole using the Canon Laser Blood Flowmeter. RESULTS: Hypercarbia resulted in a 16% increase in blood velocity and a 22% increase in blood flow (p<0.05)...

Ohta K, Yachie A, Development of vascular biology over the past 10 years: heme oxygenase-1 in cardiovascular homeostasis, J Endovasc Ther. 2004 Dec;11 Suppl 2: II140-50.

... Moreover, the reaction is also the major source of carbon dioxide (CO2) in the body, which is a physiologically important gaseous vasodilator that inhibits SMC proliferation.

Ozkan M, Koramaz I, Ulus AT, Tavil Y, Filizlioglu H, Baykan EC, Eryilmaz S, Inan B, Katircioglu SF, Ozyurda U, Effect of carbon dioxide insufflation on free internal thoracic artery flows: is it a vasodilator? J Thorac Cardiovasc Surg. 2004 Sep;128(3):354-6.

...CONCLUSIONS: Carbon dioxide insufflation of the internal thoracic artery is an efficient technique to increase the flow and seems to be safe, simple, and reliable. When the internal thoracic artery is harvested in a carbon dioxide-insufflated fashion, arterial spasm and reduced early flow may be avoided, even without vasodilator agents such as papaverine.

Wise RG, Ide K, Poulin MJ, Tracey I, Resting fluctuations in arterial carbon dioxide induce significant low frequency variations in BOLD signal, Neuroimage. 2004 Apr;21(4):1652-64.

... Carbon dioxide is a potent cerebral vasodilator...

Nakahata K, Kinoshita H, Hirano Y, Kimoto Y, Iranami H, Hatano Y, Mild hypercapnia induces vasodilation via adenosine triphosphate-sensitive K+ channels in parenchymal microvessels of the rat cerebral cortex, Anesthesiology. 2003 Dec;99(6):1333-9.

BACKGROUND: Carbon dioxide is an important vasodilator of cerebral blood vessels...

Kashiba M, Kajimura M, Goda N, Suematsu M, From O2 to H2S: a landscape view of gas biology, Keio J Med. 2002 Mar;51(1):1-10.

... Carbon dioxide (CO2) is generated mainly through the Krebs cycle as a result of glucose oxidation and serves as a potent vasodilator...

Djurberg HG, Tjan GT, Al Moutaery KR, Enhanced catheter propagation with hypercapnia during superselective cerebral catherisation, Neuroradiology. 1998 Jul;40(7):466-8.

... Carbon dioxide, a most potent cerebral vasodilator, was temporarily added to the inspired gases of two anaesthetised patients undergoing superselective embolisation of an arteriovenous malformation, when the microcatheter had been impacted for a considerable time. Successful propagation of the microcatheter into the malformation was achieved in both patients after a relatively short period of hypercapnia.

References for CO2 vasodilation effect

Buteyko KP, Odintsova MP, Dyomin DV, Hyper- and Hypoxemia Effects on the Peripheral Vascular Tone, Materials of the Second Siberian Research Conference of Therapists, Irkutsk, 1964a.

Buteyko KP, Dyomin DV, Odintsova MP, Regressive Analysis in Differentiating Aerated Blood Gas Component Effects on Peripheral Arteriole Functional Conditions, Materials of the Second Siberian Research Conference of Therapists, Irkutsk, 1964b.

Buteyko KP, Zhuk EA, MIkaelyan AL, Electrocardiogram for Isolated Aortal Stenosis, Cardiologiya (Cardiology, USSR), 1964c, N 2, p. 67.

Buteyko KP, Dyomin DV, Odintsova MP, Ventilation of the Lungs and Arterial Vascular Tone Interconnection in Patients with High Blood Pressure and Angina Pectoris, Phyziologichny Zhurnal (Physiological Magazine, Ukrainian SSR) 1965. V. 11, N 5 (in Ukrainian).

Buteyko KP, Odintsova MP, Dyomin DV, Hyper- and Hypoxemia Effects on the Arterial Vascular Tone. Sovetskaya Meditsina (Soviet Medicine), 1967, N3, p.44-49.

Coetzee A, Holland D, Foëx P, Ryder A, Jones L, The effect of hypocapnia on coronary blood flow and myocardial function in the dog, Anesthesia and Analgesia 1984 Nov; 63(11): p. 991-997.

Dutton R, Levitzky M, Berkman R, Carbon dioxide and liver blood flow, Bull Eur Physiopathol Respir. 1976 Mar-Apr; 12(2): p. 265-273.

Gilmour DG, Douglas IH, Aitkenhead AR, Hothersall AP, Horton PW, Ledingham IM, Colon blood flow in the dog: effects of changes in arterial carbon dioxide tension, Cardiovasc Res 1980 Jan; 14(1): 11-20.

Foëx P, Ryder WA, Effect of CO2 on the systemic and coronary circulations and on coronary sinus blood gas tensions, Bull Eur Physiopathol Respir 1979 Jul-Aug; 15(4): p.625-638.

Fujita Y, Sakai T, Ohsumi A, Takaori M, Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle, Anesthesia and Analgesia 1989 Aug; 69(2): p. 152-157.

Hashimoto K, Okazaki K, Okutsu Y, The effects of hypocapnia and hypercapnia on tissue surface PO2 in hemorrhaged dogs [Article in Japanese], Masui 1989 Oct; 38(10): p. 1271-1274.

Henderson Y, Acapnia and shock. - I. Carbon dioxide as a factor in the regulation of the heart rate, American Journal of Physiology 1908, 21: p. 126-156.

Hughes RL, Mathie RT, Fitch W, Campbell D, Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound , J Appl Physiol. 1979 Aug; 47(2): p. 290-295.

Litchfield PM, A brief overview of the chemistry of respiration and the breathing heart wave, California Biofeedback, 2003 Spring, 19(1).

Macey PM, Woo MA, Harper RM, Hyperoxic brain effects are normalized by addition of CO2, PLoS Med. 2007 May; 4(5): p. e173.

McArdle WD, Katch FI, Katch VL, Essentials of exercise physiology (2nd edition); Lippincott, Williams and Wilkins, London 2000.

Okazaki K, Okutsu Y, Fukunaga A, Effect of carbon dioxide (hypocapnia and hypercapnia) on tissue blood flow and oxygenation of liver, kidneys and skeletal muscle in the dog, Masui 1989 Apr, 38 (4): p. 457-464.

Santiago TV & Edelman NH, Brain blood flow and control of breathing, in Handbook of Physiology, Section 3: The respiratory system, vol. II, ed. by AP Fishman. American Physiological Society, Betheda, Maryland, 1986, p. 163-179.

Starling E & Lovatt EC, Principles of human physiology, 14-th ed., 1968, Lea & Febiger, Philadelphia.

Tsuda Y, Kimura K, Yoneda S, Hartmann A, Etani H, Hashikawa K, Kamada T, Effect of hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebrovascular disorders, Eur Neurol. 1987; 27(3): p.155-163.

Wexels JC, Myhre ES, Mjøs OD, Effects of carbon dioxide and pH on myocardial blood-flow and metabolism in the dog, Clin Physiol. 1985 Dec; 5(6): p.575-588.

* Illustrations by Victor Lunn-Rockliffe

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