Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances

Daugherty, Robert M.; Scott, Jerry B.; Dabney, J. M.; Haddy, Francis J.

doi:10.1152/ajplegacy.1967.213.5.1102

Cited by 144 publications

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“…Complex interactions among a number of factors that may be influenced by development may be involved in the circulatory changes during respiratory acidosis. Individual vesselsmay dilate because of the local effects of CO2• This has been shown experimentally in a variety of vascular beds including cerebral (20), mesenteric (7), coronary (9), renal (13), and limb (13,29). On the other hand, hypercapnia provokes peripheral vasoconstriction via an effect both on the central nervous system (15) and peripheral chemoreceptors (27).…”

Section: Discussionmentioning

confidence: 99%

“…Nonlinearity characterized some of the responses of regional blood flows as well. These variable responses are not surprising when one considers that regional blood flow in hypercapnia depends upon complex interactions ofa number of factors including local vasodilation by CO 2 (7,9,13,20,29), vasodilation mediated by the pulmonary inflation reflex (12,32), vasoconstriction induced by a central effect of CO2 on vasomotor centers (15), and vasoconstriction induced by effectson peripheral chemoreceptors (27). Given the complicated nature of these interactions, one might anticipate considerable differences in the response to respiratory acidosis before and after birth.…”

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Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

1984

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SummaryThe effects of changes in PaC02on the circulation are complex, involving local vasodilation, vasodilation mediated by the pulmonary inflation reflex, and vasoconstriction due to effects on central vasomotor centers and peripheral chemoreceptors. One might anticipate that some or all of these inight differ between the fetus in uteroand the newborn. Distribution of cardiac output was measured in unanesthetized fetal (n =6) and newborn (n = 7) sheep, using the radioactive microsphere technique. Paco, rose from 44 to 70 (fetus) and 38 to 60 torr (newborn) with the addition of CO2 to room air. In the fetus, there were significant increases in central nervous system (CNS), diaphragm, and lung blood flows. No organ showed a significant decrease in flow. Local vasodilation by CO 2 was the likely cause of the increased flow to CNS. The large increase in pulmonary blood flow was most likely due to the associated rise in fetal Pao, (23 to 28 torr) that accompanied respiratory acidosis and the presence of fetal breathing movements. The rise in diaphragmatic blood flow was -likely the result of fetal breathing. In the newborn, CNS and diaphragm flows rose, but unlike the fetus, spleen and stomach flows decreased. These decreased flows in the hypercapnic newborn may have been due to stimulation of either central vasomotor centers or peripheral chemoreceptors.Abbreviations CNS, central nervous system . DAo, descending aorta DA, ductus arteriosus I, aortic isthmus PA, pulmonary artery (2, blood flow C, radioactive countsStudies of the redistribution of cardiac output induced by hypoxia in fetal and adult animals (I, 4, 10) have shown that cardiac, cerebral, and adrenal oxygen delivery is preserved at the expense of other organs. Redistribution is accomplished by a local effect of hypoxia which dilates cerebral and coronary vessels, while the chemoreceptor reflex produces vasoconstriction in skeletal muscle and splanchnic beds (16).The circulatory effects of changes in Paco-, on the other hand, have not been as carefully studied . In particular, there are no data comparing effects before and after birth. The response of cardiac output and its regional distribution to changes in Paco, has been looked at in an acute fetal preparation but blood flow was measured only in major arteries (3). Only recently has the regional blood flow response been described in quantitative detail in a conscious adult animal (21). These studies done on adult sheep have shown that the effect of CO2 on the circulation is nonlinear. Cardiac output is unchanged as Paco; increases from 36 to 58 mm Hg; however, a 35% increase occurs as Paco, is further increased to 75 mm Hg. Nonlinearity characterized some of the responses of regional blood flows as well. These variable responses are not surprising when one considers that regional blood flow in hypercapnia depends upon complex interactions ofa number of factors including local vasodilation by CO 2 (7,9, 13, 20, 29), vasodilation mediated by the pulmonary inflation reflex (12, 32), vasoconstriction ind...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

1984

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“…The arterial CO 2 tension (PaCO 2 ) plays a role in regulating a variety of circulations such as cerebral, coronary and visceral circulations (Sokolo , 1960;Daugherty et al, 1967;Cullen & Eager, 1974;Hughes et al, 1979). Although an increase in PCO 2 generally induces vasodilation except the pulmonary vasculature (Hyde et al, 1964), the mechanism underlying the vasodilatory e ect of PCO 2 seems to be complex and remains to be clari®ed.…”

Section: Introductionmentioning

confidence: 99%

Involvement of barium‐sensitive K⁺ channels in endothelium‐dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds

Okazaki

Endou

Okumura

1998

British J Pharmacology

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1 We examined the vasodilatory e ect of hypercapnia in the rat isolated mesenteric vascular bed. The preparation was perfused constantly (5 ml min 71 with oxygenated Krebs-Ringer solution, and the perfusion pressure was measured. In order to keep the extracellular pH (pHe) constant (around 7.35) against a change in CO 2 , adequate amounts of NaHCO 3 were added to Krebs-Ringer solution. 2 In the endothelium intact preparations, an increase in CO 2 from 2.5% to 10% in increments of 2.5% decreased the 10 mM phenylephrine (PE)-produced increase in the perfusion pressure in a concentrationdependent manner. Denudation of the endothelium by CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-l-propanesulphonate) (5 mg l 71 , 90 s perfusion) abolished the vasodilatory e ect of hypercapnia. 3 An increase in CO 2 from 5% to 10% reduced the increases in the perfusion pressure produced by 10 mM PE and 400 nM U-46619 by 48% and 44%, respectively. N G -monomethyl-L-arginine (100 mM) and indomethacin (10 mM) did not a ect the vasodilatory e ect of hypercapnia, whereas the vasodilatory response of the preparation to hypercapnia disappeared when the preparation was contracted by 60 mM K + instead of PE or U-46619. 4 The vasodilatory e ect of hypercapnia observed in the PE-or U-46619-precontracted preparation was a ected by neither tetraethylammonium (1 mM), apamin (500 mM), glibenclamide (10 mM), nor 4-aminopyridine (1.5 mM). On the other hand, pretreatment with Ba 2+ at a concentration of 0.3 mM abolished the hypercapnia-produced vasodilation. 5 An increase in the concentration of K + in Krebs-Ringer solution from 4.5 mM to 12.5 mM in increments of 2 mM reduced the PE-produced increase in the perfusion pressure in a concentrationdependent manner. Pretreatment of the preparations with not only Ba 2+ (0.3 mM) but also CHAPS abolished the vasodilatory e ect of K + . 6 The results suggest that an increase in CO 2 produces vasodilation by an endothelium-dependent mechanism in the rat mesenteric vascular bed. The membrane hyperpolarization of the endothelial cell by an activation of the inward recti®er K + channel seems to be the mechanism underlying the hypercapnia-produced vasodilation. Neither nitric oxide nor prostaglandins are involved in this response.

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“…Six guinea pigs had Po 2 values less than 100 mg Hg. None of the Po 2 values was less than 30 mm Hg, which is reported to be the degree of hypoxemia necessary to influence vascular resistance directly 1 "' 17 and inhibit responses to constrictor stimuli in limb vasculature. 1 " Furthermore, the guinea pigs with low These values were calculated from the data in Figure 6 and the analysis of variance in Table 3.…”

Section: Discussionmentioning

confidence: 87%

Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.

Schmid¹,

Mayer²,

Mark³

et al. 1977

Circulation Research

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SUMMARY We investigated neurogenic, non-neurogenic, and structural contributions to vascular resistance in hindquarters in five groups of guinea pigs after heart failure produced by (1) constriction of the pulmonary artery (RHF), (2) constriction of the ascending aorta (LHF A ), and (3) constriction of the descending thoracic aorta (LHF D ); (4) after left ventricular hypertrophy produced by mild constriction of the ascending aorta (LVH); and (5) after sham surgery. Pressure-flow curves were used to assess vascular resistance in the isolated, perfused hindquarters. In RHF and LHF A , vascular resistance tended to increase and for different reasons. In the LHF A group, sympathectomy produced the greatest vasodilation. Therefore, neurogenic influences predominated. The high neurogenic tone may have been related to reduced arterial pulse pressure (P < 0.05) and reflexes arising in arterial baroreceptors. In contrast, the LHF D group had increased arterial pressure and pulse pressure (P < 0.05) and normal neurogenic vasoconstriction. However, non-neurogenic vasoconstriction was increased probably as a result of increased vascular responsiveness to constrictor stimuli. In the RHF group, papaverine produced the greatest vasodilation (P < 0.05). Therefore, non-neurogenic influences predominated. This was attributed to both increased vascular responsiveness and to altered humoral stimuli. Similar maximal vasodilation indicated that structural factors contributed equally to vascular resistance in all the groups. These results indicate differences in the regulation of vascular resistance in anesthetized, guinea pig models of right and left heart failure.THE RELATIVE importance of neurogenic, humoral, vascular reactive, and structural contributions to vascular resistance in heart failure has not been established. Some investigators have suggested that the neurogenic contribution is predominant. "4 Others have reported observations that detract from this concept. In one study, for example, the reflex vasoconstrictor response to carotid occlusion was less in dogs with right heart failure than in normal dogs. 5 In two other studies reported from our own laboratory, the neurogenic influence, as estimated from the vasodilator response to sympathectomy, was not abnormally increased in hamsters with cardiomyopathy 6 or in dogs with right heart failure. 7 These observations have led us to consider the possibility that various types of heart failure might differ with regard to the relative importance of the factors regulating vascular resistance. Theoretical considerations would appear to support this possibility. Mechanoreceptors in the right and left atria may mediate different compensatory changes. Brennan et al. 8 have suggested that mechanoreceptors in the right atrium modulate plasma levels of renin. Brennan et al. 8 and Johnson et al. reflex control of vascular resistances. Thus, in left and right heart failure, which could stress different populations of mechanoreceptors, the factors contributing to vascular resistance mi...

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Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances

Cited by 144 publications

References 0 publications

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

Involvement of barium‐sensitive K⁺ channels in endothelium‐dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds

Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.

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Local effects of O2 and CO2 on limb, renal, and coronary vascular resistances

Cited by 144 publications

References 0 publications

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

Distribution of Cardiac Output in Fetal and Neonatal Lambs with Acute Respiratory Acidosis

Involvement of barium‐sensitive K+ channels in endothelium‐dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds

Differences in the regulation of vascular resistance in guinea pigs with right and left heart failure.

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Involvement of barium‐sensitive K⁺ channels in endothelium‐dependent vasodilation produced by hypercapnia in rat mesenteric vascular beds