Effects of Ischemic Reperfusion Injury and Remote Conditioning on Passive Leg Raising-Induced Brachial-Artery Dilation.

OBJECTIVES: Passive leg raising (PLR) has been proposed to assess arterial vasodilator reserve and possibly endothelial function. Since endothelial function is sensitive to ischemic-reperfusion (I-R) injury, we determined the effects of I-R injury and ischemic conditioning on PLR-induced brachial-artery dilation (BAD), i.e. PLR-BAD. METHODS: We induced PLR-BAD before and after ipsilateral arm I-R injury (7.5 min of occlusion) in 20 healthy males aged 29 ± 6 years. The protocol was repeated in combination with remote conditioning stimuli (3 × 30 s of contralateral arm occlusions). RESULTS: PLR resulted in significant BAD (3.85%, p < 0.001) before but not after prolonged ischemia (0.25%, p = 0.38). I-R injury, along with either preischemic or postischemic conditioning restored the PLR-BAD response (before: 3.11%, p < 0.001 and after: 3.74%, p < 0.001). CONCLUSIONS: I-R injury blunts the BAD induced by PLR. Remote pre- and postconditioning restore this response. These findings are similar to those previously reported using hyperemia and ultrasound to assess BAD.

Spinal anesthesia using Taylor's approach helps avoid general anesthesia in short stature asthmatic patient.

The case history of a 35-year-old female patient with short stature is presented. She was posted for rectopexy in view of rectal prolapse. She was a known case of bronchial asthma. She had crowding of intervertebral spaces, which made administration of spinal anesthesia via the normal route very difficult. Taylor's approach for administration of the same was tried and proved successful, thus saving the patient from receiving general anesthesia in the presence of bronchial asthma, for a perineal surgery. The possible cause for the difficulty in administration of spinal anesthesia and the Taylor's approach are discussed, and reports of similar cases reviewed.

The ankle-brachial index is related to left ventricular ejection fraction in bonnet macaques.

UNLABELLED: Low ankle-brachial index (ABI) is a marker of peripheral arterial disease associated with higher cardiovascular risk. ABI has been found to be influenced by left ventricular ejection fraction (LVEF), but this relation is confounded by atherosclerosis. OBJECTIVES: Since nonhuman primates have a low incidence of atherosclerosis, we sought to evaluate the effect of LVEF on ABI in 24 healthy female bonnet macaques (age 83 ± 21 months). METHODS: LVEF was determined by echocardiography during anesthesia with ketamine. ABI was determined using automatic blood pressure cuff. RESULTS: Mean LVEF was 73 ± 6%. Mean ABI was 1.03 (range 0.78-1.17) with similar right and left lower limb values (p = 0.78). On univariate analysis, mean ABI was significantly correlated with LVEF (r = 0.58, p = 0.003) but not with age, crown-rump length or weight. Mean LVEF increased in a stepwise manner from lowest to highest ABI tertile (68 ± 6 vs. 73 ± 4 vs. 77 ± 5%, p = 0.008). On ordinal regression and forced multivariate linear analyses, ABI status was independently related to LVEF. CONCLUSIONS: ABI is influenced by left ventricular systolic function but not age, height, weight or mass index in bonnet macaques. Left ventricular systolic function should be accounted for when considering ABI measurements.

Comparison of passive leg raising and hyperemia on macrovascular and microvascular responses.

Passive leg raising is a simple diagnostic maneuver that has been proposed as a measure of arterial vasodilator reserve and possibly endothelial function. While passive leg raising has previously been shown to lower blood pressure, increase flow velocity and cause brachial artery dilation, its effects on microvascular flow has not been well studied. Also, passive leg raising has been directly compared previously to upper arm but never to lower arm occlusion of blood flow induced hyperemia responses. We compared changes in macrovascular indices measured by brachial artery ultrasound and microvascular perfusion measured by Laser Doppler Flowmetry induced by passive leg raising to those provoked by upper arm and lower arm induced hyperemia in healthy subjects. Upper arm induced hyperemia increased mean flow velocity by 398%, induced brachial artery dilatation by 16.3%, and increased microvascular perfusion by 246% (p<.05 for all). Lower arm induced hyperemia increased flow velocity by 227%, induced brachial artery dilatation by 10.8%, and increased microvascular perfusion by 281%. Passive leg raising increased flow velocity by 29% and brachial artery dilatation by 5.6% (p<.05 for all), but did not change microvascular perfusion (-5%, p=ns). In conclusion, passive leg raising increases flow velocity orders of magnitude less than does upper arm or lower arm induced hyperemia. Passive leg raising-induced brachial artery dilatation is less robust than either of these hyperemic techniques. Finally, although upper arm and lower arm hyperemia elicits macrovascular and microvascular responses, passive leg raising elicits only macrovascular responses.

The effects of ischemia with and without remote conditioning on hyperemia induced decline in carotid-radial pulse wave velocity.

Ischemic conditioning has long held promise for preventing ischemic-reperfusion (I-R) injury. Although a number of studies have evaluated the effects of brief repeated episodes of ischemia before a prolonged ischemic episode on the cardiovascular system using clinical endpoints, more sensitive techniques by which to measure its effects are lacking. Since endothelial function is sensitive to I-R injury, flow mediated dilation of the brachial artery has been proposed for this purpose, but has significant limitations. Hyperemia normally decreases carotid to radial pulse wave velocity (PWV). Accordingly, we sought to determine the effects of I-R injury and ischemic conditioning on the hyperemic change (Δ) in PWV. We induced hyperemia by release of arterial cuff occlusion before and after ipsilateral arm I-R injury (7.5min occlusion) in 25 healthy males, age 29±6 years. The protocol was repeated on 2 occasions in combination with either pre- or post- conditioning stimuli (3× 30s contralateral arm occlusions). Hyperemia resulted in a significant decrease (-13.7%, p<.001) before but not after prolonged ischemia (-0.88%, p=0.40). I-R along with either pre- or post-ischemic conditioning restored the PWV decline (pre: -11.0%, p<0.001; post: -9.9%, p<0.001). In conclusion, 7.5min ischemia blunts the normal PWV decline produced by hyperemia. Remote pre- and post-conditioning restores this response. This technique may be useful for the assessment of novel treatment strategies and mechanisms underlying remote pre- and post-ischemic conditioning in protecting the cardiovascular system.