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Arterial Resistance (arterial + resistance)
Selected AbstractsIntratesticular arterial resistance and testicular volume in infertile men with subclinical varicoceleJOURNAL OF CLINICAL ULTRASOUND, Issue 8 2004Nevbahar Akcar MD Abstract Purpose The aim of this study was to evaluate whether intratesticular arterial resistance and testicular volume differed between infertile men with subclinical varicoceles and infertile men without varicoceles. Materials and Methods Fifty-eight infertile men were examined by gray-scale and color Doppler sonography for presence of varicocele, testicular volume, and arterial resistance. For men in the study group, mean testicular volume and resistance index (RI) in testes with varicoceles were compared with those in the contralateral testis by the paired t-test; statistical analyses between the study and control groups were performed by independent t-tests. Results Twenty-seven men had left-sided varicoceles (96% of which were subclinical), and 31 infertile men without varicoceles served as controls. Mean volumes of the right and left testes of study subjects were 14.8 ml and 14.6 ml, respectively, and in controls were 14.2 ml and 13.6 ml, respectively. Mean RI values for the right and left testes of study subjects were 0.61 and 0.58, respectively, and in controls were 0.61 and 0.58, respectively. There were no statistically significant differences in volume or RI, either between the right and left testes within patient groups or between the control and study groups' combined mean values. While the mean intertesticular volume differences for the study and control groups were 2.2 ml and 3.4 ml, respectively, the mean intertesticular RI differences were 0.04 and 0.07, respectively. These values also did not differ significantly between the 2 groups. Conclusions Subclinical varicocele is not associated with ipsilateral testicular atrophy, and does not affect the intratesticular arterial RI. © 2004 Wiley Periodicals, Inc. J Clin Ultrasound 32:389,393, 2004 [source] A distinct nitric oxide and adenosine A1 receptor dependent hepatic artery vasodilatatory response in the CCl4 -cirrhotic liverLIVER INTERNATIONAL, Issue 7 2010Alexander Zipprich Abstract Increase of portal venous vascular resistance is counteracted by decrease of hepatic arterial vascular resistance (hepatic arterial buffer response). This process is mediated by adenosine in normal livers. In cirrhosis, hepatic arterial vascular resistance is decreased but the involvement of adenosine in this process is unknown. The aim of our study was to identify the signalling pathway responsible for the decreased hepatic arterial resistance in cirrhotic livers. Methods: Cirrhosis was induced by CCl4. Using a bivascular liver perfusion dose,response curves to adenosine of the HA were performed in the presence and the absence of pan-adenosine blocker (8-SPT), A1 blocker (caffeine) or nitric oxide synthase-blocker (l -NMMA) after preconstriction with an ,1-agonist (methoxamine). Western blot of the HA were used to measure the density of the A1 and A2a receptors. Results: Adenosine caused a dose dependent relaxation of the hepatic artery of both cirrhotic and control animals that were blocked in both groups by 8-SPT (P<0.02). The response to adenosine was greater in cirrhotic rats (P=0.016). Both l -NMMA (P=0.003) and caffeine reduced the response to adenosine in cirrhotic but not in control animals. Western blot analysis showed a higher density of A1 and a lower density of A2a receptor in cirrhotic animals (P<0.05). Conclusion: The adenosine-induced vasodilatation of the HA is increased in cirrhotic rats suggesting a role for adenosine-NO in the decreased hepatic arterial vascular resistance found in cirrhosis. This significantly greater response in cirrhosis by the A1 receptor follows the same pathway that is seen in hypoxic conditions in extra-hepatic tissues. [source] Changes in pulmonary arterial pressure in term-infants with hypoxic,ischemic encephalopathyPEDIATRICS INTERNATIONAL, Issue 6 2009Jing Liu Abstract Background:, Hypoxic,ischemic encephalopathy (HIE) is an important complication that results from birth asphyxia or some other adverse conditions and has a high risk of neonatal morbidity and mortality. It is unclear, however, whether the elevated pulmonary arterial pressure (PAP) can aggravate the condition and prognosis of HIE. The purpose of the present study was to investigate the relationship between the changes of PAP and HIE in term infants after birth asphyxia. Methods:, The left/right ventricle pre-ejection phase (LPEP/RPEP), left/right ventricle ejection time (LVET/RVET) and the ratios of LPEP/LVET and RPET/RVET were evaluated in 40 term infants with HIE and 40 healthy controls on days 1, 3, 7, and 12,14 after birth using echocardiogram. PAP such as pulmonary arterial diastolic pressure (PADP, mmHg), pulmonary arterial resistance (PAR, mmHg), and pulmonary arterial resistance/systemic resistance ratio (PAR/RS) was calculated using these indexes. Patient mortality was also evaluated. Results:, PADP, PAR, and PAR/RS were significantly higher in HIE patients than in healthy controls during the first week after birth, particularly in severe-degree HIE patients. And until the end of the first week of life, these indexes may return to the levels of healthy controls. Persistent fetal circulation (PFC) was found in nine patients (7/16 severe, 2/12 moderate HIE patients), and non-PFC was found in mild HIE patients. Two patients with PFC died. No patients without PFC died. The course of HIE was longer in patients with pulmonary hypertension than in those without. Conclusion:, Increased PAP is an important pathophysiological process that may influence the course and prognoses of HIE in infants after birth asphyxia, particular in severe HIE patients who often have PFC. Thus it is important to assess changes in PAP using echocardiography. [source] | ||||||||||