Regional blood flow during simulated diving in the conscious Weddell seal

1979 ◽  
Vol 47 (5) ◽  
pp. 968-973 ◽  
Author(s):  
W. M. Zapol ◽  
G. C. Liggins ◽  
R. C. Schneider ◽  
J. Qvist ◽  
M. T. Snider ◽  
...  

Changes in regional blood flow during simulated normobaric diving were studied in the conscious Antarctic Weddell seal (Leptonychotes weddelli) by injecting 25-microns radioactive microspheres into the left ventricle. Injections were performed before and 8--12 min after submersion of the head in iced seawater. Diving was associated with a fall in cardiac output from a mean control value of 39.8 +/- 10.2 to 5.6 +/- 3.4 l/min (mean +/- SD) and in heart rate from 52 +/- 15 to 15 +/- 4 beats/min. Blood flow to the splanchnic and peripheral vascular bed was reduced by more than 90%, cerebral blood flow was unchanged, right and left ventricular blood flow decreased by 85%, and adrenal blood flow decreased by 39%. The pulmonary fraction of the injected microsphere dose increased from 7.9 to 29.9% during diving. This may signify a large increase of peripheral arteriovenous shunting during the dive and/or increased bronchial artery blood flow. It is concluded that blood flow during diving is directed to organs and tissues according to their metabolic requirements.

1992 ◽  
Vol 72 (4) ◽  
pp. 1563-1570 ◽  
Author(s):  
G. Piedimonte ◽  
J. I. Hoffman ◽  
W. K. Husseini ◽  
W. L. Hiser ◽  
J. A. Nadel

Stimulation of sensory nerves in the airway mucosa causes local release of the neuropeptides substance P and calcitonin gene-related peptide (CGRP). In this study we used a modification of the reference-sample microsphere technique to measure changes in regional blood flow and cardiac output distribution produced in the rat by substance P, CGRP, and capsaicin (a drug that releases endogenous neuropeptides from sensory nerves). Three sets of microspheres labeled with different radionuclides were injected into the left ventricle of anesthetized F344 rats before, immediately after, and 5 min after left ventricular injections of capsaicin, substance P, or CGRP. The reference blood sample was withdrawn from the abdominal aorta and was simultaneously replaced with 0.9% NaCl at 37 degrees C. We found that stimulation of sensory nerves with a low dose of capsaicin causes a large and selective increase in microvascular blood flow in the extrapulmonary airways. The effect of capsaicin is mimicked by systemic injection of substance P but not by CGRP, suggesting that substance P is the main agent of neurogenic vasodilation in rat airways.


1990 ◽  
Vol 69 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
D. A. White ◽  
G. H. Parsons

Tracheal blood flow increases greater than twofold in response to eucapnic hyperventilation of dry gas in anesthetized sheep. To determine whether this occurs at normal minute ventilation, we studied sheep in which tracheal blood flow was measured in response to humid and dry gas ventilation while 1) awake and spontaneously breathing and 2) anesthetized and intubated during isocapnic mechanical ventilation. In additional sheep, three tracheal mucosal temperatures were measured during humid and dry gas mechanical ventilation to measure airway tissue cooling. Tracheal blood flow was determined by use of a left atrial injection of 15-microns-diam radiolabeled microspheres. Previously implanted flow probes on the pulmonary artery and the common bronchial artery allowed continuous recording of cardiac output and bronchial blood flow. Tracheal blood flow in awake spontaneously breathing sheep was 10.8 +/- 5.6 (SD) ml.min-1.100 g wet wt-1 while humid gas was breathed, and it was unchanged with dry gas. In contrast, isocapnic ventilation of intubated animals with dry gas resulted in a 10-fold increase in blood flow to the most proximal two-ring tracheal segment compared with that seen while humid gases were spontaneously ventilated [101 +/- 75 vs. 11 +/- 6 (SD) ml.min-1.100 g-1, P less than 0.05]. Despite a 10-fold increase in proximal tracheal blood flow, there was no response in distal tracheal and bronchial blood flow, as indicated by no change in the common bronchial artery blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 268 (3) ◽  
pp. H1202-H1207
Author(s):  
A. Roitstein ◽  
B. V. Cheinberg ◽  
J. Kedem ◽  
J. Tse ◽  
H. R. Weiss ◽  
...  

In a dog model of left ventricular hypertrophy (LVH) created by aortic valve plication, we examined the hypothesis that regional myocardial inotropic and metabolic responses to alpha-adrenergic stimulation would be diminished due to decreased alpha-adrenoceptor number. After systemic beta-adrenergic blockade, phenylephrine (PE, 5 micrograms.kg-1.min-1) was infused into the left anterior descending artery in eight LVH and nine control open-chest anesthetized dogs. The circumflex region served as control. In both regions, local segment work was calculated as the integrated products of force (miniature transducer) and segment shortening (ultrasonic crystals). Local myocardial O2 consumption was calculated from regional blood flow (microspheres) and O2 saturation (microspectrophotometry). A saturation radioligand binding assay was used to determine adrenoceptor number and affinity. In control animals in the treated region, PE increased work from 815 +/- 140 to 1,493 +/- 149 g.mm.min-1. In LVH, work was not significantly altered (688 +/- 142 vs. 730 +/- 149 g.mm.min-1). Regional blood flow was elevated in controls (81 +/- 10 to 141 +/- 24 ml.min-1.100 g-1) but was not changed in LVH (105 +/- 12 vs. 123 +/- 18 ml.min-1.100 g-1). In controls, but not in LVH, myocardial O2 consumption was almost doubled during PE infusion (6.2 +/- 0.9 vs. 12.0 +/- 2.1 ml O2.min-1.100 g-1). alpha-Adrenoceptor number and dissociation constants values were not different between control and LVH (15.7 +/- 2.8 vs. 16.4 +/- 2.7 fmol/mg protein; 13.2 +/- 3.4 vs. 16.9 +/- 4.3 nm, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 250 (5) ◽  
pp. H778-H785 ◽  
Author(s):  
M. Akaishi ◽  
R. M. Schneider ◽  
R. J. Mercier ◽  
J. B. Agarwal ◽  
R. H. Helfant ◽  
...  

The quantitative effects of graded ischemia on the phases of contraction in ischemic and nonischemic myocardium were studied in 10 open-chest dogs. During progressive coronary stenosis, an index of the overall severity of ischemia, total myocardial blood flow deficit (TMFD), was measured using microspheres. Segment shortening (% delta L) during the isovolumic and ejection phases of systole in the ischemic and nonischemic zones was obtained with ultrasonic crystals. In the ischemic zone, total systolic and ejection phase % delta L decreased progressively as stenosis increased; isovolumic phase % delta L showed segment elongation (bulging) during mild ischemia, which was unchanged as ischemia became severe. Total % delta L in the nonischemic zone increased progressively with increasing stenosis, reaching 132 +/- 20% of the control value when TMFD was 24.8 +/- 6.5% of total expected left ventricular (LV) myocardial blood flow. The increase in total % delta L was entirely attributable to increased ejection % delta L and correlated with indices of preload (multivariate r = 0.65) and afterload (multivariate r = 0.62). Multiple linear regression analysis revealed that augmented contraction in the nonischemic zone was best described (multivariate r = 0.94) by a combination of four hemodynamic variables estimating LV preload and afterload, which correlated in turn with the overall severity of ischemia. Thus systolic bulging in the ischemic zone is primarily an isovolumic phase phenomenon that develops initially with mild ischemia. Little additional change occurs in the isovolumic phase as ischemic severity increases, although further reductions in shortening occur in the ejection phase.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document