Hemodynamic and tissue blood flow responses to long-term pneumoperitoneum and hypercapnia in the pig.

BACKGROUND: Increased peritoneal blood flow may influence the ability of cancer cells to adhere to and survive on the peritoneal surface during and after laparoscopic cancer surgery. Carbon dioxide (CO2) pneumoperitoneum is associated with a marked blood flow increase in the peritoneum. However, it is not clear whether the vasodilatory effect in the peritoneum is related to a local or systemic effect of CO2. METHODS: In this study, 21 pigs were exposed to pneumoperitoneum produced with either CO2 (n = 7) or helium (He) (n = 7) insufflation at 10 mmHg for 4 h, or to two consecutive levels of hypercapnia (7 and 11 kPa) (n = 7) produced by the addition of CO2 to the inhalational gas mixture. Tissue blood flow measurements were performed using the colored microsphere technique. RESULTS: Blood flow in peritoneal tissue increased during CO2, but not He, pneumoperitoneum, whereas it did not change at any level of hypercapnia alone. There was no change in blood flow in most organs at the partial pressure of CO2 (PaCO2) level of 7 kPa. However, at a PaCO2 of 11 kPa, blood flow was increased in the central nervous system, myocardium, and some gastrointestinal organs. The blood flow decreased markedly in all striated muscular tissues during both levels of hypercapnia. CONCLUSION: The effect of CO2 on peritoneal blood flow during laparoscopic surgery is a local effect, and not attributable to central hemodynamic effects of CO2 pneumoperitoneum or high systemic levels of CO2.

Effect of carbon dioxide pneumoperitoneum on tissue blood flow in the peritoneum, rectus abdominis, and diaphragm muscles.

BACKGROUND: Changes in local blood flow may play a role in the pathogenesis of port-site metastasis. This study aimed to investigate the effect of pneumoperitoneum induced by carbon dioxide (CO2) on the blood flow in the peritoneum and abdominal wall muscle layers, which are target structures for this phenomenon. METHODS: The study was performed on domestic farm swine of both genders weighing 20 to 25 kg. Intraabdominal pressures (IAP) of 0, 5, and 10 mmHg were produced by either CO2 ( n = 9) or helium (He) ( n = 6) insufflations. The colored microsphere technique was used to measure blood flow distributions in the parietal peritoneum, rectus abdominis, and diaphragm muscles. RESULTS: Insufflation of CO2 was associated with a threefold increase in blood flow of the parietal peritoneum at both 5 and 10 mmHg IAP ( p < 0.001 for both pressure levels). In contrast, insufflation of He caused a significant decrease in blood flow in the parietal peritoneum at both 5 and 10 mmHg ( p < 0.05). In the rectus abdominis and diaphragm muscles, blood flow remained unchanged after insufflation of CO2 at both 5 and 10 mmHg IAP. However, after insufflation of He, there was a substantial decrease in blood flow both in the rectus abdominis and diaphragm muscles at both 5 mmHg ( p < 0.01 and p < 0.05, respectively) and 10 mmHg ( p < 0.001 and p < 0.01, respectively). CONCLUSIONS: Despite high intraabdominal pressure, tissues surrounding the abdominal cavity, particularly the peritoneum, respond to insufflation of CO2 with increased blood flow, which may favor the growth of tumor cells.

Mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine.

Acid back diffusion into the rat stomach mucosa leads to gastric vasodilation. We hypothesized that histamine, if released from the rat mucosa under such conditions, is mast cell derived and involved in the vasodilator response. Gastric blood flow (GBF) and luminal histamine were measured in an ex vivo chamber. Venous histamine was measured from totally isolated stomachs. Mucosal mast cells (MMC), submucosal connective tissue mast cells (CTMC), and chromogranin A-immunoreactive cells (CgA IR) were assessed morphometrically. After mucosal exposure to 1.5 M NaCl, the mucosa was subjected to saline at pH 5.5 (control) or pH 1.0 (H(+) back diffusion) for 60 min. H(+) back diffusion evoked a marked gastric hyperemia, increase of luminal and venous histamine, and decreased numbers of MMC and CTMC. CgA IR cells were not influenced. Depletion of mast cells with dexamethasone abolished (and stabilization of mast cells with ketotifen attenuated) both hyperemia and histamine release in response to H(+) back diffusion. GBF responses to H(+) back diffusion were attenuated by H(1) and abolished by H(3) but not H(2) receptor blockers. Our data conform to the idea that mast cells are involved in the gastric hyperemic response to acid back diffusion via release of histamine.

Effect of increased intraabdominal pressure on cardiac output and tissue blood flow assessed by color-labeled microspheres in the pig.

BACKGROUND: Studies of the hemodynamic effects associated with the pneumoperitoneum have had controversial results. We set out to investigate the effect of increased intraabdominal pressure (IAP) on cardiac output and tissue blood flow in various intraabdominal and extraabdominal organs using the color-labeled microsphere (CLM) technique. METHODS: IAP was induced by CO2 insufflation in anesthetized pigs; 0, 5, and 10 mmHg was used in the low-pressure group and 0, 15, and 24 mmHg in the high-pressure group. Tissue blood flow (ml.min-1.g-1) and cardiac output (CO) (ml/min) were determined by the CLM technique. RESULTS: CO decreased at IAP > or = 15 mmHg. Arterial PaCO2 and hydrogen ion concentration increased in response to all levels of IAP. Arterial PaO2, oxygen saturation, and bicarbonate ion concentration remained unchanged. Low IAP did not influence tissue blood flows in most of the organs. However, in the spleen, pancreas, esophagus, and gastric mucosal specimens, tissue blood flow was significantly decreased at 24 mmHg. CONCLUSION: The level of IAP used in current practice (10-12 mmHg) appears to be safe with regard to hemodynamic variables and tissues blood flow; however, higher levels may induce a decrease in cardiac output and tissue blood flow.

Substance P may attenuate gastric hyperemia by a mast cell-dependent mechanism in the damaged gastric mucosa.

Calcitonin gene-related peptide (CGRP) released from sensory neurons, which are closely apposed to mast cells and blood vessels, mediates gastric hyperemia in response to acid challenge of the damaged mucosa. Substance P (SP) is coreleased with CGRP from sensory neurons, but the role of this peptide in gastric blood flow regulation is largely unknown. Chambered rat stomachs were exposed to 1.5 M NaCl and acidic saline after treatment with SP, aprotinin (serine protease inhibitor), and the mast cell stabilizers ketotifen and sodium cromoglycate (SCG). Gastric hyperemia (measured with a laser Doppler flow velocimeter) after hypertonic injury and acid challenge was nearly abolished by SP. Aprotinin infused together with SP and pretreatment with ketotifen and SCG before SP restored the gastric hyperemia. Ketotifen and SCG inhibited mast cell degranulation in SP-treated rats. Preservation of gastric hyperemia was correlated with improved mucosal repair. These data suggest that impaired hyperemia by SP during acid challenge of the gastric mucosa may be mediated by a mast cell-dependent mechanism involving the release of proteases from mast cells.